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Patho II, Renal > Structure - Function > Flashcards

Structure - Function Flashcards

1
Q

What is the cup shaped around the glomerulus

A

BOWMAN’S CAPUSULE

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2
Q

Smooth muscle cells found between / supporting glomerular capillaries, which can contract to regulate blood flow into the glomerulus.

They also have phagocytic properties similar to monocytes and release inflammatory cytokines and growth factors.

A

Mesangial Cells

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3
Q

What is special about the glomerular capillaries

A

They are fenestrated, and allow large amounts of solute-rich fluid (Ions and large molecules, not protein or blood cells) to pass through

They have podocytes - which make up the visceral epithelium of bowman’s capsule

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4
Q

Where does the filtrate enter the (bowman’s) capsular space

A

Filtration slits of the podocytes

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5
Q

Clefts between the foot processes of the podocytes

A

Filtration slits

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6
Q

Most nephrons are _____ They are the “hard workers” and have a shorter loop of henle

A

Cortical Nephrons

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7
Q

About 15% of nephrons are ______ They have a long loop of henle

A

Juxtaglomerular Nephrons

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8
Q

What do juxtaglomerular nephrons specialize in

A

CONCENTRATING URINE

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9
Q

Where does renal filtration occur?

A

Glomerulus

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10
Q

Where does renal reabsorption and secretion occur?

A

Tubules

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11
Q

Name the two kinds of capillaries found in nephrons

A

Glomerular - filtration!

Peritubular -

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12
Q

The only capillaries in the body that are fed and drained by an arteriole

A

Glomerular capillaries

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13
Q

When filtrate reabsorbed by the tubules, how does it return to the blood stream

A

via peritubular capillaries

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14
Q

What allows the blood pressure in the glomerular capillary bed to be so high?

A

The fact that these glomerular capillaries are fed and drained by an arteriole

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15
Q

On what forces does glomerular filtration depend

A

STARLING forces - hydrostatic and osmotic pressures

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16
Q

What makes glomeruli efficient filters?

A
  1. large surface area
  2. Surface is very permeable to water
  3. High glomerular BP (55 mmHg) (higher than capsule pressure)
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17
Q

Glomerular BP?

A

55mmHg

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18
Q

What opposes glomerular filtration?

A

Osmotic pressure in the plasma from protein

Fluid pressure in Bowman’s space

  1. Increase plasma protein (dehydration, polycythemia)
  2. Increase BS pressure
  3. Decrease BP
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19
Q

What favors glomerular filtration?

A

Glomerular capillary BP

  1. raise systemic BP
  2. Decrease pressure in BS
  3. Decrease plasma protein (blood loss, no transfusion)
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20
Q

Tubular cells are joined by _____ through which substances can _______

A

Tight junction, diffuse

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21
Q

Percentage of urea reabsorbed

A

44%

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22
Q

Percentage of Na reabsorbed

A

99.5%

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23
Q

Percentage of water reabsorbed

A

99%

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24
Q

Examples of things which are secreted in the tubules

A

H+

K+

Organic anions

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25
Q

Tubule secretion is particularly important for which homeostatic mechanism

A

Controlling blood pH (H+ secretion)

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26
Q

Normal GFR

A

90/120 ml/min

< 60 = disease

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27
Q

GFR affected by

A
  1. Filtration surface area
  2. Membrane permeability and Net Filtration Pressure (NFP)
  3. Blood pressure / flow to glomerulus
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28
Q

Key mechanisms kidneys use to regulate water and ions

A

Water reabsorption

Na reabsorption / secretion

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29
Q

Range of daily urine volume

A

400 - 2500mL

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30
Q

Renal salt wasting

A

Hypo-aldosteronism

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31
Q

Order of operations in nephron

A

Afferent arteriole > glomerulus > Prox convoluted tubule > Descending loope of henle > Loop > thin ascending loop > thick ascending loop > distal convoluted tubule > (cortex, medulla) > Collecting duct > papilla of renal pyramid > minor and major calyces >renal pelvis (Hilum) > Ureter

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32
Q

What makes up the renal corpuscle

A

Glomerulus, bowman’s capsule, mesangial cells

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33
Q

Major disorders that disrupt the glomerular filtration barrier

A

DMII, HTN, Glomerulonephritis (autoimmune)

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34
Q

Where does sodium reabsorption occur and how is it transported?

A

Occurs in all tubular segments EXCEPT the descending loop of Henle (for the countercurrent!)

Transported passively, by diffusion, from the tubular lumen to the epithelial cells. Then transported actively, via Na/K pump, from the epithelial cells to the systemic capillaries

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35
Q

By what mechanism is water reabsorbed

A

Osmosis (passive) - but ** determined by the movement of sodium and presence of aquaporins **

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36
Q

Sites for water / Na balance

A

Renal Tubules

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37
Q

Where would one find aquaporins?

A

Proximal convoluted tubule +++

Descending, loop, ascending?

NONE in collectinge ducts UNLESS YOU HAVE ADH

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38
Q

ADH is produced where and alongside what?

A

Produced in HYPOTHALAMUS

STORED in POSTERIOR PITUITARY

alongside oxytocin

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39
Q

How does ADH lead to increased aquaporins

A

increased plasma osmolarity > ADH from post pituitary >
binds receptors on basolateral membrane of COLLECTING DUCTS >
increased cAMP / PO4 >
AQP fuse w luminal membrane

40
Q

How is sodium transported in renal tubules?

A

Transported passively, by diffusion, from the tubular lumen to the epithelial cells.

Then transported actively, via Na/K pump, from the epithelial cells to the systemic capillaries

41
Q

Why is active transport of Na out of the tubule epithelial cells necessary?

A

To keep intracellular Na low and drive the diffusion gradient

42
Q

Things which might disrupt the homeostasis of passive / active Na reabsorption and subsequent H20 / glucose drafting?

A

Broken AQPs

Lack of ATP in kidney

Tubular damage w interstitial fibrosis

43
Q

How to baroreceptors in the atria and carotid arteries affect ADH

A

Lower BP at carotid / atrial baroreceptors will inhibit ADH, so the kidneys will hold on to water and increased blood volume / BP

44
Q

How does SIADH affect fluid homeostasis

A
  1. Too much ADH > too much water reabsorbed / retained

2. High BP, low Na

45
Q

How does Diabetes Insipidus affect fluid homeostasis?

A
  1. Not enough or ineffective ADH
  2. Low BP, high Na
  3. Large, dilute volumes urine
46
Q

Where does concentration of urine happen/

A

Loop of Henle

47
Q

What special function does the special structure of the loop of henle provide?

A

Countercurrent Multiplier

48
Q

Osmolarity of filtrate in proximal tubule and beginning of descending loop vs plasma

A

IT’S THE SAME IT’S THE SAME

49
Q

Describe how the osmolarity of filtrate changes throughout the tubules

A

PCT and beginning of descending loop (same as plasma)

Osmolarity increases (concentration) as filtrate travels down the descending limb - because only water is reabsorbed here. Impermeable to solutes.

Osmolarity decreases (dilutes) as filtrate travels up the ascending limb - because Na is reabsorbed. Permeable to solutes.

Filtrate entering the DCT is very dilute - as low as 70mOsm

Osmolarity either increases, decreases, or stays the same as filtrate travels down collecting duct - depending on body’s needs, presence of ADH etc

50
Q

What contributes to the medullary osmotic gradient

A

Urea recycling

51
Q

How dilute can filtrate be by the time it reaches the DCT ?

A

Very dilute - as low as 70mOsm

52
Q

How concentrated can urine become?

A

1200 mOsm

53
Q

Key controller of Na reabsorption?

A

Aldosterone

54
Q

Aldosterone site / action

A

Steroid, from adrenal cortex

Increases Na reabsorption from distal tubules and collecting ducts

** fine- tuning here - bulk reabsorption already happening in earlier tubules **

55
Q

Increases Na reabsorption from distal tubules and collecting ducts by dumping K

A

Aldosterone

Hold Na, at the expense of K

56
Q

JGA consists of

A

JG cells + Macula Densa

57
Q

Enlarged, specialized smooth muscle cells that secrete renin and control blood flow to glomerulus

A

JG cells

58
Q

Are JG cells considered endocrine?

A

YES

59
Q

What kind of receptors to JG cells use to detect BP shifts in afferent arteriole?

A

Mechanoreceptors

60
Q

How to renin and aldosterone relate?

A

JG cells detect Low BP > JG cells secrete Renin > Angiotensinogen / I / II > Aldosterone

61
Q

A group of tall, closely packed cells in the DCT which detect changes in Na / osmolarity via chemoreceptors

A

Macula Densa

62
Q

What does low Na in the DCT mean for Macula Densa?

A

Low Na = decreased filtration&raquo_space; JG cells release renin (Paracrine signaling!!)

63
Q

What controls aldosterone?

A

Renin, Angiotensin II&raquo_space;
Adrenal Cortex >
Aldosterone >
Na and H20 retention

64
Q

Three triggers for Renin release

A
  1. Low BP (JGA, less stretch = more renin)
  2. Low Na (Macula)
  3. SNS stimulation (JG)
65
Q

Atrial Natriuretic Peptide and Na

A

Increased BP > cardiac distention > ANP released

ANP > decreased aldosterone > Na dumped
ANP > afferent dilation, efferent constriction > Increased GFR

66
Q

Major extracellular buffering system

A

CO2 / HCO3 system

67
Q

Major intracellular buffers

A

Phosphate and proteins

68
Q

How do the kidney’s alter the body’s pH?

A

By altering the plasma HCO3 concentration

HCO3 is filtered, then reabsorbed or secreted in tubules according to body’s pH needs

Normally, all filtered HCO3 is “reabsorbed” (H exchange mechanism)

69
Q

A “low oxygen” environment, this area of the kidney is particularly prone to ischemia

A

Medulla!

70
Q

The structure of this area makes it particularly vulnerable to deposition of immune complexes, compliment fixation, and damage from HTN and glycosylation

A

Glomerulus!

highly vascular, fenestrated structure

71
Q

This area gets clogged by things that shouldn’t have made it through the glomerulus and is therefore prone to ischemia

A

Tubules!

RBC, WBC, Protein, Fat, Stones

72
Q

These structures are more prone to malformation, obstruction, and masses

A

“Post renal” structures - ureters, bladder

73
Q

Renal medulla is particularly prone to what kind of problem

A

Ischemia

74
Q

Glomerulus is particularly prone to what kinds of problems

A

Due to fenestrated vasculature:

Deposition of immune complexes, complement
HTN damage
Glycosylation

75
Q

Tubules are particularly prone to

A

Ischemia, clogged by large molecules that make it through damaged glomeruli (WBC, RBC, protein etc)

76
Q

Post renal structures are particularly prone to what kinds of problems

A

Malformation
Obstruction
Masses

77
Q

What “pre renal” structures can cause renal problems?

A

Vascular - Renal Artery

General blood volume / perfusion

DRUGS (NSAIDs, ACEi, diuretics)

78
Q

Heterogenous group of disorders characterized by rapid deterioration of renal function (GFR), rapid elevation of BUN, and S Cr, oliguria

A

ACUTE renal failure

79
Q

Acute Renal Failure, Pre-renal causes (30%)

A

CV, volume depletion (ischemia)

Drug induced (NSAIDs, ACE, diuretics)

80
Q

Acute Renal Failure, Intrarenal causes (60%)

A

Inflammatory diseases

Acute Tubular Necrosis

81
Q

Acute Renal Failure, Post Renal causes (10%)

A

OBSTRUCTION

Cancer

Congenital abnormalities

82
Q

60% of acute renal failure is caused by

A

Intrarenal problems, mostly Acute Tubular Necrosis

*ATN, when blood supply to kidney is severely reduced or blocked. Tubular cells slough off and form casts

83
Q

30% of acute renal failure is caused by

A

Pre renal, hemodynamic

84
Q

10% of acute renal failure is caused by

A

Post renal, OBSTRUCTION

85
Q

Slow, progressive loss of renal function associated with:

Systemic diseases (HTN, DM, SLE) or

Intrinsic kidney disease (kidney stones, acute kidney injury, chronic glomerulonephritis, chronic pyelonephritis, obstructive uropathies, or vascular disorders)

A

Chronic Kidney Disease

86
Q

Clinical definition of CKD

A

GFR less than 60 ml/min/1.73 m2 for 3 months or more

Irrespective of the initial cause of the renal damage

87
Q

Anatomical changes to kidney in CKD

A

Granular surface
Smaller size

Decreased function
high urine protein

88
Q

Stage 1 CKD

A

GFR > 90

No obvious disease. GFR being compensated by higher kidney pressure

89
Q

Stage 2 CKD

A

GFR 60-89

Early evidence of bone disease (VD3)
Creeping SrCr
EPO anemia
Mild HTN

90
Q

Stage 3 CKD

A

GFR 30-59

Elevated SrCr and Urea
Mod HTN
High Triglycerides
Metabolic Acidosis

91
Q

Stage 4 CKD

A

GFR 15-29

Hyperkalemia
Na / H2O retention
Increasing SrCr / Urea

92
Q

Stage 5 CKD

A

GFR 0-14

Significant Uremia
Death

93
Q

GFR for Kidney Failure

A

< 15

94
Q

When do symptomatic changes appear in renal failure

A

Not until renal function declines to < 25% of normal (75% loss) - when adaptive reserves have bee exhausted

95
Q

What causes the symptoms of renal failure

A

Symptoms result from:
increased levels of creatinine, urea, and potassium

alterations in salt and water balance

96
Q

Intact nephron hypothesis

A

when nephrons are lost, the surviving nephrons step up their game to sustain normal kidney function

Patho II, Renal (2 decks)

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