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URI > Renal structure and function > Flashcards

Renal structure and function Flashcards

1
Q

How is the ultrafiltrate produced by the glomerulus?

A
  • Efferent arteriole thinner than afferent = pressure gradient
  • Ultrafiltrate from capillaries between afferent and efferent
  • Podocytes around capillaries prevent passage of proteins
  • Fenestrated lining of capillaries
  • Negative change of basement membrane
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2
Q

Why is the basement membrane of the glomerulus negatively charged?

A
  • Made up of acellular glycocalyx
  • Thick (physical barrier)
  • Negative charge (repels anions)
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3
Q

What components of blood can pass thorugh the glomerular barriers easily?

A
  • Micromolecules i.e.:
  • Urea
  • Amino acids
  • Glucose
  • Toxins
  • Salts
  • Small hormones
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4
Q

What components are not contained within the normal ultrafiltrate?

A
  • Macromolecules i.e.:
  • Proteins
  • Cells
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5
Q

How do podocytes aid the production of the ultrafiltrate?

A
  • Make up inner epithelial layer of Bowman’s capsule
  • Have pedicels with gaps
  • Final barrier
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6
Q

What components are reabsorbed from teh ultrafiltrate in the tubule?

A
  • Plasma proteins if present
  • Glucose
  • Amino acids
  • Hormones
  • Vitamins
  • Salts/electrolytes
  • Water
  • Urea (partially)
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7
Q

What is filtration dependent on?

A
  • Molecular weight
  • Small molecules less than MW 700 Daltons filtered witout restriction
  • Medium: MW 17000 Daltons filtered less
  • Large: MW 70000 Daltons restricted completely
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8
Q

What is meant by glomerular filtration rate?

A
  • Volume of fluid filtered per unit time
  • Measure of kidney function
  • Is scaled to bodyweight (thus affected by lean mass)
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9
Q

Where does the majority of the reabsorption of the ultrafiltrate occur and why?

A
  • Proximal tubule
  • Is structurally and functionally organised for bulk reabsorption
  • Outer cortex
  • Cortex receives most blood flow
  • Involves cortical glomeruli
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10
Q

What proprtion of glucose and amino acids is reabsorbed from teh ultrafiltrate?

A

100%

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11
Q

Describe the process of ultrafiltrate reabsorption

A
  • Coupled to movement of Na+ ions
  • Generally iso-osmotic
  • Filtered proteins reabsorbed
  • Waste products retained in tubule to be excreted
  • Primary and secondary active transport
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12
Q

How are proteins reabsorbed from the ultrafiltrate?

A

Endocytosis via recetpros megalin and cubulin)

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13
Q

Decribe primary active transport in ultrafiltrate reabsorption

A
  • Directly uses ATP
  • ATP to transport Na across basolateral membrane
  • Creates concetration difference and difference in electrical charge due to K leak
  • Na passively across apical membrane
  • More Na into peritubular capillaries
  • Ca-ATPase, H-ATPase and H/K-ATPase also use this
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14
Q

Why is ATP used to transport Na across the basolateral membrane in primary active transport for ultrafiltrate reabsorption?

A

Na/K+ ATPase not present in apical membrane

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15
Q

Describe secondary active transport in ultrafiltrate reabsorption

A
  • Uses ATP indireclty as uses concentration gradient created by primary Na+ linked glucose transport
  • Primary creates concentration difference
  • Drives apical Na uptake, couples with other substances to reabsorb them
  • Some molecules exchanged for Na
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16
Q

Explain the effects of hyperglycaemia on urine production

A
  • Infection risk (sugary water attracting bacteria)
  • Osmotic effects, draws water into tubules and so increased urine production
  • Glucose symporters reach saturation, no more water reabsorbed
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17
Q

What is nephrotic syndrome?

A

Protein appearing in urine

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18
Q

What are the signs of nephrotic syndrome

A
  • Weight loss
  • Oedema
  • Ascites
  • Hypoalbuminaemia
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19
Q

How does oedema occur in nephrotic syndrome?

A
  • Altered colloid osmotic pressure

- Abdominal leakage

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20
Q

How does weight loss occur in nephrotic syndrome?

A
  • Loss of protein
  • Liver accomodates
  • Lose weight
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21
Q

Describe teh process of nephrotic syndrome

A
  • Amyloid blocks glomerular basement membrane leads to loss of normal barrier function thus proteinuria, loss os plasma protein leading to oedema
  • Chronic protein loss triggers renal inflammation leading to renal failure
  • Chronic proteinuria leads to hypovolaemia acivating RAAS can lead to hypertension
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22
Q

What are the effects of hypertension on filtration?

A

Expansion of capillaries and so increased passage of large molecules

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23
Q

What is angiotensin II?

A
  • Peptide hormone
  • Causes vasoconstriction => increased blood pressure
  • Results in enzyme binding (not protein production)
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24
Q

What are the primary functions of ADH?

A
  • Retain water in body

- Constrict blood vessels

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25
Q

Give the biochemical class, site of production, site of action and if water or fat soluble for ADH

A
  • Short peptide
  • Hypothalamus
  • Kidneys (aquaporins)
  • Water
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26
Q

Give the biochemical class, site of production, site of action and if water or fat soluble for aldosterone

A
  • Steroid
  • Adrenal cortex
  • Kidneys
  • Fat
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27
Q

Give the biochemical class, site of production, site of action and if water or fat soluble for angiotensin II

A
  • Peptide
  • ACE acting on AT1 in the blood
  • Blood
  • Water
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28
Q

Give the biochemical class, site of production, site of action and if water or fat soluble for erythropoeitin

A
  • Glycoprotein
  • Kidney
  • Bone marrow
  • Water
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29
Q

Give the biochemical class, site of production, site of action and if water or fat soluble for renin

A
  • Protein
  • Juxtaglomerular apparatus
  • Angiotensinogen in blood
  • Water
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30
Q

What is the effect of hypernatraemia on renal function

A
  • High ECF Na induces natriuresis to cause net loss of Na ions
  • Hyper inhibits aldosterone
  • Hyponatraemia induces Na retention to recover Na ions
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31
Q

Where is sodium mostly found?

A

In the ECF

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32
Q

Where is potassium mostly found?

A

In the ICF

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33
Q

What is the main method of Na control?

A
  • Basolateral pump

- Control total body sodium not concentration

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34
Q

What are the key hormones in controlling ECF Na

A
  • Aldosterone
  • ADH
  • Natriuretic peptides e.g. ANP
  • RAAS
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35
Q

Describe the role of aldosterone

A
  • RAAS stimulates aldosterone release
  • Upregulates sodium receptors in order to reabsorb sodium
  • Acts to reabsorbed Na and thus increase secretion of K
  • Increase ECF volume and blood pressure
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36
Q

How does aldosterone carry out its function?

A
  • Increases expression of sodium receptors
  • ENaC on collecting duct
  • Basolateral Na/K ATPase on distal tubule
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37
Q

What is the effect of K concentration on aldosterone

A
  • Increased K concentration stimulates aldosterone
  • Retention of Na/secretion of K is reciprocal
  • High potassium intake leads to aldosterone activation
  • Secretion of K and reabsorption of Na
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38
Q

What is the function of ADH?

A
  • Acts to conserve water
  • Increase water retention (prevent diuresis)
  • In high concentrations has vasopressor effect to raise BP
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39
Q

How does ADH carry out its function?

A
  • Mainly effect on distal tubule

- Increase expression of receptos in cortical and distal collecting duct

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40
Q

What is RAAS?

A

Renin Angiotensin Aldosterone System

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41
Q

What is the function of RAAS?

A
  • Stimulates production of aldosterone
42
Q

How does RAAS carry out its function?

A
  • Decreased blood pressure
  • Decreased perfusion to kidney (sensed in efferent arteriole)
  • More renin secretion
  • Conversion of angiotensinogen to angiotensin II
  • Stimulates adrenal gland to produce aldosterone
43
Q

What is the effect of angiotensin II on sodium channels?

A
  • Insertion of Na+ channels
  • Inproximal tubule: apical Na/H exchanger, basolateral Na+(HCO3-)3 and Na/KATPase
  • In thick ascending limb: apical Na/H exchanger and Na+K+2Cl-
  • In collecting duct: ENaC
44
Q

What does ENaC stand for?

A

Epithelial Na+ Channel

45
Q

What transport mechanisms for Na+, Cl-, K+ are used in the proximal tubule?

A
  • basolateral Na/K-ATPase
  • Na/H exchange transporter
  • Due to carbonic anhydrase in lumen, net effect is HCO3- reabsorption
46
Q

What transport mechanisms for Na+, Cl-, K+ are used in the loop of Henle?

A
  • High Na and Cl in thinAL, some leave by passive diffusion
  • Na+/K+/2Cl- in thick AL (1Na, 1K and 2Cl into interstitium, into epithelial cell, K+ acively into tubule by ROMK channel, net reabsorption of Na and 2Cl)
47
Q

What transport mechanisms for Na+, Cl-, K+ are used in the distal tubule?

A
  • 1na, 2Cl transporter (NCC)
48
Q

What transport mechanisms for Na+, Cl-, K+ are used in the collecting ducts?

A
  • Net positive charge in tubular lumen aids paracellular uptake of remaining positively charged ions in tubule (e.g. Na, K, Ca, Mg)
  • Principle cells: ENaC, K/Cl cotransport secretor, NaKATPase, K+ leak (basolateral), Cl- leak (basolateral)
  • Alpha-intercalated: K/H antiport, HCO3-/Cl- antiport (Cl- reabsorption, basolateral), Cl- leak (baso), K+ leak (baso)
  • Beta-intercalated: HCO3-/Cl- antiport (HCO3- secretion), K/H antiport, Cl- and K+ leak (baso)
49
Q

How does the H+ ATPase transport mechanism work in the collecting duct?

A
  • type B intercalated cells
  • Establishes H+ gradient
  • Drives secretion of HCO3- coupled to reabsorption of Cl-
50
Q

Explain what occurs when Na needs to be excreted

A
  • If need to get rid of Na for example (Na+ load, ECF volume or BP high)
  • Renin secretion inhibited
  • Aldosterone deendent Na+ reabsortpion does not occur
  • Excess Na+ excreted in urine
51
Q

What are some causes of hypokalaemia?

A
  • Renal loss increased (CKD), diuretic therapy
  • Gastric loss (diarrhoea, vomiting)
  • Shift in biodistribution (ICF to ECF, e.g. insulin treatment, hyperthyroidism)
  • iatrogenic (nephrotoxic drugs, laxatives, bicarbonate therapy alkalosis)
52
Q

What are the 3 main methods of K control?

A
  • ECF/ICF shifts (short term buffer)
  • Renal excretion
  • GI excretion
53
Q

What may cause chronic hyprekalaemia?

A
  • Oliguric or anuric renal failure
  • Urinary tract trauma or obstruction
  • ACE inhibitors
  • Potassium-sparing diuretics
  • Hypoaldosteronism
  • Hypoadrenocorticism
54
Q

Where is potassium reabsorbed?

A
  • Mainly proximal tubule (active reabsorption)
  • Some in Loop of Henle
  • Fine tuning in collecting duct
55
Q

Where is potassium secreted in the nephron?

A
  • The distal tubule
56
Q

Describe the mechanism behind potassium secretion

A
  • Principle cell main route
  • Aldosterone
  • Increased Na/K ATPase in basolateral of principle cells (drivign force for K secretion)
  • K secretion through ROMK small (SK) or big conductance channels (BK)
  • High potassium increases aldosterone, drives Na uptake and K loss
  • Sodium entry via ENaC stimulates K secretion via apical leak channels
  • Functional cotransport of potassium chloride affects potassium secretion
57
Q

What are the mechanisms of potassium reabsorption?

A
  • Alpha-intercalated cell, active K reabsorption driven by apical membrane proton potassium pump
  • pH sensitive, acivaded by acidosis potassium restriction and aldosterone
58
Q

What may cause hyperkalaemia?

A
  • Imparied internal redistribution (insulin resistance, beta blockers)
  • Increased potassium leak (cell destruction, acidaemia)- Structure abnormalities in the kidney (decreased GFR, decreased filtration, reduced abilty to compensate for rapid changes in K load)
  • Function abnormalities in kidney (decreased luminal flow, metabolic acidosis, hypoaldosteronism)
59
Q

Where is ANP stored and what stimulates its release?

A
  • Right atrium of heart

- Stimulated by increased stretch due to increased blood volume

60
Q

What is the function of ANP?

A

To increase sodium excretion

61
Q

What happens when ANP is secreted?

A
  • Renal vasodilation
  • Increased GFR
  • Decreased renin (opposes RAAS)
  • Decreased aldosterone
  • Decreased reabsorption of Na
  • Decreased ADH secretion
62
Q

Relate the physical properties of water to its physiological function

A
  • Water is polar due to polarity of H-O bonds
  • Properties of water are due to hydrogen bonding between molecules (loose association with each other)
  • Leads to unique properties
63
Q

What are the 2 “compartments” total body water can be divided into?

A
  • Extracellular fluid (ECF) (20%)

- Intracellular fluid (ICF) (40%)

64
Q

What are the components ECF can be split into?

A
  • Plasma volume (5%)
  • Interstitial fluid (15%)
  • Transvellular fluid (<1%)
65
Q

What are the main solutes found in ECF?

A
  • Sodium
  • Chloride
  • Bicarbonate
66
Q

What are the main solutes found in ICF?

A
  • Potassium
  • Magnesium
  • Protein
67
Q

Define concentration

A
  • A measure of how much of a given solute is dissolved in a given volume of solvent (usually moles per litre (dm^3))
68
Q

What is oncotic pressure?

A
  • Colloid osmotic pressure
  • Proportion of total osmotic pressure in plasma exerted by colloids
  • Produced from endogenous plasma proteins or synthetic colloids
69
Q

What are colloids?

A

Large molecular weight particles present in solution

70
Q

How do colloids generate pressure?

A
  • do not cross from arterial vessels into interstitial fluids
  • Create oncotic pressure
71
Q

What is tonicity?

A
  • The effective osmolality of a solution/osmotic pressure of a fluid when compared with plasma
  • Equal to sum of concentration of solutes which have capacity to exert an osmotic force across the membrane
  • State of a solution in respect of osmotic pressure
72
Q

What is a hypotonic solution?

A

Surrounding environment has less solutes

73
Q

What is a hypertonic solution?

A

Surrounding environment has more solutes

74
Q

What is an isotonic solution?

A

Surrounding environment has same concentration of solutes

75
Q

What is an osmole?

A

The number of ions or particles into which a solute dissociates in solution
- e.g. 1 mole of NaCl = 2 osmoles

76
Q

How is osmosis affected by osmolality?

A
  • Osmolality is the number of osmoles of a solute per kg solvent
  • Osmosis is dependent on the number of particles
  • Osmolarity is the number of osmoles per litre of solution
77
Q

Define osmolality

A

The number of osmoles of a solute per kg solvent

78
Q

Deinfe osmolarity

A

The number of osmoles per litre of solution

79
Q

Define molarity

A

The number of moles per litre (M)

- 5M solution = 5 moles per lite

80
Q

Define molality

A

the number of moles per kg of solvent (m)

  • 5m solution - concentration of 5 moles/kg
  • Is always constant
81
Q

What is meant by “equivalents”?

A
  • The mount of material that will combine with 1 mole of OH-, H+ or electrons
  • E.g. in HCL, 1 mol hydrogen combines with 1 mol chlorine, so amount of chlorine needed is 1 equivalent
  • Can be given as mEq/L
82
Q

How can equivalents be determined?

A
  • By their mass
  • mass of one equivalent can be found by dividing atomic mass by its valence
  • .e.g calcium: 50/2 = 20g/Eq
83
Q

Give the mmols for 1 equivalent of monovalent, divalent and trivalent ions

A
  • Mono: 1mmol
  • Di: 0.5mmol
  • Tri: 0.333mmol
84
Q

Define osmosis

A
  • The process by which molecules of a solvent tend to pass through a semipermeable membrane from a more to a more concentrated to a less concentrated one
  • In order to balance energy levels
85
Q

Explain the effects of adding a solute on osmosis

A
  • Water moves to balance energy levels
  • Solutes decreased entropy (water molecules organise around them)
  • Side with greater entropy (thus more energy) will lose water molecules to side with lower energy
86
Q

What is water potential

A
  • The tendency of water molecules to move out a solution
  • Always from high to low
  • Pure water, potential = 0
  • Is equal to osmotic potential plus any additional pressure on the system
87
Q

What is osmotic pressure?

A

The pressure exerted by the oslite particles in the solution which prevents movement of water across a membrane

88
Q

What are ineffective osmoles?

A

Ones that do not exert any osmotic pressure e.g. urea

89
Q

What are effective osmoles?

A

Ones that are able to dictate the direction and extent of diffusion e.g. Na+ or glucose
- Tonicity is a measure of only effective osmoles

90
Q

Describe the process of exchange of water between the plasma and interstitial spaces

A
  • Formation of ISF from plasma
  • Water taken on by animal
  • Enters circulatory system
  • When enters arterial region, pressure and pores allow filtration of fluids and salts into interstitial fluid
  • Excess dealt with lymphatics system
  • Some absorbed by venous portion of system driven by osmosis
  • Net filtration is sum of these processes
  • Large particles cannot move from plasma to ISF
91
Q

What is hypotonic fluid loss?

A

Loss of water but no loss of salts e.g. water deprivation

92
Q

What is the effect of hypotonic fluid loss on ECF tonicity and ECF volume

A
  • Hypertonic ECF (water out of cells)

- Increases ECF volume to preserve circulating fluid volume

93
Q

What is isotonic fluid loss?

A

Loss of fuids and salts e.g. trauma leading to blood loss

94
Q

What are the effects of isotonic fluid loss on ECF tonicity and ECF volume?

A

No effect on tonicity, loss of ECF volume

95
Q

What is hypertonic fluid loss?

A

Loss of salt more than water, worst kind of fluid loss. E.g. salt depletion

96
Q

What are the effects of hypertonic fluid loss on ECF tonicity and ECF volume?

A
  • Hypotonic ECF (water moving into cells)

- ECF volume decreases, compounding fluid loss

97
Q

What is the effect of isotonic crystalline fluids (IV) on plasma volume, ISF and ICV?

A
  • PV: expanded proprtionally to its volume of ECF
  • ISF: expanded
  • ICV: unchanged
98
Q

What is the effect of hypertonic crystalline fluid on plasma volume, ISF and ICV?

A
  • Transient expansion in relation to ISF, draws water out from ISF initially as moves around to arterial system, water and salts pushed and filtered into ISF
  • ISF expanded
  • ICV decreased (pulling water out of cells)
99
Q

What is the effect of colloid fluid on plasma volume, ISF and ICV

A
  • PV: sustained expansion (water from ISF to plasma volume as colloids cannot move into cells)
  • ISF: unchanged in healthy tissue
  • ICV: unchanged
100
Q

What is the effect of rapid vs fast changes in ECF tonicity?

A
  • Rapid alter cell volume (may cause neurological complication)
  • Slow (and moderate) have no effect on ICF volume
101
Q

What is the effect of extracellular hypertonicity in gene expression?

A
  • Increases expression of genes encoding proteins that increases intracellular osmoles
  • Membrane transporters
  • Enzymes that synthesise solute

URI (15 decks)

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