Renal 1 Flashcards

0
Q

Blood flow runs in parallel, enters through ___, exit ___ > peri-tubular capillaries in the juxto-medullary nephron - we have the longer loops of henle the peri-tubular capillaries are known as the ___.

A
  • afferent glomerulus
  • efferent
  • vasa recta
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1
Q

4 Major Terms:

1) This only occurs at the glomerulus?
2) This is going from tubule to blood?
3) This is going from blood to the tubule?
4) This is exiting passed the collecting duct?

A

1) Filtration
2) Reabsorption
3) Secretion
4) Excretion

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2
Q

Filtration is through the ___ into the ___.

A

Glomerulus

PCT

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3
Q
Intermediate structure (basically an epithelial cell) this is the working portion of any of those actions, excluding filtration. 
Reabsorption, secretion primarily focused on the tubule and what lines it are epithelial cells and then the capillaries via the endothelium. The interface btw the epithelial cell and the endothelial cell is where we get the actual movement. Where we can think of \_\_\_ and \_\_\_.
A

Secretion & reabsorption

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4
Q

Filtrate:
Concentration of these contents as we go through the nephron:
___ & ___ are important as these can be markers of kidney disease or injury. These increase as we exit towards the ___, thus we know its most likely not being reabsorbed back into the blood, stays in the tubule and will eventually become urine.

A
  • Creatinine & urea

- collecting tubule

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5
Q

Filtrate:
Proteins by the time they reach the end of the ___ they are almost gone, we have reabsorbed them. Here is where we reabsorb the majority of ___ & ___ (by the time we leave the ___) - giving us an idea of how much work is being done here.

A
  • PCT
  • glucose & amino acids
  • PCT
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6
Q

Filtrate:
___ line the proximal convoluted tubule - can reabsorb ___ & ___ a certain amount of times, if we increase the load we will put more work on them and they will die out/turn over faster. This gives us an idea of how diabetics/hyperglycemia can injure the kidney.

A
  • Epithelial cells
  • Glucose & amino acids

*The increased work causes increased epithelial cell turnover. Will reach a point where we can not make new cells at the same rate they are dying off, will have a hole or a non-functioning portion of the PCT. Why we need to manage/cut out glucose.

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7
Q

To estimate kidney function can give ___ (synthetic compound) it behaves like creatinine in that it is freely filtered. So that we know if these agents make their way to the ___ they will make their way to the ___. Freely filtered, not reabsorbed, not secreted.

A
  • Inulin
  • Glomerulus
  • PCT
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8
Q

Majority of Bicarb - have a sharp drop in the ___. At this point is where we usually have to engage ___ & ___ to help buffer the urine and again when we use these to buffer the urine we lose bases, so by using these two we create a ___.

A
  • PCT
  • Phosphates & ammonia
  • new Bicarb
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9
Q

? ? ? = sharp increase (especially with ?) as we get towards the latter end of the nephron there is fine tuning.

____ (in the beginning portion) we concentrate the urine in order to fine tune based on the bodies needs. Increase in these by the time we get to the ___ and ___. Try to drop these particular electrolytes and fine tune with the bodies needs.

A
  • K, Cl, Na
  • K
  • Loop of Henle
  • Distal tubule & collecting duct
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10
Q

Filtrate:

1) Thus __, __, __, __, __ all increase in the distal tubule and collecting duct in order to be peed out.
2) ___ & ___ (___) sharply decrease in the PCT because they are being reabsorbed.
3) ___ sharp drop in the PCT as well.

A

1) Creatinine, urea, Na, K, Cl
2) Amino acids & glucose (proteins)
3) Bicarb

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11
Q

Tubuloglomerular Feedback: thinking about the normal functions of the kidney so that when we injure/damage/cause inflammation will decrease these functions.

1) ___ deals with increase in load-this causes us to inhibit renin. Renin leads to aldosterone, aldosterone normally acts on the distal portion of the nephron (around the DCT) so by increasing the Na/K atpase pump we have increased sodium reabsorption. If we sense an increase in pressure > inhibit renin > inhibit aldosterone > inhibit increase in Na/K pump > inhibition of Na reabsorption.
2) ___ beta 1 adrenergics these will stimulate renin release, and there we want to conserve fluid volume. In a situation where we are fighting a bear, main focus is to increase blood flow to heart, lungs, muscles, not the best time to be creating wastes (kidneys/GI system).
3) ___ at the distal portion of the nephron we sense sodium chloride content, if there is high salt content it will give us an idea that we are overloaded. Therefore we inhibit renin > decrease aldosterone > decrease the action of the Na/K pump and therefore we decrease sodium reabsorption.

A

1) Baroreceptor mechanism
2) Sympathetic nerve mechanism
3) Macula densa mechanism

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12
Q

In the ___ is the ___, the sodium-glucose transporter. We can piggyback onto the concentration gradient of ___.

~Using this high sodium to low sodium inside the cell gradient, glucose can piggyback on top of that and make its way back into the blood.

On the vasolateral side - right next to the capillary or epithelial cells we have the ___ transporter - basically this follows the concentration gradient of ___.

~High glucose in the cell and low glucose in the blood > going from high to low and will follow that gradient.

*Reason why we have increased work on both sides, hyperglycemic patient you will overload both ends.

A
  • PCT
  • SGLT2
  • sodium
  • GLUT2
  • glucose
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13
Q

Acid Base Regulation:
Bicarb is a primary/initial buffer, bicarb itself is freely filtered, so any bicarb that makes its way to the ___ will find its way to the ___.

A
  • glomerulus

- PCT

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14
Q

Think of this epithelial cell as functioning in the distal tubule.

  • If we run out of bicarb we then have to use any ___ that we have left over or that we created as well as any ___. This helps to buffer any acid in the urine so we do not burn our urinary tract.
  • Remember that when we use ___ or ___ we create a new bicarb in that process.
A
  • phosphates
  • ammonia
  • phosphates
  • ammonia
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15
Q

Metabolic Acidosis: Someone drank battery acid > severely decrease your pH > increase acid filtration:
~Acute = respiratory
~Metabolic correction will take longer by increasing our acid filtration, getting rid of the acid that makes its way to the nephron. Use our ___ as well as ___ & ___ that help excrete the majority of urine as well as make or regenerate new bicarb all with the goal of returning us to a normal pH.

A
  • bicarb
  • phosphates
  • ammonia
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16
Q

Hypochloremic Metabolic Alkalosis: Losing chloride or alkalosis. Start with vomiting > first losing hydrogen therefore we become basic > hypo-ventilate to increase CO2 levels and help to decrease the pH.
~Focusing on chloride and idea of electroneutrality. Chloride is -1 if we lose this -1 charge we try to increase our reabsorption of this -1 in the form of ___. But in doing so we are essentially exacerbating this alkalosis, making us more basic. Intervention is to give ___ & ___ to stop ___ reabsorption & hopefully correct for these losses.

A
  • Bicarb
  • NaCl
  • K
  • bicarb
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17
Q

Hypochloremic Metabolic Alkalosis:
NaCl & K focus would be the + charge on this potassium & with NaCl in dealing with electroneutrality issue. Remember this ___ ___ is a reaction to this -1 charge (from loss of chloride) so we need to try to stop this increased reabsorption which is exacerbating the alkalosis.

A

bicarb reabsorption

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18
Q

Metabolic Alkalosis:
~Here we have an addition of base. Increased pH compensation is to hypo-ventilate to increase CO2 levels.
~Renal correction initial insult results in base addition or increase in pH so we can correct by decreasing our ___ of ___ and therefore increasing our excretion in the urine.

A

reabsorption of bicarb

19
Q

Respiratory Acidosis:
~Focus on how the kidneys compensate, get to the point of some sort of respiratory injury leading us to increased acid.
~Our kidneys will compensate by increasing the titration or getting rid of acid. ___ is our first buffer, then we move to ___ & ___.

A
  • Bicarb
  • phosphates
  • ammonia
20
Q

Respiratory Alkalosis:
~With respiratory alkalosis we increase ventilation and therefore decrease PCO2. Affect acid levels by decreasing protons and therefore increasing pH.
~Kidneys compensate by decreasing the acid titration, stop excreting it, hold onto ___ (acid, H+).

A

protons

21
Q

Potassium:
Potassium channel on apical side facing the lumen, the side that faces our capillaries (blood) is the basolateral side. There is the ___ on the basolateral side which is regulated by ___ = increases the expression of this pump. So we get the reabsorption of ___ (into blood) & by doing so we kick out ___ into the tubules.

A
  • Na/K pump (uses ATP)
  • aldosterone
  • sodium
  • potassium
22
Q

Potassium:
~We also have an ___ on the apical side. Acidosis can lead to ___. This exchanger contributes to this condition by stopping any sort of exchange here by not reabsorbing more acid into our acidotic condition thus we do not ___ ___.
~Inhibit this from working thus not sending potassium into the tubules, therefore holding onto potassium contributing to our hyperkalemic state.

A
  • H+/K exchanger (H+ in, K+ out)
  • Hyperkalemia
  • secrete potassium
23
Q

At the distal tubule, basically at the end of the nephron, so we are ___ anything in this region at the end of the nephron most likely this will end up as filtrate or ultra-filtrate - going to be urine.

A

secreting

24
Q

Fluid Homeostasis:
We have ___ ___ which are regulated by ___, these are basically just water channels.
Water can cross this membrane on its own (can cross any membrane on its own), just not that quickly, by increasing ___ & it then acting on these specific cells in the ___ ___ we increase the amount of water channels and therefore increase the amount of ___ ___.

A
  • Aquaporin channels
  • ADH
  • ADH
  • collecting tubule
  • water reabsorption
25
Q

___ & ___ will result in increased Na+ & water retention.

___ & ___ will result in loss of Na & water in the urine.

A
  • Aldosterone & Angiotensin 2

- Natriuretic peptides & Urodilatin

26
Q

~Urine & Blood studies most helpful in evaluating kidney function:

  • Urinalysis, Tests of GFR
  • ___ = If any of this makes its way to the glomerulus should make its way to the PCT & from there does not get reabsorbed. If in the PCT, it should be in the urine. As decreased function of the glomerulus occurs should see an increase in ___ ___.
  • ___ = breakdown products of protein metabolism.

~One of the best ways to evaluate kidney function is to look at structure - diagnostic tests = imaging, biopsy

A
  • Creatinine
  • plasma or serum Creatinine
  • BUN
27
Q

*Creatinine and urea should be making its way into the urine. Should see rise in these levels as we make our way through the nephron (not getting more as we go through nephron just becoming more
concentrated).
~We can increase creatinine levels in the urine with 2 factors in general:
1) Increase ___ of ___
2) Increased creatinine excreted by the kidney, this is associated with ?

A

1) Breakdown of muscle

2) GFR

28
Q

*If GFR working efficiently our plasma creatinine levels should be really low.
*Creatinine enters the glomerulus > PCT > pee out (this is normal functioning kidney/nephron/glomerulus).
~As our ___ slows down d/t injury our plasma creatinine increases. Not getting rid of creatinine in the normal process of the nephron.

A

~GFR

29
Q

~Both ___ & ___ are measures of GFR this can also be tested with ___. Similar to creatinine this is freely filtered, not reabsorbed, not secreted, this will be excreted.
~___ more reliable indicator of renal function than ___.

A

~Urea & Creatinine
~Inulin
~Serum creatinine
~BUN

30
Q

1) Elevation of BUN & creatinine levels, related to decrease in GFR. Associated with a number of renal diseases?
2) Elevation of urea in blood. Sign of failing excretory system and other metabolic and endocrine abnormalities?
3) Increased concentration of protein in the urine, due to leakiness of glomerular filtration barrier and/or nephron abnormalities?

A

1) Azotemia
2) Uremia
3) Proteinuria/albuminuria

31
Q

1) Presence of blood in the urine?
2) Presence of lipids in the urine?
3) Decreased urine production?
4) No urine flow?
5) Presence of bacteria in the urine?
6) Presence of leukocytes in the urine?

A

1) Hematuria
2) Lipiduria
3) Oliguria
4) Anuria
5) Bacteriuria
6) Pyuria

32
Q

1) Inflammation of the glomeruli?
2) Sign of mild glomerular abnormalities?
3) UTI is characterized by ___ & ___, infection may be symptomatic or asymptomatic affecting the kidney or bladder.
4) ??? = Renal stones, manifested by ___, ___ & recurrent stone formation.

A

1) Glomerulonephritis
2) Asymptomatic hematuria or proteinuria
3) Bacteriuria & pyuria
4) Nephrolithiasis
- renal colic
- hematuria

33
Q
  • This is known as clear cell - because with biopsy these cells have a high lipid and glycogen content when you process the tissue for histologic analysis and bleach it out > cells look clear
  • Patients will have pain, blood in the urine
  • This in general is really hard to treat
A

Renal Cell Carcinoma (RCC)

34
Q

With neoplasms staging is related to ??

A

size & spreading

35
Q

___ is a protective mechanism so if infections are going upstream (making their way up) this can be problematic.

A

Unidirectional flow

36
Q

We have maintained that infection then inflammation for a longer period of time. Remember with the later stages of inflammation is to activate fibroblasts and make scar tissue these processes can scar the kidney itself?
decrease kidney function = unable to get rid of wastes

A

Chronic Pyelonephritis

37
Q

*Take home point if an individual has a predisposition to ??? then they are predisposed to forming more.

A

form one stone

38
Q

CKD = In both dominant and recessive forms ___ will develop. This will assist in leading to ESRD.
~ ___ primarily has cyst on affected kidney itself
~ ___ cysts can appear in other organs in the abdominal viscera

A

HTN
~Recessive
~Dominant

39
Q

Glomerular Disorders: Remember there are 3 cells that make up the glomerulus:

1) ___ (part of the glomerular capillaries).
2) ___ (specialized smooth muscle cells that can constrict & dilate. Upon injury contain phenotype to be secretory, now secreting ECM leading to fibrosis, scarring & hardening of glomerulus > decreased functioning of the glomerulus & therefore decreased filtration).
3) ___ (wrap around the capillaries and provide barrier for movement of molecules based on size and charge).

A

1) Endothelial cells
2) Mesangial cells
3) Podocytes

40
Q

Glomerular Disorders - Secondary Classifications:
Glucose likes to stick to proteins. Thus in the kidney they like to stick to endothelial cells which have proteins on them. This association is a stimulus for inflammation. If you maintain high levels of glucose this association becomes permanent and therefore inflammation becomes permanent > scarring of the glomerular capillaries > scarring the glomerulus > decreasing its function and therefore function of the kidney in general.

A

Diabetic Nephropathy

41
Q

Glomerular Disorders - Secondary Classifications:
There is an antibody that for whatever reason is recognizing the basement membrane (endothelial cells sit on top of the basement membrane). This complex that binds elicits inflammatory response from there. Depositing on glomerular basement membrane.
~These ABs can also recognize the basement membrane in the lungs, often times will see the complex form in the lungs as well as the kidneys.

A

Goodpasture Syndrome

42
Q

Glomerular Disorders - Secondary Classifications:
Circulating antigen-AB that will just happen to deposit into the mesangial region of the glomerulus, it is as if we are attacking the glomerulus but really just attacking the antigen-AB complex. Damages the glomerulus.

A

Systemic Lupus Erythematosus

43
Q

Glomerular Disorders - Getting deposition of circulating complex.

1) Type 3 Hypersensitivity with ???
2) Anti-GBM (attacking the basement membrane itself) ???
3) Creating ABs directly attacking the glomerulus itself as well ???

Think is the initial insult direct to the glomerulus or is it deposition of complex that just happens to bind or deposit into tissue & we are reacting to that complex being in the glomerulus itself.

A

1) SLE
2) Goodpasture Syndrome
3) Membranous Nephropathy

44
Q

Acute Glomerulonephritis:
Don’t know why but there is deposition of immunoglobulin A into the glomerulus (IgA usually present in ducts and tracts, specifically respiratory and GI tract). IgA will find its way & will react & bind to the glomerulus this will cause a reaction & as with lupus or post-infectious will get the same sort of events that follow.

*Will have blood in the urine (hematuria)
BUT note that edema, proteinuria & HTN are NOT PRESENT

A

IgA Nephropathy, Berger Disease

45
Q

Injury to podocytes will affect the negative charge - thus things that are negatively charged won’t be repelled as much and will be able to move to the PCT and eventually the urine (example of negative charged items that can make their way because of this injury are PROTEINS).

A

Minimal Change Disease

46
Q

___ help filtration by preventing movement based on size and charge.

A

Podocytes