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Semester 3 > Urinary 1-6 > Flashcards

Urinary 1-6 Flashcards

1
Q

What is the main function of the urinary system?

A

Control concentrations of key substances in extracellular fluid - homeostasis

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2
Q

What results from failure to control ECF volume?

A

Changes in blood pressure, tissue fluid and cell function

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3
Q

What reults from failure to control ECF osmolarity?

A

Cells shrink or swell

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4
Q

What are membranes permeable to?

A

Very permeable to water, selective to other types of molecules and electrolytes

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5
Q

What is osmolality?

A

Solute per kg of solvent - functionally the same as osmolarity.

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6
Q

What is osmolarity?

A

Number of osmoles of solute per litre - total concentration of substances which do not cross the membrane freely

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7
Q

Is potassium concentration higher intra cellularly or extra cellularly?

A

Intracellularly (sodium opposite)

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8
Q

What are the main anions extra cellularly?

A

Cl- and HCO3-

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9
Q

What controls the pH of extra cellular fluid?

A

HCO3

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10
Q

How do the kidneys control homeostasis?

A

Control volume

Control osmolarity

help to control pH

Excrete some waste products

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11
Q

What substances are 100% reabsorbed?

A

HCO3, glucose and amino acids

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12
Q

What % of cardiac output goes to the kidneys? (at rest)

A

25%

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13
Q

What is the functional unit of the kidney?

A

Nephron - filter unit connected to a long tube for reabsorption

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14
Q

In order, what are the regions of the nephron?

A

Prox. con. tubule (cortex) -> loop of henle (into and out of medulla) -> dist. con. tubule (cortex) -> collecting duct (passes through the medulla to pelvis)

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15
Q

What is the glomerulus?

A

Highly specialised filter.

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16
Q

What is filtered through the glomerulus?

A

Water, electrolytes and small molecules - NOT large proteins

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17
Q

What causes filtration through the glomerulus?

A

Pressure from the capillaries to the afferent arterioles.

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18
Q

Where is the major site of reabsorption in the kidneys?

A

Proximal convoluted tubule -

60-70% Na and water

80-90% K

90% HCO3

100% glucose and aa (usually)

reabsorbed materials leave by peritubular capillaries

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19
Q

What are the 2 membranes lining the tubular cell?

A

Luminal (luminal side)

Basolateral (ECF side)

POLARISED

allow transport across the epithelium

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20
Q

What controls tranport across the tubular cell membranes?

A

Na-K pump - couple other substances to energy from sodium movement. Water follows osmotically

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21
Q

What is the main function of the loop of henle?

A

Create a gradient oof increading osmolarity in the medulla by counter-current multiplication - produces concentrated urine as water is reabsorbed

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22
Q

How is the distal convoluted tubule different to the prox.?

A

Variable reabsorption of electrolytes and water.

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23
Q

What is the function of the dis. con. tubule?

A

Removes more Na and Cl and actively secretes H ions

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24
Q

What is diluresis?

A

large volumes of dilute urine

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25
Q

What controls sodium recovery?

A

Renin angiotensin system - controls ECF volume

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26
Q

What controls water recovery?

A

Anti diuretic hormone - controls permeability of DCT and collecting duct to water - this controls the ECF osmolarity

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27
Q

How might you gather an image of the renal tract?

A

Ultrasound

CT scan

MRI

KUB

Micturating Cystogram

Urethrogram

Retrograde Pyelogram

Antegrade Pyelogram

Arteriography

DMSA scan

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28
Q

Where do the kidneys lie?

A

Each side of the vertebral column betwen T12 and L3

Retroperitoneal

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29
Q

Where are the renal corpuscles found?

A

Cortex

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30
Q

Where are the tubules found?

A

Pass from the cortex through the medulla

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31
Q

What is the renal corpuscle?

A

Glomerulus and bowmans capsule

Produces ultrafiltrate plasma

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32
Q

What is another name for the collecting duct?

A

Ducts of Bellini

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33
Q

What is the renal papilla?

A

Location where the medullary pyramids empty urine into the minor calyx

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34
Q

What is at the vascular pol of the corpuscle?

A

Afferent and efferent arterioles and glomerulous

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35
Q

What dos the urinary pole consist of?

A

Bowman’s capsule

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36
Q

What are the filtration barriers of the nephron?

A

Capillary endothelium and visceral layer of Bowman’s capsule

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37
Q

What does the parietal layer of Bowman’s capsule do?

A

Makes a “funnel” to collect ultrafiltrate which drains into the prox. con. tubule at urinary pole

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38
Q

Describe the capillary endothelium in the nephron

A

Fenestrated with podocytes investing into it with slits between them.

Endothelium and podocytes share the basement membrane

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39
Q

What type of epithelium lines the prox.con.tubule?

A

Simply cuboidal with pronounced brush border

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40
Q

What is the longest part of the tubule?

A

Proximal

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41
Q

What are the 4 parts of the Loop of henle?

A

Pars recta

Thin descending limb

Thin ascending limb

Thick ascending limb

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42
Q

What is the epithelium of the thin limb of the loop of henle?

A

Simple squamous

No active transport

No brush border

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43
Q

What is the epithelium in the thick ascending limb of the loop of henle?

A

Simple cuboidal, no brush border

Active transport

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44
Q

Describe the distal convoluted tubule

A

Cortical

Makes contact with its parent glomerulus

Contains numerous mitochondria

No brush border adn larger lumen than PCT

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45
Q

What makes up the juxtaglomerular apparatus?

A

The macula densa of the distal convoluted tubule

Juxtaglomerular cells of afferent arteriole of glomerulus

Extraglomerular meangial cells (aka lacis cells)

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46
Q

What is the collecting duct?

A

Continuation of the DCT via collecting tube

Similar appearance to the thick limbs of loop of Henle but lumen is larger and tend to be more irregular rather than circular

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47
Q

What are the renal pyramids?

A

Progressively larger ducts formed by merging of collecting ducts

Emplty at renal papilla

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48
Q

What are the layers of the ureter?

A

2 layers of smooth muscle - only a third appears in the lower 1/3 of the ureter

Lined by transitional epithelium aka urinary epithelium or urothelium

It is a muscular tube

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49
Q

What are the histological layers of the bladder?

A

3 layers of muscle

Outer adventitia

Transitional epithelium

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50
Q

What is urothelium?

A

Stratified epithelium

“umbrella cells” on the surface layer which make the epithelium impermeable

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51
Q

What is the amniotic fluid made of?

A

Weak urine produced by the metanephric kidney from the end of the first trimester

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52
Q

What function do the mesonephric ducts have in an adult?

A

Male - reproductive function

Female - receed in development of the feotus - non-existant in adult life

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53
Q

What might cause abnormally low amniotic fluid volume?

A

Renal agenesis

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54
Q

What is another name for an ectopic kidney and how might this occur?

A

Pelvic kidney

Failure to ascend. Maintains fetal blood supply from iliac vessels or distal aorta

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55
Q

How might a horse shoe kidney occur?

A

Developing kidneys make contact in their ascen, fusion occurs. Most common in lower poles. Bridge of parenchyma called isthmus. When it reaches the inferior mesenteric artery it can rise no further.

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56
Q

What does a horseshoe kidney increase the risk of?

A

Hydronephrosis, kidney stones and renal cell carcinoma

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57
Q

Explain the embyological basis for the presence of accessory/supermumerary renal arteries.

A

Remain attached following ascent of kidneys and continues to supply kidney

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58
Q

What might cause duplication of the ureter?

A

Division of the ureteric bud

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59
Q

Why might a patient with ectopic ureteral orrifices suffer from incontinence?

A

No sphincter to control release of urine from ectopic ureteral orifice

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60
Q

Which nephrons have the longest loop of henle?

A

Lower nephrons (juxtamedullary), closer to the medulla penetrate further into the medulla with longer loop of henles.

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61
Q

What is the capillary arrangement of the nephrons?

A

Cortical - random

juxtamedullary - organised and structured. loops counter flow to loop of henle

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62
Q

How much blood is filtered throughn the glomeruli?

A

20% of the flow

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63
Q

Where are the glomeruli found?

A

Cortex

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64
Q

What are the 3 filter layers of the kidney?

A

Capillary endothelium

Basement membrane

Podocyte layer

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65
Q

Describe the basement membrane.

A

Acellular gelatinous layer of collagen/glycoproteins

Permeable to small proteins

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66
Q

Why do proteins not pass through the basement membrane?

A

Glycoproteins (- charge) repel protein movement

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67
Q

Describe the podocyte layer of the filtration barrier.

A

Pseudopodia interdigitate and form filtration slits

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68
Q

What causes proteinuria?

A

In many disease processes the negative charge on the filtration barrier is lost so that proteins are more readily filtered

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69
Q

What type of forces are involved in filtering plasma to form ultra filtrate?

A

Only physical forces:

  1. Hydrostatic forces in the capillary (regulated). Favours filtration
  2. Hydrostatic pressure in bowmans capsule. Oopposes filtration
  3. Osmotic pressure difference between the capillary and tubular lumen. Opposes filtration
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70
Q

What is tubular secretion and how does it work?

A

Transfer of materials from peritubular capillaries to renal tubular lumen.

Caused mainly by active transport.

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71
Q

What is usually secreted in tubular secretion?

A

Usually only a few substances which are in great excess or are natural poisons

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72
Q

What drives reabsorption in the PCT?

A

Sodium uptake - pumped across basolateral membrane by 3Na-2K-ATPase. Na moves across luminal membrane down conc gradient. This utilises a membrane transporter or channel. Water follows osmotically.

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73
Q

What sodium transporters are in the PCT?

A

Na-H antiporter

Na-Glucose symporter

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74
Q

What sodium tansporters are in the Loop of Henle?

A

Na-K-2Cl symporter

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75
Q

What sodium transporter is in the early DCT?

A

Na-Cl symporter

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76
Q

What sodium transporter is in the late DCT and CD?

A

Epithelial Na channels

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77
Q

How might a substance move against its concentration gradient?

A

Co-transport eg. SGLUT moves glucose against its concentration out of the PCT by co-transport with sodium via a symport.

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78
Q

What is the renal threshold for glucose?

A

200mg/100ml - plasma conc of a substance at which Tm is reached and the substance starts spilling into the urine

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79
Q

What is Tm for glucose in men and women?

A

Men = 375mg/min

Women = 300mg/min

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80
Q

How does organic cation secretion occur?

A

Passive carrier-mediated diffusion across the basolateral membrane down favourable concentration and electrical gradients created by the 3Na-2K-ATPase pump.

Secretion into the lumen occurs by a H+-OC+ exchanger that is driven by the H+ gradient created by the Na-H antiport (anions are the same)

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81
Q

Define renal plasma flow.

A

The amount of plasma that perfuses the kidney per unit time.

usually 605ml/min

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82
Q

What is haematocrit?

A

Percentage of a volume of blood sample occupied by cells

83
Q

What is filtration fraction?

A

Proportion of a substance that is actually filtered - 605ml of plasma enters the glomerulus and only 20% is filtered. Therefore 125ml is filtered through into bowman’s space, 408ml passes into peritubular capillaries

(GFR/RPF)

84
Q

What is glomerular filtration rate and how is it measured?

A

The quantity of filtrate formed each minute

Need to be able to measure a substance as it is filtered and use this as an indication of how well the kidney works. Chosen substance must not be altered in any way as it travels through the nephron - completely cleared from the plasma that is filtered, not reabsorbed or secreted

85
Q

Define clearance

A

The volume of plasma from which a substance X can be completely cleared to the urine per unit time

eg clearance for urea in a normal kidney is about 665ml/min so the kidenys remove all the urea from 65ml of plasma per min.

(Urine concentration of substance x urine flow rate) / (plasma conc of the substance)

86
Q

How is filtered fluid different to the remaining plasma fluid?

A

Filtrate in bowman’s capsule is identical to normal plasma, - proteins

Remaining plasma fluid contains the cells and proteins not filtered

87
Q

How is filtration regulated?

A

autoregulation by myogenic responses. Decrease in pressure in the glomerular capillay (blood pressure) causes afferent resistance to increase by constriction of the afferent arteriole. Increase in pressure of glomerular capillary causes a decrease in afferent resistance by relaxation of the afferent arteriole wall

This maintains the GFR when blood pressure is within physiological limits (80-180 mmHg)

88
Q

What cells recognise and respond to changes in the amount of NaCl reaching the distal tubule?

A

Macula densa cells NaK2Cl cotransporter. ATP can be released and converted to adenosine. This is recognised by A1 receptors on extraglomerular mesengial cells triggering a rise in intracellular calcium. This causes contraction of the smooth muscle in the walls of the arterioles - vasoconstriction and decrease of GFR. Prostaglandins are released for vasodilation.

89
Q

What region of the loop of henle reabsorbs salts and water?

A

Salts in ascending limb

Water in descending

90
Q

What causes secretion of K and reaborption of Na and water in the DCT?

A

Aldosterone

91
Q

How can you change the plasma volume?

A

Must add or remove an isosmotic solution - not change osmolarity

Move osmoles, water follows

92
Q

How much Na is reabsorbed in each region of the nephron?

A

PCT - 67%

Loop - 25%

DCT - 5%

Collecting duct - 2.5%

0.5% remains at the end approx

93
Q

Where is no water reabsorbed?

A

Ascending limbs of loop of henle

DCT (vv little)

94
Q

What is glomerulotubular balance?

A

Balance between glomerulous and PCT

2nd line of defence which blunts sodium excretion response to any GFR changes which occur despite autoregulation

Reabsorption of Na in the PCT is a % of filtered load not set amount (unless Tm exceeded)

95
Q

Is Na reabsorption trans or paracellular?

A

Transcellular

96
Q

Is chloride reabsorption trans or paracellular?

A

Both - trans i active, para is passive. Na ion reabsorption, Cl is implied

97
Q

What are the 2 regions of the PCT?

A

S1 - Na reabsorption. No movement of Cl or urea - increase conc. Stabilises osmolarity.

S2 and 3 - Conc grad. of Cl and urea from S1

(Osmolarity of PCT is constant)

98
Q

What transporters are in the membrane of S1/S2 and 3?

A
99
Q

What are the tranasporters in the TAL?

A

Lmenal membrane - NakCC2 and ROMK

Basolateral - NAKATPase and Cl transporters

100
Q

What is the most energy consuming area of teh nephron?

A

Thick ascending limb

101
Q

Why is the ROMK on the lumenal membrane of the TAL necessary?

A

Maintain some K in the lumen to allow NaKCC2 transporter to work

102
Q

Describe the structure of the descending limb of the loop of henle.

A

V few transporters. Lots of aquaporins

103
Q

What is the ascending limb of the loop of henle known as?

A

Diluting segment - tubule fluid leaving the loop is hypo-osmotic compared to plasma

104
Q

What is the importnat transporter in the DCT?

A

luminal - NCC transporter and calcium channel

basolateral - NCX, 3Na2K ATPase and chlorine channel - Ca removed, Na in (NCX) conc gradient established by NaKATPase.

105
Q

What are the 2 types of cells in the DCT?

A

Principle - reabsorption of NA ions via ENaC

Type B intercalated cells - active reabsorption of Chloride. Intercalated cells (secrete H ions or HCO3 ions)

106
Q

How do principle cells work?

A

Reabsorption of Na ions via ENA channel on apical membrane

3Na2KATPase in basolateral is the driving force

Active Na uon uptake through a channel and not a cotransporter means there is no accompanying anion

Produces a lumen with - charge providing a driving force for Cl ionuptake via paracellular route

This - charge in the lumen has an important role in K secretion into the lumen

Variable water uptake through ACP dependent on action of ADH

107
Q

Where are baroreceptors?

A

Nerve endings in the carotd sinus and aortic arch

108
Q

How are long term changes in blood pressure controled?

A

Complex interation of neurohumoral responses directed at controlling sodium balance and thus extracellular fluid volume. Plasma is part of this therefore volume of each is linked

  1. Renin-angiotensin-aldosterone system (RAAS)
  2. Sympathetic nervous system
  3. Antidiuretic hormone (ADH)
  4. Atrial natriuretic peptide (ANP)
109
Q

Describe the RAAS.

A

Renin is released from granular cells of juxtaglomerular apparatus

3 factors

reduced NaCl delivery to distal tubule

reduced perfusion pressure in kidney causes the release of renin - baroreceptors in afferent arteriole

sympathetic stimulation to JGA increases release of renin

110
Q

Where is renin stored?

A

Stored and released from granular cells of afferent arterioles

111
Q

What causes the relerase of renin in the kidney?

A

Decreased circulating volume - decreased NaCl conc at macula densa causes sympathetic stimulation to JGA. Decreased renal perfusion pressure is sensed by renal baroreceptors.

112
Q

Describe the formation of active angiotensin.

A

Angiotensinogen -> angiotensin I -> angiotensin II (active form)

converted by renin then ACE

113
Q

What effect does angiotensin have on the kidney?

A

vasoconstriction

enhance action of Na-H exchanger in apical membrane

Stimulates Na reabsorption by causing the release of aldosterone from the adrenal cortex

Increase thirst sensation in hypothalamus and cause ADH release

114
Q

How does aldosterone work in the kidney?

A

Stimulates Na and H2O reabsorption

Acts on principal cells of collecting duct

Activates apical Na channel and apical K channel

Also increases basolateral Na extrusion viaNaKATPase

(increases expression of ENaC and NaKATPase in preinciple cells of collecting duct)

115
Q

What is the effect of ACE inhibitors and when might they be used?

A

Reduce hypertension - prevent reabsorption of Na and water and prevent vasoconstriction by preventing the formation of angiotensin II

ACE also converts bradykinin to peptide fragments (breaks it down) which usually acts as a vasodilator

116
Q

What effect does the sympathetic nervous system have on the renal blood flow?

A

High stimulation reduces renal blood flow - decrease GFR - decrease Na excretion

Activates apical Na/H exchanger and basolateral Na/KATPase in PCT

Stimulates renin release from JGcells - increase Ang II / increaes aldosterone

117
Q

What is the role of ADH?

A

Formation of concentrated urine by retaining water and control plasma osmolarity

Release stimulated by increase in plasma osmolarity or severe hypovolaemia

Stimulates Na reabsorption

Acts on thick ascending limb

118
Q

What do natriuretic peptides do and where is it?

A

Promote Na excretion

Synthesized and stored in atrial myocytes

Released from atrial cells in response to stretch

Low pressure sensors in the atria

Reduced effective circulating volume inhibits the release of ANP- reduced filling of heart - less stretch

119
Q

What are the actions of NP on the kidney?

A

Vasodilation of afferent arterioles

Increased blood flow -> increases GFR

Inhibits Na reabsorption along the nephron

Acts in opposite direction to the other neurohumoral regulators

120
Q

What do prostaglandins do?

A

Act as vasodilators

enhance glomerular filtration and reduce Na reabsorption

May have important protective function

Act as a buffer to excessive vasoconstriction produced by SNS and RAAS

Important when levels of Ang II are high

121
Q

What do NASIDs do and when might this be a problem?

A

Inhibit cyclo-oxygenase (COX) pathway involved in formation of prostaglandins. Therefore if NSAIDs are administrated when renal perfusion is compromised can further decrease GFR -> acute renal failure.

122
Q

What is classified as hypertension?

A

Systolic BP >140

diastolic > 90

123
Q

What causes hypertenison?

A

In around 95% of cases the cause is unkown - essential hypertension. May be genetic factors, environmental.

If cause can be defind it is known as secondary hypertension - must treat primary cause

124
Q

What might cause secondary hypertension?

A

Renovascular disease

Chronic renal disease

Aldosteronism

Cushings syndrome

125
Q

How can renovascular disease cause hypertension?

A

Occlusion of the renal artery (stenosis) causes a fall in perfusion pressure in that kidney

Decreased perfusion pressure leads to increased renin production

Activation of the RAAS

Vasoconstriction and Na retention at other kidney

126
Q

How can renal parenchymal disase cause secondary hypertension?

A

Earlier stage may be a loss of vasodilator substances

Later, Na and water retention due to inadequate glomerular filtration - volume-dependent hypertension

127
Q

How does Conn’s syndrom cause hypertension?

A

Aldosterone secreting adenoma therefore causing an increased reabsorption of Na and water

128
Q

How can Cushing’s syndrome cause hypertension?

A

Excess secretion of glucocorticoid cortisol - at high concs acts on aldosterone receptors - Na and water retention

129
Q

What is a phaeochromocytoma and how can it cause hypertension?

A

Tumour of the adrenal medulla that secretes catacholamines (adrenaline and noradrenaline)

130
Q

What can result from hypertension that makes it “the silent killer”?

A
131
Q

How is hypertension treated?

A

Secondary - treat primary cause

ACE inhibitors, Ang II receptor antagonists - diuretic and vasodilator effects

Thiazide diuretics - inhibit Na-Cl co-transport on apical membrane of cells in distal tubule - other diuretics will but not first line choice

Vasodilators - L-type Ca channel blockers - reduce Ca entry to vascular smooth muscle cells -> relaxation of vascular smooth muscle. Alpha 1 receptor blockers reduce sympathetic tone

Beta blockers of B1 receptors in the heart will reduce effects of sympathetic output - reduce heart rate and contractility- not used in first line treatment but would be if there are other indications such as previous MI

Non-pharmacological approaches can be taken.

132
Q

How is a disorder of water balance manifested?

A

Changes in body fluid osmolarity

133
Q

How is a disorder in Na balance manifested?

A

Changes in body fluid volume

134
Q

On average, how much does a person urinate per day and how much water do they ingest? What does this mean for the osmolarity of urine?

A

1-1.5L/day urine

600-1000 mosm/day ingested

Excretion must match consumption therefore water lost is 1000mosmL in 1L

135
Q

What senses changes in plasma osmolarity?

A

Osmoreceptors in the Organum Vasculoum of the Laminae Terminalis (OVLT) of the hypothalamus. (anterior and ventral to the 3rd ventricle). Fenestrated leaky endothelium exposed directly to the systemic circulation

136
Q

What are the 2 efferent pathways that enable a changes in plasma osmolarity to be corrected?

A

thirst - brain alters drinking behaviour

ADH - Kidney excretes water

137
Q

What is ADH?

A

Anti diuretic hormone. 9 AA long peptide.

138
Q

When is osmolarity compromised?

A

When faced with circulatory collapse the kidneys continue to conserve water even though this will reduce osmolarity of body fluids

139
Q

What are the effects of ADH on the body?

A

Vasoconstriction in glomerulus can decrease the effective filtering surface area

Increases Na, K and Cl reabsorption in ascending limb

Increases water absorption in the DCT and CD

Increased secretion of K into the CD

Increased urea reabsorption in the CD

140
Q

How does ADH effect water reabsorption?

A

Inserts aquaporin 2 channels into the apical membrane making it permeable to water. The basolateral membrane already has aquaporin 3/4 in it so is already permeable. This allows water to move freely across the membrane. In the absence of ADH, aquaporin 2 is removed

141
Q

Does an increase or decrease in osmolarity cause the release of ADH?

A

Increase - more water reabsorbed to create a more dilute ECF

142
Q

Describe the osmolarity at the cortico-medullary border.

A

isosmotic

143
Q

Describe the osmolarity of the medullary intersticium

A

Hyperosmotic - increasing gradient down to the papilla

144
Q

How would the medullary intersticium be made isosmotic?

A

Block NaKCl transporters with a loop diuretic

145
Q

How is a hyperosmotic interstitual fluid created at the tubular bend of the loop of henle if only passive transport is occuring?

A

Urea is also present. Na diffuses down its concentration gradient to increase the osmolarity further (200 mosm difference) - counter current multiplier by the loop of henle. Maintained by the vasa recta acting as a counter current exchanger

146
Q

What is urea recycling?

A

Urea is moved out of the collecting duct (more so in the presence of ADH) into the surrounding interstitium. This increases the osmotic gradient and enables water to follow by diffusion. Urea is often taken up again by the ascending loop of henle and recycled back to the collecting duct to continue its journey towards excretion

147
Q

How is the plasma pH controlled by the kidneys?

A

Filter and variably recover hydrogen carbonate and actively secrete hydrogen ions

148
Q

What pH range in the blood is safe and normal?

A

7.38-7.42

<7.30 acidaemia

>7.42 alkalaemia

149
Q

Why is alkalaemia dangerous?

A

Lowers free calcium - increases excitability of nerves - >7.45 - parasthesia and tetany

150
Q

Why is acidaemia dangerous?

A

Increased plasma potassium

Affects many enzymes - reduced cardia and skeletal muscle contractility, reduced glycolysis in many tissues, reduced hepatic function

severe effects below 7.1, life threatening below 7

151
Q
A
152
Q

How much hydrogen carbonate is dissolved compared to CO2?

A

20 times as much hydrogen carbonate as dissolved CO2. This ratio determines the pH

153
Q

How is the concentration of hydrogen carbonate controlled?

A

By the kidney. Disturbed by metabolic and renal disease

154
Q

What is the difference between pH correction and compensation?

A

Correction - remove the original problem to fix it

Compensation - fix the problem by bringing the ratio back to normal using the other component. Eg. if CO2 is changed, use HCO3- to fix it

155
Q

How is metabolic acidosis conpensated for?

A

Chnging ventilation:

  • peripheral chemoreceptors
  • increased ventilation lowers pCO2
  • restores pH towards normal
156
Q

What does acidosis mean?

A

Change in the buffer base - if conc. HCO3- changes, acid/alkalosis, CO2 changes - acidaemia…

157
Q

Why can metabolic alkalosis only be partially compensated for by ventilation?

A

To keep more CO2 would mean reducing O2 intake which is not a viable option after a point. Therefore, generally, HCO3 conc is corrected and CO2 is compensated

158
Q

How can HCO3 be created?

A

Metabolic activity of the kidneys produces large quantities of CO2 which can react with water to produce HCO3- to enter plasma and H+ to enter urine.

Can also make HCO3- from amino acids (particularly glutamine) producing NH4- to enter the urine

159
Q

Where is HCO3 recovered in teh kidneys?

A

80-90% in prox con tubule

remainder in thick ascending imb of the loop of henle

160
Q

How is HCO3- recovered in the loop of henle?

A

Coupled to the movement of Na+ out and H+ in. Reactes with H+ -> H2O + CO2 which moves into the tubular cell and reformed to HCO3- by reaction again with H2O

161
Q

How is HCO3- created in the prox con tubule?

A

Glutamine broken down to produce alphaketoglutarate which makes HCO3- and ammonium (ammonia + hydrogen first, then reaction to ammonium). HCO3- is moved into ECF and NH4+ into lumen.

162
Q

How is HCO3- created in the distal convoluted tubule?

A

By this poit all filteres HCO3= is usually recovered, Na gradient insufficient to drive H+ secretion so need active secretion of H+ into lumen. Here it is buffered by filtered phosphate and excreted ammonia. H+ is generated from metabolic CO2 and HCO3- is produced which enters the ECF

163
Q

What is the minimum urine pH?

A

4.5 - no HCO3=, some H+ buffered by phosphate (titratable acid), rest attached to ammonia as ammonium

Total acid excretion 50-100mmol H+ per day. This keeps plasma [HCO3] normal

164
Q

What are the cellular responses to acidosis?

A

Enhanced H+/Na+ exchange - full recovery of all filtered HCO3-

Enhanced ammonium productin in prox tube

Increased activity of H+ ATPase in distal tubule

Increased capacity to export HCO3- from tubular cells to ECF

165
Q

What is the cellular response to metabolic acidosis?

A

Acids produced metabolically produce H+ and an ion. H+ reacts with HCO3- producing CO2 which is breathed out. So some HCO3- is replaced by anion from acid

166
Q

What is the anion gap?

A

Indicates whether any HCO3- has been replaced with something other than Cl-

= ([Na+]+[K+]) - ([Cl-]+[HCO3-]) (unaccounted anions)

Normally 10-15mmol/l. Increased if anions from metabolic acid has replaced plasma HCO3-

Sometimes renal problems can reduce [HCO3-] without increaseing the anion gap as it is replaced with Cl-

167
Q

If the anion gap does not change but the blood is acid, what is the cause?

A

Disease of the kidney - HCO3- replaced with Cl-

168
Q

When might metabolic alkalosis occur and why might this be particularly difficult to correct?

A

Increase HCO3- after persistant comiting. Should be easy to correct as HCO3- infusions excreted extremely rapidly (rise in intra-cellular pH reduces H+ excretion and HCO3- recovery

However, if there is also volume depletion, capacity to lose HCO3- is less, because of high rates of recovery of Na+ favouring HCO3- recovery and H+ secretion as well

169
Q

How do acid base disturbances effect potassium?

A

Metabolic acidosis associated with hyperkalaemia as K+ moves out of cells and more K+ is reabsorbed in the nephron. These conditions favour H+ excretion and HCO3- recovery and therefore metabolic alkalosis

Metabolic alkalosis is associated with hypokalaemia as K+ moves into cells and less K+ is reabsorbed. This causes HCO3- excretion to be favoured and can therefore cause metabolic acidosis

170
Q

What % of body weight is water?

A

60%

171
Q

How much of the body’s water is ICF/ECF?

A

2/3 ICF

1/3 ECF

172
Q

Where is K+ measured to determine hypo/hyperkalaemia?

A

Intertitial fluid

173
Q

How much potassium is in the ICF?

A

98% of the bodies ICF

174
Q

How is the ICF & ECF [K+] maintained?

A

Na-K ATPase moves out of ECF into cells

K+ channels move K+ out of cells into ECF

175
Q

What is the resting membrane potential?

A

-90mV (ICF more negative)

176
Q

Why is the regulation of K+ so importatn?

A

The resting membrane potential of cells is dependent on the [K+] in ICF and ECF

(Increase ECF [K+] depolarizes the cell membrane potential, decrease causes hyperpolarization of the cell)

These changes have a profound effect on excitability of cardia and neuromuscular tissues and hence their function. (IC K+ important in cellular function)

177
Q

How much K+ is lost in the GI tract?

A

5-10%

178
Q

What is responsible for the long term control of K+?

A

Kidneys

Slow to act. Approx 6-12 hrs to excrete a load of potassium

179
Q

What factors promote the uptake of K+ into cells?

A

Hormones

Alkalosis (decrease ECF H+)

Increased K+ in ECF

180
Q

What hormones promote the uptake of K+ into cells?

A

Insulin - K+ in splanchnic blood stimulated insulin secretion by pancreas and in return insulin stimulates K+ uptake by muscle cells and the liver via increase in Na-K-ATPase

Aldosterone - K+ stimultaes aldosterone secretion…

Catecholamines - acts via beta 2 adrenoreceptors which in turn stimulate Na-K-ATPase which stimulates teh cell uptake of K+

181
Q

What factors promote the K+ shift out of cells

A

Low WCF [K+]

Exercise

Cell lysis

Increase in ECF osmolarity

Acidosis - increase ECF [H+] shift of H+ into cells, reciprocal K+ shift out

182
Q

How does excercise affect ICF and ECF K+?

A
183
Q

How does cell lysis effect K+ ICF and ECF?

A
184
Q

How does plasma tonicity affect K+ ICF and ECF?

A
185
Q

How does acid base disturbance affect the ECF K+?

A
186
Q

Where in the nephron is K+ reabsorbed and secreted?

A
187
Q

What tubular factors affect K+ secretion by principal cells?

A

Aldosterone

K+ in EFC

Acid base status

188
Q

What luminal factors affect K+ secretion by principal cells?

A

increase DCT flow rate, increaes K+ loss

Increase sodium delivery to distal tubule results in more K+ loss

189
Q

What cells in the DCT and collecting duct absorb K+?

A

Intercalated cells via an active process. Mediated by H+ K+ ATPase in apical membrane

190
Q

When may hyperkalcaemia be expected to occur?

A

Untreate diabetic ketoacidosis

Treatment with ACEI

Addisons disease

Kidney failure

Cushings syndrom

Poor perfusion of the kidney due to renal artery stenosis

191
Q

What effects does changes in ECF {K+] have?

A

Alter cell membrane resting potential

Alter neuro muscular excitability

Result in arrhthmias, cardiac arrest, muscle paralysis

192
Q

What might hyperkalaemia be due to?

A

Problems of external balance - increased intake (only causes problems in the presence of renal dysfunction unless inappropriate doses given IV),

Inadequate renal excretion - acute/chronic kidney injury or reduced aldosterone with normally functioning kidneys

Internal shifts - diabetic ketoacidosis, other metabolic acidosis, cell lysis (muscle cruch injury)

193
Q

When might there be reduced aldosterone?

A

Adrenal insufficiency

Drugs which reduce/block aldosterone action

K sparing diuretics

ACEI

194
Q

What effect does hyperkalaemia have on cardia tissue?

A

Depolarizes it -> more Na channels remain in inactive form, heart less excitable

195
Q

What are the clinical features of hyperkalaemia?

A

Heart - altered excitability -> arrhythmias, heart block

GI - neuromuscular dysfunction -> paralytic ileus

Acidosis

196
Q

What ECG changes may be brought about by hyperkalaemia?

A

Ventricular fibrillation

Atrial standstill, intraventicular block

Prolonged PR interval, depressed ST segment, high T wave

197
Q

What is the emergency treatment for hyperkalcaemia?

A

Reduce K+ effect on heart - IV calcium gluconate

Shift K+ into ICF - glucose +insulin IV/nebulised beta agonists (salbutamol)

Remove excess K+ - dialysis

198
Q

What are the long term treatments of hyperkalcaemia?

A

Treat cause

Reduce intake

Measures to remove excess K+ (dialysis, oral K+ binding resins to bind K+ in gut)

199
Q

What might hypokalaemia be due to?

A

Problems of external balance - excessive loss (GI/kidney)

Problems of internal balance - shifts of K into ICF eg metabolic alkalosis

200
Q

What effect does hypokalaemia have on the resting membrane potential of cardiac cells?

A

Hyoerpolarises -> more fast Na channels available in active form -> heart more excitable

201
Q

What are the clinical features of hypokalaemia?

A

Heart - altered excitability -> arrhythmias

GI - neuromuscular dysfunction -> paralytic ileus

Skeletal muscle - neuromuscular dysfunction -> muscle weakness

Renal - dysfunction of collecting duct cells -> unresponsive to ADH -> nephrogenic diabetes insipidus

202
Q

What are the ECG changes associated with hypokalaemia?

A

Low T wave

High U wave

Low ST segment

203
Q

What is the treatment of hypokalaemia?

A

Treat cause

Potassium replacement - IV/oral

If due to increased mineralocorticoid activity, potassium sparing diuretics which block action of aldosterone on principle cells

204
Q
A

Semester 3 (19 decks)

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