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Med 3 > Renal > Flashcards

Renal Flashcards

1
Q

Functional unit of the kidney

A

Nephron, each kidney has roughly 1x10^6 nephrons

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2
Q

Types of nephron and their location

A

Cortical (85%), majority in cortex

Juxtamedullary (15%), majority in medulla

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3
Q

5 distinct regions of the nephron

A

Bowman’s capsule

Proximal convoluted tubule

Loop of henle

Distal convoluted tubule

Collecting duct

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4
Q

Structures that make up the renal corpuscle

A

Bowman’s capsule

Glomerular capillaries

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5
Q

Juxtaglomerular apparatus and its functions

A

Distal convoluted tubule and glomerular afferent arteriole

Autoregulation, renin release (salt water balance)

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6
Q

Functions of nephron

A

Renal corpuscle filters initial blood to form filtrate / ultrafiltrate / tubular fluid

Tubular system (cortical and medullary) controls concentration and content of urine

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7
Q

Blood supply to the nephron

A

Glomerular capillary bed (within bowman’s capsule)

Peritubular capillary bed (wraps around remainder of nephron)

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8
Q

Functions of the blood supply to the nephrons

A

Glomerular - high hydrostatic pressure (60mmHg) for filtration

Peritubular - low pressure (20 mmHg) for reabsorption and secretion

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9
Q

Outline vasa recta

A

Peritubular capillaries wrap around loop of henle and provide O2 and nutrients to innermost regions of medulla

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10
Q

Cardiac output to the kidneys

A

25%,

Important role in cleaning blood and homeostasis

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11
Q

Outline the filtration fraction

A

20% of plasma that enters glomerular capillaries is filtered, 19% reabsorbed, 1% excreted externally

Remaining 80% leaves via efferent arteriole and is returned by Peritubular capillaries to systemic circulation

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12
Q

Define glomerular filtration rate

A

Volume of fluid entering bowman’s capsule per unit time

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13
Q

Outline process of ultrafiltrate formation

A

Fluid driven from capillaries into bowman’s capsule, across glomerular filter by capillary hydrostatic pressure

Efferent arterioles smaller than afferent, maintaining pressure

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14
Q

Structure of glomerular filter

A

Glomerular capillaries separated from podocytes by basement membrane

Mesangial cells provide structural support and are contractile

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15
Q

Characteristics of the glomerular capillary membrane

A

Endothelium- very charged glycoproteins repel anionic proteins

Podocytes have filtrations slits

Normally all contents of plasma except trace amounts of plasma proteins appear in filtrate

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16
Q

How can GFR be altered

A

Kf (filtration coefficient)

Starling forces by patho/physiological conditions / drugs

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17
Q

State the ways in which capillary hydrostatic pressure can change

A

Constriction of afferent / efferent arterioles

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18
Q

Outline the impact of constriction of afferent arteriole on GFR

A

Increase renal vascular resistance, decrease renal vascular resistance

Decreases intraglomerular pressure and GFR

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19
Q

Outline the impact of changes in colloid osmotic pressure on GFR

A

Decrease in protein concentration (hypo proteinaemia), increase in GFR

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20
Q

Outline the impact of changes in bowman’s space pressure on GFR

A

Increase in bowman’s space pressure by renal stone, decrease in GFR

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21
Q

Outline the impact of changes in Kf on GFR

A

Increase in Kf via drugs or conditions, decrease in GFR

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22
Q

Outline the use of insulin as an indicator of GFR

A

Freely filtered, not reabsorbed / secreted / metabolised

No effect on renal toxic

Easily measured in urine

Mass filtered = mass excreted

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23
Q

Function of the kidneys

A

Filter and excrete waste products

Control water and electrolyte balance

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24
Q

Location of kidneys

A

Retroperitoneal

T12- L3

R kidney usually lower due to presence of liver

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25
Q

State the layers encasing the kidneys from deep to superficial

A

Renal capsule

Perirenal fat

Renal fascial (and suprarenal glands)

Pararenal fat (mainly posterolateral)

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26
Q

Outline structure of the kidneys

A

Renal parenchyma split into outer cortex and inner medulla

Cortex extends into inner medulla, creating renal pyramids

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27
Q

Outline internal structure of kidneys

A

Apex of pyramids - renal papilla

In middle of pyramids - minor calyx

Base of pyramids - major calyx

Connection of pyramids - renal pelvis

Renal pelvis attached to ureter

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28
Q

Outline the arterial supply of the kidneys

A

R and L renal arteries (L1-2), enter at hilum at split

R renal artery (crosses IVC posteriorly) slightly longer due to aorta being left of midline

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29
Q

Venous drainage of the kidneys

A

R and L renal veins

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30
Q

State the equation for GFR, using insulin clearance

A

GFR = (UI x V)/ Pl

UI- urine conc of insulin

V - urine flow rate

Pl- plasma conc of insulin

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31
Q

State the equation of eGFR using creatinine clearance

A

eGFR = ([U]CR x V) / [P] CR

V - urine flow rate

[U]CR - urine conc of creatinine
[P] CR- plasma conc of creatinine

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32
Q

Define renal plasma flow

A

Amount of plasma that perfumes the kidneys per unit time

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33
Q

State the purpose of renal plasma and renal blood flow measurements (RPF and RBF)

A

Indicators of renal health

RPF can be used to estimate RBF

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34
Q

Outline the relationship between renal plasma flow (RPF) and glomerular filtration rate (GFR)

A

The greater, the greater

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35
Q

Outline the method to estimate renal plasma flow

A

Mass excreted (of indicator substance) = mass (of indicator substance) delivered to kidneys

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36
Q

Give an example of an indicator used to estimate renal plasma flow

A

Para - aminohippuric acid (PAH), freely filtered and secreted

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37
Q

Outline the movement of para-aminohippuric acid (PAH) with regards to the nephron

A

Enters glomerular capillaries, some filtered and most leaves via efferent arteriole

PAH secreted out of Peritubular capillaries and into tubular lumen via transporters on proximal tubule

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38
Q

State the equation regarding clearance of para aminiohippuric acid (PAH)

A

Total mass PAH excreted = total mass PAH presented to kidney

= (plasma conc) x (plasma vol / unit time)
= RPF
= 600mL/min

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39
Q

State the condition in which all para-aminohippuric acid (PAH) is secreted from Peritubular fluid to proximal tubule

A

Tubular transport maximum (Tm) not exceeded, low plasma concentrations of PAH

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40
Q

Define filtration fraction

A

Proportion of plasma that forms filtrate

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41
Q

State the equation linking filtration fraction, glomerular filtration rate and renal plasma flow

A

FF = GFR/ RPF
= 120/600
= 20%

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42
Q

State the relationship between filtration fraction and collie pressure

A

The greater, the greater

Hence greater forces for tubular reabsorption at proximal tubule

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43
Q

Define haematocrit

A

Proportion of blood volume occupied by RBCs

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44
Q

Outline the amount of blood and plasma received at the kidney per minute

A

Cardiac output = 5L / min

Kidney receives 20-25% of output
= 1300ml blood or 600ml plasma / min

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45
Q

Mechanism of autoregulation by the kidneys

A

Occurs between arterial blood pressure of 90-180 mmHg

Ensures fluid and solute excretion remains constant during normal changes in arterial BP

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46
Q

Outline the myotonic mechanism which changes afferent arteriolar resistance

A

Afferent arteriole contracts in response to pressure and stretch

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47
Q

Outline the tubuloglomerular feedback mechanism which changes afferent arteriolar resistance

A

Increase of NaCl in filtrate detected by macular densa of juxtaglomerular apparatus

Causes contraction of afferent arteriole via adenosine / ATP

Vasoconstriction of afferent arteriole reduces blood getting into glomerular capillaries which decreases GFR

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48
Q

State the make up of the juxtaglomerular apparatus

A

Macula densa (of loop of henle - distal convoluted tubule junction) and granular / juxtaglomerular cells (of afferent arteriole)

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49
Q

Summarise the pathway of the autoregulation mechanisms in response to increased BP

A

Increased RBF and GFR triggers myogenic mechanism and tubuloglomerular feedback

Mechanisms trigger afferent arteriolar contraction (through pressure / stretch and adenosine / ATP production) causing decrease in capillary hydrostatic pressure

Decrease in RBF and GFR

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50
Q

State the factors affecting renal blood flow (RBF) and glomerular filtration rate (GFR)

A

Vasoconstrictors (sympathetic nerves, angiotensin II)- decrease

Vasodilators (prostaglandins, PGE2, PGI2)- increase

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51
Q

Outline the mechanism in which vasoconstrictors influence renal blood flow (RBF) and glomerular filtration rate (GFR)

A

Activation by decreased BP

Efferent arteriole more sensitive to AgII than afferent (at low concs), therefore will dominate and help maintain GFR in presence of hypotension

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52
Q

Outline the process in which NSAIDs and COX inhibitors may exacerbate vasoconstriction

A

Drugs block synthesis of prostaglandins, interfering with preservation of RBF

If RBF already low, excessive vasoconstriction and ischaemia may lead to renal tubular necrosis

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53
Q

State conditions / situations in which the renal threshold for glucose is exceeded, causing glucose excretion in urine

A

Untreated diabetes mellitus

Hyperthyroidism

Fanconi syndrome

Familial renal glucosuria

Pregnancy

Drugs

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54
Q

State the equation linking filtered glucose load, GFR and plasma glucose conc

A

Filtered glucose load = GFR x plasma

Glucose conc

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55
Q

State the equation linking glucose, excretion, urine flow (V) and urine glucose conc

A

Glucose excretion = urine (V) x urine glucose conc

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56
Q

State the equation linking glucose reabsorbed, glucose filtered and glucose excreted

A

Glucose reabsorbed = glucose filtered - glucose excreted

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57
Q

State the equation linking filtered glucose load, GFR and plasma glucose conc

A

Filtered glucose load = GFR x plasma glucose conc

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58
Q

State the plasma solute concentration of Na+

A

135-145 mmol/ L

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59
Q

State the plasma solute concentration of K +

A

3.5 - 5.0 mmol /L

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60
Q

State the plasma solute concentration of Cl-

A

100-106 mmol/ L

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61
Q

State the plasma solute concentration of HCO3-

A

21-28mmol/L

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62
Q

State the plasma solute concentration of H+

A

37-43mmol/L

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63
Q

State the plasma solute concentration of glucose

A

3.9-5.6 mmol/L

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64
Q

State the plasma solute concentration of protein

A

60-84 g /L

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65
Q

Outline how the concentration of constituents of plasma solute and ultrafiltrate differ

A

Similar due to free movement through filtration barrier

Except protein, held back by filtration barrier so very low concentrations in ultrafiltrate

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66
Q

State the approximate GFR in a normal 70kg person

A

120ml / min

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67
Q

State the approximate RPF in a normal 70kg person

A

600 ml / min

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68
Q

State the approx PVC in a normal 70kg person

A

40%

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69
Q

State the approximate RBF in a normal 70kg person

A

1 L/min

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70
Q

State the approx cardiac output in a normal 70kg person

A

5L/min

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71
Q

Outline the histology of the epithelial cells of the nephron and the corresponding Peritubular capillaries

A

Tubular epithelium with basolateral membrane facing Peritubular fluid and apical / luminal membrane facing lumen of nephron

Peritubular fluid separates nephron and capillary

Tight junctions between epithelial cells

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72
Q

State the transport pathways between epithelial cells of the nephron and Peritubular capillaries

A

Transcellular / transepithelial transport across cells

Paracellular transport - between cells

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73
Q

Outline the function of Na + / K + ATPase pumps in the basolateral membrane of the nephron

A

Pump Na+ out in exchange for K+, creating Na+ conc

Promotes movement of Na+ to move from lumen to peritubular fluid via tubular epithelium

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74
Q

Outline the function of the peritubular capillaries with regards to reabsorption

A

Hydrostatic pressure in Peritubular capillaries is low ( 10 mmHg), facilitating reabsorption from Peritubular fluid

Increased colloid osmotic pressure favours this

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75
Q

Outline the reabsorption that takes place at the proximal convoluted tubule

A

Bulk - 60-70% of filtered load of Na+, H2O, Cl-, K+ and other solutes, and nearly all filtered glucose and amino acids are reabsorbed, coupled with Na+ reabsorption

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76
Q

Outline the properties of the proximal convoluted tubule which prevents build up of significant osmotic gradients

A

Leaky tight junctions between tubular epithelial cells

Presence of aquaporin -1 (membrane proteins acting as H2O channels)

Peritubular fluid = isometric with plasma

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77
Q

Outline the transport of Na+, glucose, AAs and PO4 from the proximal convoluted tubule to peritubular fluid

A

Na+ readily enter epithelial cells, crossing apical membrane from tubular lumen, down gradients created by Na+ pump on the basolateral membrane

Other molecules move via symptom treatment with Na+

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78
Q

State the 4 mechanisms by which Na+ enters the tubular epithelium from the tubular lumen via the apical membrane

A

Na+ / H+ exchange

Coupled with entry with glucose, AAs and PO4 via symporters

Membrane channels

Passive through tight junctions into lateral space

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79
Q

Outline the transport of HCO3- from the proximal convoluted tubule to peritubular fluid

A

H+ +HCO3-, forms carbonic acid

Dissociates due to CA into CO2 and H2O

CO2 and H2O move into tubular epithelium and are converted back to H+ and HCO3- by CA

HCO3- transported to peritubular fluid via Na+ transporter in basolateral membrane

H+ continues to move between cell and lumen

80
Q

Outline the adaptations to the transport of HCO3- under alkalotic conditions

A

Excrete more filtered HCO3- into urine and reabsorb less

81
Q

Outline the adaptions to the transport of HCO3- under acidic conditions

A

Production of new HCO3- (normal system is already close to capacity)

82
Q

Outline the transport of H2O from the proximal convoluted tubule to peritubular fluid

A

Via leaky tight junctions

Via aquaporin 1 (AQP1) channels in apical and basolateral membranes

Reabsorbed by osmotic pressure grad due to Na+ reabsorption

Facilitated by oncotic pressure and low hydrostatic pressure in capillaries

83
Q

Outline the mechanism of solute drag

A

Free and passive oncotic flow of H2O results in solutes being carried through to be reabsorbed

84
Q

Outline the transport of K+, Cl- and urea from the proximal convoluted tubule to peritubular fluid

A

K+ via solvent drag

Cl- via paracellular and transcellular transport

Urea via paracellular and transcellular transport after concentration due to H2O movement

85
Q

Outline the structure of the loop of henle

A

Descending thin limb

Ascending limb (initially thin, then thick)

86
Q

Outline the nature of the descending thin limb with regards to H2O and other solutes

A

Highly permeable to H2O due to AQP1

Less permeable to NaCl and urea, movement is largely passive

87
Q

Outline the nature of the ascending limb with regards to H2O and other solutes

A

Impermeable to H2O

Na+, Cl- and K+ reabsorbed, mainly at thick limb

Thin limb involved in passive reabsorption

88
Q

Outline the function of Na+ / K+ ATPase pumps in the basolateral membrane of the thick ascending limb

A

Pump Na+ out in exchange for K+, creating Na+ concentration gradient

Promotes movement of Na+ to move from lumen to peritubular fluid via tubular epithelium

89
Q

Outline the function of symporter proteins on the apical membrane of the thick ascending limb

A

Move Na+ and 2 Cl- across membrane into epithelial cells, down concentration gradient

90
Q

Outline the movement of Na+ from the lumen to the Peritubular fluid

A

Into epithelial cells via symporter proteins on the apical membrane

Into peritubular fluid via Na+ pumps on basolateral membrane

91
Q

Outline the movement of Cl- from the lumen to the Peritubular fluid

A

Into epithelial cells via symporter proteins on apical membrane

Into peritubular fluid via Cl- channels on basolateral membrane

92
Q

Outline the movement of K+ from the lumen to the Peritubular fluid

A

Into epithelial cells via symporter proteins on apical membrane

Into peritubular fluid via K+ channels on basolateral membrane

Mainly diffusion back into lumen, creating +ve charge within lumen

93
Q

State the driving force behind paracellular transport of +vely charged ions

A

Diffusion of K+ from epithelial cells back into lumen, creating +ve charge within lumen

94
Q

Outline the function of Na+ / H+ antiporters on the apical membrane of the thick ascending limb

A

Secretion of H+ into lumen from epithelial cells

Used to reabsorb HCO3- into the lumen

95
Q

State the consequences of salts moving out of the thick ascending limb without the accompaniment of H2O

A

Osmolality (dilution) of tubular fluid

Interstitial fluid becomes hyperosmotic, important in renal concentrating mechanism

96
Q

Outline the nature of the tubular fluid arriving at the early distal tubule

A

Further reduction in volume

Hyperosmotic with respect to plasma due to reabsorption of salts

97
Q

Function of early distal tubule

A

Continues active dilution, reabsorption of salt without water causes osmolality to fall further

98
Q

Mechanisms functioning at the early distal tubule

A

Continues active dilution, reabsorption of salt without water causes osmolality to fall further

99
Q

Mechanisms functioning at the early distal tubule

A

Na+ pumps drive transport of many solutes

Na+ /Cl- symporter transports into epithelial cells from lumen

Cl- channels allows Cl- to leave epithelial cells and into peritubular fluid

Ca2+, Mg2+ and K+ reabsorption

H+ excretion via Na+ / H+ exchange or H+ pump

100
Q

State the target of drug action of thiazides

A

Na+ / Cl- protein symporter transporter

101
Q

State the function of principal cells

A

Reabsorb Na+ and H2O

Secrete K+

102
Q

State the function of the intercalated cells

A

Regulate acid base balance due to high intracellular concs of carbonic anhydrase

103
Q

State the location from which aldosterone is released from

A

Zona glomerulosa of adrenal cortex

104
Q

State the effects of aldosterone on solute handling in the late distal tubule and cortical collecting duct

A

Enhances Na+ and K+ reabsorption in principal cells

Enhances H+ secretion in intercalated cells

105
Q

Outline the methods by which aldosterone enhances Na+ reabsorption in principal cells

A

Increased number and activity of apical Na+ channels

Increased activity of basolateral Na+ pump

106
Q

Outline the methods by which aldosterone enhances K+ reabsorption in principal cells

A

Increased number and activity of apical K+ channels

Increased activity of basolateral Na+ pump

Increased Na+ reabsorption

107
Q

Outline the method by which aldosterone enhances H+ secretion in intercalated cells

A

Stimulates H+ - ATPase pump

108
Q

State the potential fates of disturbed aldosterone levels

A

Hyperaldosteronism (aldosterone excess) - metabolic alkalosis, hypokalaemia

Hypoaldosteronism (type 4 renal tubular acidosis)- hyperkalemia

109
Q

Outline the production of diuresis, in the absence of ADH

A

Tubular fluid entering distal tubule always hyposmotic to plasma

Late distal tubule and collecting duct have low permeability to H2O

110
Q

Outline the production of antidiuresis in the presence of ADH

A

Increases permeability of late distal tubule and collecting duct by increasing stimulation of AQP2 on the principal cells

Water exits the lumen by osmosis into interstitial fluid

111
Q

Functions of ADH

A

Regulation of urine and extracellular fluid osmolality

112
Q

Outline the urea permeability of the nephron, in the absence of ADH

A

Restricted to proximal tubule and inner medulla

113
Q

Outline the urea permeability of the nephron in the presence of ADH

A

ADH dependent urea transporter on apical membrane in inner medullary collecting duct concentrates urea

Urea diffuses out of lumen and into medullary interstitium

114
Q

Purpose of urea reabsorption

A

Maintains osmotic gradient between interstitium and collecting duct lumen

Urea diffuses into tip of loop of henle and is recycled

115
Q

Outline the regions of the nephron with low urea permeability in the absence of ADH

A

Descending thin limb

Ascending thick limb

Distal tubule

Collecting duct

116
Q

Relationship between urea permeability and ADH

A

Proportional

117
Q

Relationship between H2O permeability and ADH

A

Proportional

118
Q

Disorders of ADH secretion / response

A

Diabetes insipidus - polyuria , polydipsia

SIADH ( syndrome of inappropriate section of ADH - hyponatremia)

Nocturnal enuresis (bed wetting)

119
Q

Location of the adrenal gland

A

Superomedially to the upper pole of each kidney

120
Q

Describe the relationships of the right adrenal gland

A

Posteriorly- diaphragm
Inferiorly- kidney
Medially - vena cava
Anteriorly - hepato-renal pouch and bare area of the liver

121
Q

Describe the relationships of the left adrenal gland

A

Postero-medially: crus of the diaphragm
Inferiorly: pancreas and splenic vessels
Anteriorly: lesser sac and stomach

122
Q

Arterial supply of the adrenal gland

A

Superior adrenal arteries - from inferior phrenic artery
Middle adrenal arteries- from aorta
Inferior adrenal arteries from renal arteries

123
Q

What is the venous drainage of the right adrenal

A

Via one central vein directly into the IVC

124
Q

What is the venous drainage of the left adrenal

A

Via one central vein into the left renal vein

125
Q

Why are diuretics so important

A

Important cardiovascular drugs
Management of CHF
Antihypertensives

A/C (D) guidelines
A: ACE inhibitor
C: Ca2+ channel inhibitor
D: diuretic

126
Q

What are the different types of diuretics

A

Osmotic agents
Loop diuretics
Thiazides
Potassium sparing agents

127
Q

What are osmotic diuretics

A

Eg mannitol
Pharmacologically inert
Freely filtered in bowmans capsule
Increased osmolality of tubular fluid in PCT and loop of henle
Reduce passive reabsorption of H2O
Used in cerebral oedema (increases osmolality and removes fluid from the brain)

128
Q

What are loop diuretics

A

Eg furosemide
High ceiling bc powerful diuretic effect
Causes 15-25% of filtered Na+ to be excreted
Block Na+ / 2Cl- / K+ symporter of thick ascending limb
Reduces hyperosmotic interstitium
Risk of dehydration

129
Q

How do loop diuretics work

A

Reduce the ability of the loop to concentrate urine by preventing creation of a hypertonic interstitium in the medulla
Increases Na+ delivery to DCT
- promotes K+ loss (risk of hypokalameia)
Decreases Na+ entry into macula densa
- promotes renin release

130
Q

Uses of loop diuretics

A

CHF- reduce pulmonary oedema, 2’ to LVF and peripheral oedema

Venodilators - iv rapid effect in acute LVF

Renal failure - to improve diuresis

131
Q

What are thiazides

A 
Moderately powerful diuretics 
Act on DCT 
Blocks Na+/Cl- cotransporter 
Inhibit active Na+ reabsorption and accompanying Cl-
Reduce circulating Cl- 
Used in mild / moderate heart failure 
- 2nd line in hypertension

Renally excreted / secreetd by weak acid transporter in PCT before acting on DCT

132
Q

What is hypokalaemia

A

K+ loss -> caused by kaliuresis

2’ to loop diuretics, thiazides

133
Q

How does aldosterona cause hypokalaemia

A

Acts on mineralcorticoid receptor (intracellular) -> goes to the nucleus and determines which genes are expressed.
MRNA and aldosterone induced proteins produced -> Na+ channels inserted into basolateral membrane : Na+ reabsorbed so K+ is lost

134
Q

What are potassium sparing diuretics

A
  • aldosterone receptor antagonists
    Na+ channel blockers (on DCT)
  • weak diuretics but in combo w K+ losing agents may reduce K+ loss
    ACEi cause hyperkalaemia so may negate effects of K+ losing diuretics
135
Q

What are aldosterone (mineralocorticoid) receptor antagonists

A

Eg spironolactone

  • antagonise aldosterone receptors
  • prevent insertion of Na+ pumps and channels
  • used in 1’/2’ hyperaldosteronism
  • used in CHF to block aldosterone actions on heart
136
Q

What are sodium channel blockers

A

Eg amiloride / triamterene
Block luminal Na+ channels in late DCT and CD
Na+ no longer retained at expense of K+

137
Q

What is renoprotection

A

Diabetes associated with renal nephropathy
Cause of chronic renal failure

ACEi slow renal damage, advocated in nephropathy/ diabetes + hypertension
- block inappropriate RAAS activation

138
Q

How to counsel a patient for taking diuretics

A 
Best taken am (so sleep isnt disturbed by needing to urinate) 
Pt will experience increased urine flow 
Pt should avoid excess salt in diet 
May cause postural hypotension 
Thiazides: may uncover / worsen diabetes 
Thiazides / LD may worsen gout 
NSAIDs may reduce effect of LD 
- electrolytes should be monitored
139
Q

Mechanism of action of spironolactone

A

Is an aldosterone antagonist
Inhibition of the mineralocorticoid receptor in the cortical collecting ducts interferes with excretion of potassium so can cause hyperkalaemia
Side effect: breast tissue growth

140
Q

Which diuretic causes abnormally tall T waves on ECG

A

Spironolactone

141
Q

Dietary advice for chronic kidney disease

A

Diet low in protein, phosphate, potassium and sodium
Protein- a source of ammonia which is normally excreted by the kidney (but less so in CKD)

Phosphate- can complex with calcium to cause renal stones

Sodium - increases blood pressure, which damages the kidney further

Potassium - not well excreted by failing kidneys and can cause cardiac arrhythmia

142
Q

How do you maintain acid base balance

A

1) buffers
2) ventilation
3) renal regulation of H+ and HCO3- (slow)

143
Q

What are the sources of H+ gain

A

From CO2 in tissue (aerobic respiration) - forms carbonic acid which then dissociates

  • metabolism of protein and other organic molecules
  • loss of HCO3- in diarrhoea
  • loss of HCO3- in urine
144
Q

What are the sources of H+ loss

A

H+ + HCO3- -> H2O + CO2 (CO2 excreted through lungs)

  • utilising H+ in metabolism of organic anions
  • loss of H+ in vomitus
  • loss of H+ in urine
145
Q

What are the buffers

A

Combine with H+ to form HB in acidosis and vice versa to maintain body pH

  • HCO3- (intra and extracellular)
  • phosphates, Hb
146
Q

How do the kidneys maintain homeostasis

A
  • excrete ‘ reabsorption H+
  • phosphate / ammonia buffers
  • regulate plasma [HCO3-]
  • excretion of filtered HCO3-
  • addition of new HCO3- to blood
147
Q

What happens in acidaemia in the kidneys

A

High plasma [H+]

- increase H+ secretion (add new HCO3- to blood) -> decreases plasma [H+]

148
Q

How can reabsorption in the proximal tubule affect an alkalosis

A

Less HCO3- reabsorbed helps alkalosis
- can’t help acidosis because working at max HCO3-
Reabsorption (1 HCO3- reabsorbed for 1 HCO3- filtered)
No net gain of HCO3-

149
Q

What is ammoniagenesis

A

Creation of new ammonia to act as a buffer in the excretion of H+ ions in urine, and new HCO3- is added to the blood

150
Q

What is ammonium / diffusion trapping

A

NH4+ transported across apical membrane into tubular fluid but nephron membrane has limited permeability: travels around the nephron in the tubular fluid until the thick limb which is permeable

151
Q

What is the effect of aldosterone on the late DCT / CCD

A

1) stimulates Na+ reabsorption (principle cells) to maintain electroneutrality
2) stimulates K+ secretion (principle cells)
3) stimulates H+ secretion (intercalated cells) also b/c stimulates H+ATPase .: 1’ aldosterone excess of 2’ hyperaldosteronism -> metabolic alkalosis

152
Q

Why are diuretics so important

A 
Important cardiovascular drugs 
- management of CHF 
- antihypertensives 
- A/C (D) guidelines 
A: antihypertensives 
C: Ca2+ channel inhibitor 
D: diuretic
153
Q

What do diuretics do

A
  • increase Na+ secretion (natriuresis)
  • Na+ flowed osmotically by H2O
  • decrease ECF / plasma vol
    :- reduces oedema and BP
154
Q

What is natriuresis

A

Excretion of sodium

155
Q

What are the different types of diuretics

A

Osmotic agents
Loop diuretics
Thiazides
Potassium sparing agents

156
Q

What are osmotic diuretics

A

Eg mannitol
Pharmacologically inert
Freely filtered in bowman’s capsule
Increases osmolality of tubular fluid in PCT and loop of henle
Reduce passive reabsorption of H2O
Used in cerebral oedema (increases osmolaltiy and removes fluid from the brain)

157
Q

What are loop diuretics

A

Reduces ability of loop to concentrate urine by preventing creation of an hypertonic interstitium in the medulla

  • increases Na+ delivery to DCT
  • promotes K+ loss (risk of hypokalaemia)
  • decreases Na+ entry into macula dense - promotes renin release

Kidney becomes refractory (less responsive) to LDs for some hours after use (regimen: o.d)

158
Q

What are the uses of loop diuretics

A

CHF
- reduce pulmonary oedema, 2’ to LVF and peripheral oedema

Venodilators
- iv, rapid effect in acute LVF

Renal failure
To improve diuresis

159
Q

What are thiazides

A

Moderately powerful diuretics eg chlorothiazide, chlorthalidone
Act on DCT (less important for Na+ balance)
Blocks Na+ /Cl- cotransporter
- inhibits active Na+ reabsorption and accompanying Cl-
- reduce circulating volume
Used in mild / moderate heart failure
2nd line in hypertension
Renally excreted / secreted by weak acid transporter in PCT before acting on DCT

160
Q

How does aldosterone cause hypokalaemia

A

Acts on mineralocorticoid receptor (intracellular) -> goes to the nucleus and determines which genes are expressed
- mRNA and aldosterone induced proteins produced -> Na+ channels inserted into basolateral membrane
Na+ reabsorbed so K+ is lost

161
Q

What are potassium sparing diuretics

A

Aldosterone receptor antagonists

  • Na+ channel blockers of DCT
  • weak diuretics but in combination with K+ losing agents may reduce K+ loss
  • ACEi cause hyperkalaemia so may negate effects of K+ losing diuretics
162
Q

What are aldosterone (mineralocorticoid) receptor antagonists

A

Eg spironolactone
- antagonise aldosterone receptors
- prevent insertion of Na+ pumps and channels
- used in 1’/2’ hyperaldosteronism eg ascites
Used in CHF to block aldosterone actions on heart

163
Q

What are sodium channel blockers

A

Eg amiloride / triamterene
Block luminal Na+ channels in late DCT and CD
Na+ no longer retained at expense of K+

164
Q

What is renoprotection

A

Diabetes associated with renal nephropathy -> cause of chronic renal failure
ACEi slow renal damage, advocated in nephropathy / diabetes + hypertension
- block inappropriate RAAS activation

165
Q

How to counsel a patient for diuretics

A 
Best taken morning so sleep isn’t disturbed by needing to urinate 
Pt will experience increased urine flow 
Avoid excess salt in diet 
May cause postural hypotension 
- thiazides may uncover or worsen diabetes 
- thiazides / LD may worsen gout 
- NSAID may reduce effect of LD
Electrolytes should be monitored
166
Q

What is hyponatremia

A

Deficiency of sodium

Common

167
Q

What is hypernatremia

A

Excess sodium

Common

168
Q

What causes hyponatremia

A

Usually H2O retention

  1. Advanced renal failure or inability to suppress secretion of ADH
  2. Effective circulating volume depletion
  3. Syndrome of inappropriate ADH secretion
  4. Hormonal changes (cortisol deficiency, hypothyroidism)
    - primary polydipsia (excessive thirst, often schizophrenic)
  5. Renal osmostat
169
Q

Treatment of hyponatremia

A

Water restriction, increase salt intake / diuretics
Depends on severity and cause
Aggressive treatment can cause central pontine myelinolysis

170
Q

What is pseudohyponatremia

A

Artefactually low serum [Na+] b/c volume displacement but hyperlipidaemia or hyperproteinaemia
Can be caused by hyperosmolar state eg hyperglycaemia in uncontrolled diabetes

171
Q

What is hypernatraemia

A

Less common than hypo b/c thirst is main defence mechanism against it
- v rare in alert pt w access to water and normal thirst
Found in pt over 60 (bc ability to create concentrated urine is worse)

172
Q

What are the causes / treatment of hypernatremia

A

Mainly H2O loss (diabetes, fever + impaired thirst)
Na+ retention eg administration of hypertonic NaCl or NaHCO3
H2O out of cells -> decrease in brain vol, lethargy, seizures, coma

Tx: decrease Na+, increase H2O

173
Q

How is K+ balance regulated

A

ECF [K+] controlled by:

  • uptake of K+ into cell
  • renal excretion and extrarenal losses
  • abnormalities can cause hypo / hyperkalaemia
174
Q

Why is the distribution of K+ important

A

Affects membrane potential
Transcellular shifts more important for Sx than external shifts
ICF K+ affects protein and glycogen synthesis
Only small [K+] ECF but small changes affect tissue excitability
Dietary K+ intake can’t be rapidly excreted renally

175
Q

What happens if K+ distribution increases

A

Depolarises membrane -> more excitable - persistent depolarisation inactivates Na+ channels : membrane excitability decreases : impaired cardiac conduction / mm weakness

176
Q

What happens is K+ distribution decreases

A

Hyperpolarises membrane -> less excitable in cardiac myocytes membrane excitability increases b/c removal of normal inactivation of Na+ channels
Impaired cardiac conduction / mm weakness

177
Q

What is the influence of insulin (glucagon) on K+

A

Increases K+ uptake into cells: activates Na+ / K+ ATPase

178
Q

What is the influence of catecholamines on K+

A

Beta-2 receptors; increase K+ uptake into cells; activates Na+/K+ ATPase

179
Q

What is the influence of plasma K+ concentration on K+

A

Increased K+ in plasma -> K+ movement into cells

Decrease K+ in plasma -> K+ moves out of cells

180
Q

What are the consequences of hypokalaemia

A

Often no Sx or if more severe non specific Sx

  1. Muscle weakness / paralysis (inc gut)
  2. Cardiac arrhythmias
  3. Rhabdomyolysis
  4. Renal dysfunction
181
Q

What are the causes of hyperkalaemia

A

Usually pt with renal failure

  1. Increased intake of oral salt or IV
  2. Movement from cells into ECF
  3. Decreased urinary excretion
182
Q

What are the consequences of hyperkalaemia

A

Mm weakness / paralysis (sustained depolarisation inactivates Na+ channels :. Decreased excitability)
Cardiac arrhythmias

183
Q

Hyperkalaemia treatments

A
  1. Antagonism of membrane actions
    - Ca2+ restores membrane excitability
  2. Increase K+ entry into cells
  3. Removal of excess K+
184
Q

What is referred pain

A

Perception of visceral pain some way away from the organ involved

Doesn’t accurately represent where the problem is
Signal from several areas of the body often travel through the same nerve pathway

185
Q

What is the relevance of the viscera

A

Innervated mostly only by autonomic nerves :. Visceral pain conducted along afferent autonomic nn (can only enter CNS where sympathetic / parasympathetic motor fibres leave)

Sensory info from viscera may be involved with reflex activity of elicit pain

186
Q

What is the difference between somatic and visceral pain

A

Somatic is epitomised by pain arising from the skin, many modalities, sensitive, well localised, often sharp, many sensory receptors

Visceral has fewer sensory endings, often in smooth muscle, poorly localised, dull, heavy or gripping, may be referred

187
Q

What is visceral pain

A

From internal organs
Mild discomfort of indigestion
Agony of a renal colic
Reproductive life
Common cause to seek medical intention
Viscera insensitive: crushing / cutting / burning
Viscera sensitive: stretching / contraction

188
Q

What are visceral afferent fibres

A

No peripheral synapse (unlike visceral efferent)
Joins a spinal nn, enter CNS along dorsal nerve root
- cell body found in dorsal root ganglion
- enters spinal cord at T1-2 (sympathetic motor outflow), S2-4 (parasympathetic outflow)

189
Q

What is the mechanism of referred pain

A

Not known
Nociceptors from several locations converge on a single tract
Pain signal from skin more common (high sensory input)
Brain associates activation of pathway with pain in skin

190
Q

Examples of referred pain

A

Appendix: RLQ, U
Bladder: lower abdomen, upper thighs
Diaphragm: shoulders
Oesophagus: along sternum, L upper thorax
Heart: base of neck, L jaw, L shoulder and arm
Intestines: back (backache / sharp pain in back), U
Kidneys: posterior costovertebral angle, radiating forwards around the flank
Liver: R shoulder
Pancreas: directly behind pancreas, LLQ, U
Spleen: L shoulder, upper 1/3 of arm
Ureter: costovertebral angle radiating to lower abdomen, testicles, inner thigh

191
Q

Routes of excretion

A 
Expired air 
Urine 
Bile 
Sebum / sweat 
Breast milk
192
Q

How does excretion in the bile work

A

Active transport process for highly polar compounds
Minor route for unmetabolised drug
Major route for drug metabolites
May be alternative route of excretion of polar drugs in patient with renal impairment
Possibility of enterohepatic re circulation

193
Q

What are the consequences of enterohepatic re circulation of drugs

A

Prolongation of drug action

Localisation of drug action

194
Q

Why are NSAIDs contraindicated with methotrexate

A

B/c competition for secretion (blocked by salicylate) :. Less secreted so toxicity increases

195
Q

How should you prescribe in renal impairment

A

Choose short acting agents
Gentamicin: increase dosage interval
- choose non renally excreted alternative
Some drugs must be avoided eg meteor in
Some require renal excretion to act :. Ineffective in renal impairment

196
Q

How do you prescribe if a patient is on dialysis

A

Excretion will be altered by the membrane permeability

Consult a specialist

197
Q

Describe the effects of excretion of drugs in milk

A

Limited evidence
Amount of drug relates to pharmacokinetics
Could have effect on baby

BNF:
Drug used with caution / contraindicated
Present in milk but not known to be harmful
Not known to be harmful

Med 3 (10 decks)

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