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Year 1 LSS > Urinaty Sytem > Flashcards

Urinaty Sytem Flashcards

1
Q

In what structures do the kidneys lie?

Where does it originate from?

What does it contain?

A

Lie in dense fibrous capsule called renal fascia

It derives from the transversalis fascia

It contains fat (for protection) but also is continuous anteriorly and contains major blood vessels (IVC and Aorta)

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2
Q

At which spinal levels can the kidneys normally be found?

A

Hilum of the kidney at around L1 (for both)

Start at around T11/T12( left) or T12 (right)

–> Because of right kidney often lower

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3
Q

To which structure does the kidney relate superiorly?

A

The kidney relates superiorly to the diaphragm

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4
Q

What are the important anatomical structures the kidneys relate to posteriorly?

Which nerves run posteriorly to the kidney?

A

Diaphragm, transverse abdominis+ posterior abdominal muscles

–> all separated from the kidney by the transversalis fascia

Nerves:

  • 11 intercostal nerve
  • subcostal nerve
  • Iliohypogastric nerve and Ilioinguinal nerve
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5
Q

Which structures doe the right kidney relate to anteriorly?

A

It lies behind the Hepatic flexure

The hilus of the kidney lies behind the 2nd part of the duodenum (curvature)

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6
Q

Which structures doe the left kidney relate to anteriorly?

A

It relates to different structures:

  • Pancreas
  • Stomach
  • Spleen
  • Splenic flexure (left upper curve of colon)
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7
Q

Summarise renal blood supply from the aorta and drainage into the IVC. Include the length of the vessels for the right and left kidney, and arrangement of blood vessels.

A
  • Kidneys get directly supplied by short branches of the aorta (20-25% of resting CO)
  • Drain into the IVC

Relations:

The aorta lies left and posterior to the IVC resulting in different blood vessel length:

Right kidney:

  • long artery, shorter vein

Left Kidney:

  • short artery, longer vein
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8
Q

How is the relation between the superior mesenteric artery and the left renal vein?

A

The left renal vein passes anteriorly over the aorta but is overlapped by the superior mesenteric artery originating superior to left renal vein

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9
Q

How are the blood vessels and the ureter /pelvis of kidney arranged in the hilum of the kidney?

A

From anterior to posterior

  1. Vein
  2. Artery
  3. The pelvis of Kidney (also inferior)
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10
Q

Summarise the structure of the kidney

A

Has a Cortex (outer part)

  • granular appearance because of random organisation

And a Medulla

  • Straited appearance because of radial arrangement of tubules and micro-vessels

The Medulla occurs in Lubules (Multi-lobular kidney in humans)

  • Each medulla part of lobule is called Pyramid
  • Each lobule has own calyx and renal papilla
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11
Q

What is the Calyx in the kidney?

A

Chambers of the kidney through which urine passes

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12
Q

What is the renal papilla?

A

It is the junction of the site where urine from medullary pyramids enters the calyx

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13
Q

Which route do the ureters take to get from the kideny to the bladder?

A
  • Run vertically down posterior abdominal wall in the vertical plane of the tips of the transverse processes of the lumbar vertebrae
  • Cross aorta at bifurcation of the common iliac arteries and the pelvic brim anterior to the sacroiliac joint
  • Descend anteromediallyto enter bladder at the level of the ischialspine
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14
Q

How are the ureters supplied with blood?

A

Basically from every major vessel they cross:

  • renal artery
  • gonadic artery
  • common iliac artery
  • internal iliac artery
  • some branches directly from the aorta

–> If only one blood supply gets blocked, nothing functions anymore

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15
Q

How is urine transported down the ureters?

A

By peristaltic contraction of SM

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16
Q

Where do the sphincters of the ureters sit?

What is their relevance?

A

3 sites of ureteric constriction:

  1. pelviuretericjunction
  2. where ureter crosses pelvic brim
  3. where ureter traverses bladder wall

–> often sites where renal stones get trapped and cause pain

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17
Q

Which epithelium lines the ureters and the bladder?

A

Specialised transitional endothelium/ urothelium

  • very tight junctions ! –> impermeable to water
  • Look stratified when relaxed but arent!
  • When stretched: show simple epithelium
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18
Q

Where does the bladder sit?

A

In the pelvis, below the peritoneum

But when filled:

Can reach into the abdominal cavity, pushes peritoneum away to also allow a direct catheter

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19
Q

What is the shape of the bladder?

A

•Triangular pyramid with apex pointing anteriorly and base posteriorly

Superior surface expands when bladder filled

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20
Q

What is the trigone in the bladder?

A

Triangular stretched part of the bladder between the entrance of the ureters and exit of the urethra

–> most bladder cancers occur in this region

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21
Q

By which structure is the bladder being held in place in males and females?

A

Females:

Pubovesical ligament around the urethra

Males:

Puboprostatic ligament around the prostate

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22
Q

What is the difference between the two sphincters of the bladder?

Where do they sit in males and females?

A

1. Internal/ Sphincter vesicae

  • Smooth muscle –> involuntary control via reflex opening in response to wall tension
  • At the neck of the bladder
  • Relaxed by PNS, contracts by SNS innervation

2. External/ Sphincter urethrae

  • Striated muscle –> voluntary control can be learned
  • In perineum (Perineal membrane)

–> In Females: right below internal sphincter, in males below the prostate gland

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23
Q

What is the difference between the male and the female urethra?

A

The male urethra is way longer and has almost two right angles within

Femal is short and straight

Also, parts have different names

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24
Q

How is the lymph drainage of the urinary system organised?

A

Lymph basically follows arterial supply

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25
Q

What are the 5 main steps in urine production of the kidney?

A
  1. Filtration
  2. Reabsorption
  3. Creation of hyper-osmotic extracellular fluid
  4. Adjustment of ion content of urine
  5. Concentration of urine
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26
Q

Of which components does the Renal corpuscle consist?

A

It consists of the

  • Bowman’s capsule (surrounding glomerulus)
  • Glomerulus (capillary network)
  • Podocytes (cells that wrap around glomerulus)
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27
Q

How does the blood supply of the renal corpuscle supports its function?

A

A big afferent and small efferent ateriole create a hypertonic environment for filtrate to leave capillaries

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28
Q

What structural components support the filtration of blood in the renal corpuscle?

A
  1. Large surface area –> many capillaries
  2. Fenestrated epithelium
  3. Modified basement membrane with many gaps

–> Allows plasma to leave blood

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29
Q

Which substances are filtered out of the blood in the renal corpuscle?

A

Everything <50.000 kDa

–> Almost everything except blood cells and bigger proteins

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30
Q

Which components of the primary filtrate are reabsorbed in the proximal convoluted tubule?

What is the mechanism behind each?

A
  • Na+uptake by basolateral Na+pump
  • Water and anions follow Na+
  • Glucose uptake by Na+/glucose co-transporter
  • Amino acids by Na+/amino acid co-transporter
  • Protein uptake by endocytosis
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31
Q

Which structural components of the proximal convoluted tubule allow reabsorption of the filtrate?

A
  • Cuboidal epithelium
  • Sealed with (fairly water-permeable) tight junctions
  • Membrane area increased to maximise rate of resorption:
  1. brush border at apical surface
  2. interdigitations of lateral membrane
  • Contains aquaporins
  • Prominent mitochondria reflect high energy requirement
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32
Q

Which structural component of the nephron creates the hyper-osmotic extracellular fluid?

What does it consist of?

A

The Loop of Henle consisting of

  1. Descending thin tubule (water reabsorption)
  2. Ascending thick limb ( generation of concentration gradient)
  3. Vasa recta (reabsorption of fluid into blood)
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33
Q

What is the function of the descending thin tubule in the loop of Henle for creation of the hyper-somitic extracellular fluid?

Which structural components contribute to this?

A

•Passive osmotic equilibrium (aquaporins present)

–> Water leaves the primary filtrate

•Simple squamous epithelium

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34
Q

What is the function of the ascending thick tubule in the loop of Henle for creation of the hyper-somitic extracellular fluid?

Which structural components contribute to this?

A

Generation of a concentration gradient

  • Na+and Cl-actively pumped out of tubular fluid
  • Results in hypo-osmotic tubular fluid, hyper-osmotic extracellular fluid

Structural components:

  • Very water-impermeable tight junctions
  • Cuboidal epithelium, few microvilli
  • High energy requirement - prominent mitochondria
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35
Q

What is the vasa rectae and which role does it play in the creation of a hyperosmotic extracellular fluid?

A
  • Blood vessels also arranged in loop
  • Blood in rapid equilibrium with extracellular fluid
  • Loop structure stabilises hyper-osmotic [Na+]

–> takes up water to maintain Na+ gradient

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36
Q

Where does the adjustment of the ion-concentration in the urine occur?

A

In the Distal convulated tubules

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37
Q

How do the distal convoluted tubules in the kidney control the adjustment of ion concentration in the urine?

Which structural components support this?

A

Site of Hormonal control

  • (late distal tubule) Vasopressin (re-equilibration of intracellular fluid)
  • Aldosterone (Ion (Na+, K+, H+ NH4+) adjustments)

Structural features:

  • Cuboidal epithelium with few microvilli
  • Complex membrane with invaginations that contain Na+ pumps
  • abundant mitochondria
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38
Q

Where does the concentration of the urine occur?

A

It occurs in the collecting tubule or duct in the medulla

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39
Q

How is the concentration of the urine in the collecting duct controlled?

A

It is controlled by ADH

  • –> Vasopressin induces aquaporin 2 molecules into the apical surface of the cell
  • –> Thereby it determines whether water can pass the membrane into the hyperosmotic environment or not
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40
Q

Which structural components are present in the collecting tubule/duct to match their function?

A
  • Tight, water impermeable junction (only aquaporins molecules can regulate water in/outflow)
  • few mitochondria (passive process)

Aquaporin 2/3 controlled by vasopressin

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41
Q

Where is the juxtaglomerular apparatus located?

Which structures does it include?

A

It is located next to the afferent vessel to the glomerulus

It consists of

  • juxtaglomerular cells of afferent arteriole
  • endocrine cells in the macula densa of distal convoluted tubule
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42
Q

What is the function of the juxtaglomerular apparatus?

A

To regulate blood pressure via hormone production

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43
Q

Explain the mechanism of blood pressure regulation via the juxtaglomerular apparatus

A

Renin secretion is inhibited via two signals

  • Stretch sensed by the juxtaglomerular cells surrounding the afferent arteriole
  • Cl- ions sensed in the macula densa of the distal convoluted tubules

–> Regulates BP via Renin-Angiotensin-Aldosterone system

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44
Q

What is glomerular filtration?

A

It is the formation of an ultrafiltrate of plasma in the glomerulus

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45
Q

What is by definition renal disease/ renal failure?

A

The fall in glomerular filtration rate

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46
Q

Where does glomerular filtration take place?

A

In the glomerulus + Bowmans capsule of the kidney

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47
Q

Which concentration do solutes in the primary urine have?

A

The same as in the blood plasma (isotonic)

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48
Q
A
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49
Q

What are the pressures that influence/drive glomerular filtration rate?

A

Driving force:

  • Pgc= hydrostatic pressure in glomerular capillaries (blood pressure)

Opposite force:

  • πgc=Oncotic pressure of proteins in the plasma
  • Pt= Hydrostatic pressure of proximal tubule
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50
Q

What is the net ultrafiltration pressure?

By which factors is it influenced?

A

Total pressure driving filtration if all pressures are added:

Puf= Pgc-Pt-πgc

Pgc= hydrostatic pressure

Pt= pressure in proximal tubule

πgc= plasma protein oncotiv pressure

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51
Q

What happens in the proximal convoluted tubule?

A

Active reabsorption and secretion of important substances

52
Q

How would you calculate the amount of a substance excreted by the kidney?

A

Have to consider everything that can happen to the substance:

Filtration

Absorption

Secretion

53
Q

Which factors influence glomerular filtration rate?

A

Basically pressure (Puf ) and ultrafiltration coefficient (Kf)(determined by surface area and membrane permeability)

GFR = Puf x Kf

54
Q

How does taking out of a kidney influence glomerular filtration rate? (Which parameter does it inlfluence)

A

It reduces the surface area of the nephron which reduces Kf

GFR = Puf x Kf

55
Q

What does the glomerular filtration rate actually show? (Verbalisation of formula)

A

Amount of fluid filtered from glomerulus in Bowmans capsule

Dependant on pressure and Koeficient

56
Q

How much blood flows to the kidney a minute?

How much of this is plasma?

A

20% of CO –> 1l/min

60% of this is plasma:

Renal plasma flow= 0.6 l/min

57
Q

What is filtration fraction?

What is its value?

A

How much of the plasma is actually filtered by the kidney

–> Normally 0.2 (20%) which means 120ml/min of plasmfilteredilterd

58
Q

Hwo can you calculate glomerular filtration rate based on renal blood flow?

A

GFR= RPF x FF

RPF= renal plasma flow –> plasma flows to kindeny/ minute

FF= Filtration fraction —> part of plasma that is filtered om kidney

59
Q

Explain the concept of myogenic autoregulation to control blood flow to the kidenys

A

Arterioles in proximal tubules react to stretch (i.e. increased blood pressure) with constriction

–> Filtration stays the same (higher pressure but less blood flow)

Arterial pressure rises → afferent arteriole stretches →

arteriole contracts → (vesselresistanceincreases)→blood flow reduces and GFR remains constant:

60
Q

What is the definition of renal clearance?

A

It is the volume of plasma that can be completely cleared of the substance per unit of time (normally ml/min)

61
Q

How can you calculate reanal clearance?

A

C = (U x V)/P ml/min

C= clearance

U= Concentration in urine

V= rate of urine production

P= concentration of substance in plasma

62
Q

How can you estimate GFR using renal clearance?

A

By measuring a substance that is only filtered in the glomerulus (not modified (reabsorbed, excreted)) in the urine/blood plasma

63
Q

Which substances can be used to measure glomerular filtration rate?

Why?

A

Inulin and Creatine (muscle metabolic product) normally measured

–> Both are only filtered and not reabsorbed/secreted into primary urine

64
Q

How can you measure renal plasma flow?

A

Normally uses PAH (Para aminohippurate) –> 100% actively excreted into plasma

–> Every ml of plasma arriving to kidney is completely cleared from this substance

Levels of PAH in urine show renal plasma flow

65
Q

Explain where water is reabsorbed in the nephron

A
66
Q

In which part of the nephron is the amount of water reabsorbtion regulated?

A

It is regulated in the collecting duct

67
Q

Which two components in the collecting duct can be regulated to alter water reabsorption?

A
  1. Water permeability of the collecting duct can be altered (e.g. via insertion of aquaporins)
  2. The osmolarity of Medulla can be altered –> other gradient
68
Q

How can you establish the cortico-medullary gradient via the countercurrent mechanism?

A
  • In the ascending loop, salt is actively pumped out which decreases osmolarity within the lumen but increased outside
  • This increased osmolarity is being neutralized by water flowing out of the tube into the interstitial compartment, which increases the osmolarity in the tube
  • Now water new fluid comes in at the top and is responsible for shifting the fluid around: in ascending loop there is now a more concentrated solution, where there is still ions pumped out to increase the osmolarity
69
Q

Why doesn’t medullary blood flow eliminate medullary osmotic gradient?

A

The osmolarity in the vasa recta also changes in a counter-current mechanism and has a very high osmolarity in the inner medulla

70
Q

Which role does urea play in concentrating the urine?

A

In regulating the osmolarity via the collecting duct:

Urea is concentrated in the collecting duct

Only the inner-medullary part of the collecting duct is permeable to urea

–> It flows don its concentration gradient and increases osmolarity in the inner medulla

71
Q

When is ADH released?

A
  • High Plasma osmolarity, sensed by osmoreceptors in the hypothalamus (>300mOs)
  • Low blood pressure (sensed by baroreceptors)
72
Q

How does ADH increase water reabsorption in the collecting duct?

A
  1. Causes the insertion of Aquaporins 2 in the luminal membrane

–> Allow water to flow into the medulla, following the concentration gradient

  1. Stimulates urea transport from collecting duct to thin ascending loop via increasing the membrane position of urea transporters —> increased osmolarity
73
Q

Where is sodium reabsorbed? (Percentages where?)

A
74
Q

How does GFR influences Na+ reabsorption?

A

Sodium reabsorption is proportional (percentages are reabsorbed) that means:

An increase in GFR causes an increase in Na+ reabsorption

–> Therefore sodium reabsorption is controlled by alteration of GFR

75
Q

What are the target sides of sympathetic activity on the urinary system?

A
  1. It increases GFR
  2. Increases reabsorption in the proximal convoluted tubule
  3. Stimulates the Juxtaglomerular apparatus
76
Q

How does Angiotensin II control the reabsorption of Na+?

A

It

  • Increases reabsorption in the proximal convoluted tubule (increased affinity of Na+/H+ cotransporters)
  • Stimulates the production of Aldosterone
77
Q

What effect does aldosterone have on the tubules of the nephron?

A

It increases Sodium reabsorption in the

  • distal convoluted tubule
  • and in the collecting duct
78
Q

How and where does Atrial natriuretic peptide influence the reabsorption of Sodium?

A

It decreases Sodium reabsorption by

  • Decreasing GFR
  • Decreasing reabsorption in proximal convoluted tubule
  • Decreasing Renin production
  • Decreasing reabsorption in collecting duct
79
Q

Which effect does Na+ in the distal convoluted tubule have?

A

A decrease in Na+ concentration causes renin secretion by the Juxtaglomerular cells:

–> Decrease in NaCl concentration at the macula densa, often due to a decrease in glomerular filtration rate

80
Q

What does an excess in aldosterone cause?

A

It leads to an hypokalaemic alkalosis

+ High BP:

81
Q

What effects does aldosterone have on ion balance in the kidney?

A
  • Increased Sodium reabsorption

(controls reabsorption of 35g Na/day)

  • Increased Potassium secretion
  • Increased hydrogen ion secretion (via activation of Na+/H+ exchanger)
82
Q

What is the effect of hypoaldosteronism?

A
83
Q

How does aldosterone increase Na+ reabsorption in the collecting duct?

A
  1. Steroid hormone binds to its receptor in cytoplasm which form a dimer when activated and migrate into nucleus – alter transcription
  • Induces expression of the apical Na channel of the collecting duct
  • induces the formation of Na-K-ATPase pumps (increased transcription of the corresponding mRNA)

–> More pumps to pump Na+ and reabsorb it!

84
Q

What are the symptoms and reasons for Liddls Syndrome?

A

An inherited disease of high blood pressure.

  • mutation in the aldosterone activated sodium channel.
  • channel is always ‘on`
  • Results in sodium retention, leading to hypertension
85
Q

How do ACE inhibitors affect the urinary system?

A

REduction in Angiotensin II and Aldosterone leading to a decrease in Na+ reabsobrion–> Decreased Extracellular Fluid –> Lowered BP

86
Q

Explain the mechanism of function of Carbonic anhydrase inhibitor diuretics

A

Na+/H+ Antiporters pump Sodium into the cell

Na+/HCO3- symporters transport sodium out of the cell

–> Both mechanisms inhibited by inhibition of Carbonic anhydrase

87
Q

What is an example of a carbonic anhydrase inhibitor?

A

Acetazolamide

88
Q

Explain the mechanism of action of an Osmo diuretic

Name examples

A
  • It increases the osmolarity of the filtrate –> less water out
  • Also, increase GFR by increasing overall Extracellular fluid and blood volume

E.g. Glucose (in diabetes) or Mannitol

89
Q

Explain the mechanism of action of Loop diuretics

A

Inhibit ion-co transporter in the thick ascending loop of Henle (transports Na+, K+, CL-)

  1. Less Na+ in Extracellular Fluid
  2. Higher osmolarity of filtrate

–> Decreased osmotic gradient

90
Q

Explain the target site and mechanism of action of Thiadize diuretics

A

Act on the distal convoluted tubule

Inhibit Na+/Cl- Cotransporter form the lumen into the cell

–> Less Na in the cell, less Na can be pumped out

91
Q

Explain the mechanism of action of Potassium-Sparing Diuretics and the effects of Aldosterone on it

A

Potassium-sparing diuretics either directly inhibit Na+ uptake from the Lumen, so Na+/K+ ATPase does not work (pumps fewer Na+ out, because less there)

–> Less sodium can enter the cell and leave into the lumen

Aldosterone stimulates Pump and channel and therefore aldosterone inhibitors are also K+ sparing

92
Q

By which cells and where is Potassium secreted?

A

it is secreted by the principal cell in the collecting duct

93
Q

How does aldosterone influence Potassium secretion?

A

Aldosterone stimmulates Na+/K+ ATPase

and also stimmulates K+ channels

–> Stimmulates K+ excretion

94
Q

How does tubular flow rate influence potassium secretion?

A

Increased flow= stimulates Ca2+ uptake which stimulates K+ channels and the excretion of K+

95
Q

How are Potassium levels regulated?

A

It is taken up into the cell via Na+/K+ channels

And excreted into the lumen via K+ channels

96
Q

What is a normal range for urine pH?

A

pH is normal aound 5-8

–> huge range (in comparison to blood) because urine regulates the blood

97
Q

What is the normal pH range for blood?

Which pH values are compatible with life?

A

Normal around 7.35-7.45

Compatible with life are values around 6.8-7.8

98
Q

What are normal bicarbonate blood concentrations?

A

22-26 mEq/L

99
Q

Where is how much bicarbonate in the nephron reabsorbed?

A
100
Q

What is the Henderson-Hasselbach equastion?

How would it look like for Bicarbonate?

A
101
Q

How is HCO3- reabsorbed in the proximal convoluted tubule?

A
  1. Carbonic anhydrase in Lumen: HCO3- + H+ = Co2+H20
  2. Co2 diffused into the cell
  3. Internal Carbonic anhydrase reverses the reaction
  4. H+ excreted into the lumen via
  • Na+/H+ antiporter
  • H+ ATPase
  1. Bicarbonate uptake via
  • 3HCO3-/NA+ cotransport
  • HCO3-/Cl- exchanger
102
Q

What is the function of the alpha cell and beta cells?

What is their relation to one another?

Where are they located

A

Both play a role in Acid-Base regulation of Kidney:

Alpha cells= Acid secreting cells

Beta cell= Bicarbonate secreting cells

–> Cells can change identity (alpha into beta, and other way around)

They are located in the collecting duct

103
Q

Where does acid/base regulation in the kidney occur?

A

It occurs in the collecting duct via Alpha/beta cells

104
Q

Hot do alpha cells in the kidney secrete H+?

A
  1. Carbonic anhydrase in Lumen: HCO3- + H+ = Co2+H20
  2. Co2 diffused into the cell
  3. Internal Carbonic anhydrase reverses the reaction
  4. H+ excreted into the lumen via
  • Na+/H+ antiporter
  • H+/K+ ATPase
  • H+ ATPase
  1. Bicarbonate uptake via
    * HCO3-/Cl- exchanger
105
Q

How do beta cells in the collecting duct secrete bicarbonate?

A

Just like alpha cells but the other way around:

  1. Carbonic anhydrase in Lumen: HCO3- + H+ = Co2+H20
  2. Co2 diffused into the cell
  3. Internal Carbonic anhydrase reverses the reaction
  4. H+ secreted into the blood via
  • Na+/H+ antiporter
  • H+/K+ ATPase
  • H+ ATPase
  1. Bicarbonate excreted via
    * HCO3-/Cl- exchanger
106
Q

How Can Bicarbonate be generated by cells in the kidney?

A

It can be synthesized from Glutamine

–> Split into bicarbonate and Ammonium

  1. Ammonium excreted via Na+/NH4+ exchanger
  2. Bicarbonate is taken up via CL- exchanger, Na+ cotransport
107
Q

How is Ammonium excreted?

A

It is transported across the membrane via an Na+/NH4+ exchanger and excreted into urine

108
Q

How do phosphate and acid-base regulation intervolve?

Why is this relevant?

A

H+ excreted can form:

HPO42- + H+ = H2PO4-

These substances can be measured in a lab

109
Q

Will a patient with low GFR always notice, that something is wrong with him?

What does it determine?

A

Clinical features are determined by the rate of deterioration

–> Someone who goes from 100% to 20% in a few days/weeks will be very unwell

—> Someone who has a slow deterioration over a very long time period won’t necessarily notice

110
Q

What is the problem with the loss of the excretory function of the kidney in renal failure?

A

Toxins will accumulate in the body

–> could e.g. cause nausea, vomiting, intoxication

111
Q

Which symptoms can be observed in a patient with kidney failure and why?

A

Tow presentations:

  1. (More common)–> No filtration of fluid –> Too much: (pulmonary) Oedema, high BP
  2. Tubules fail to reabsorb fluid (less common) –> too much water excretion, low BP, nausea etc.
112
Q

Why is it important to differentiate between blood sodium levels and total body sodium?

A

Because they can be very different:

CKD AND AKI (acute kidney injury) ARE OFTEN ASSOCIATED WITH HYPONATRAEMIA

113
Q

How can renal failure disturb acid-base balance?

A

It often comes to a metabolic acidosis –> Kidneys can’t excrete enough H+

114
Q

How can an acidosis lead to hyperkalemia?

A

Buffered by H+ions passing into cells in exchange for K+ions – therefore aggravates tendency to hyperkalaemia

acidosis causes potassium to move from cells to extracellular fluid (plasma) in exchange for hydrogen ions, and alkalosis causes the reverse movement of potassium and hydrogen ions.

115
Q

How does renal failure lead to Hyperkalaemia?

A

Renal failure can lead to a failure to excrete potassium in the distal tubule

116
Q

What does hyperkalaemia lead to?

A
  1. Exacerbated by acidosis - causes shift of potassium from intracellular to extracellular space
  2. Can cause cardiac arrhythmias (usually initial loss of p waves and also bradycardia) and arrest
  3. Can effect neural and muscular activity
117
Q

How can a loss of the metabolic function of the kidney impact blood cells?

A

Kidney failure can lead to anaemia because of reduced erythropoietin levels

118
Q

What do low 1-25VitD levels in renal failure lead to?

A

uLow 1-25 VitD levels result in poor intestinal calcium absorption, hypocalcaemia (short term) and hyperparathyroidism (longer term)

119
Q

Why have patients with kidney disease an increased Cardiovascular risk?

A

Direct mechanism is unclear but it leads to:

  • Hypertension
  • Secondary cardiac effects
  • Endothelial effects
  • Lipid abnormalities
120
Q

How can you differentiate between chronic and acute renal failure?

A

Barely any difference but: History and Kidney size

121
Q

Evaluate the use of Urea as a method of assessing GFR

A

–Poor indicator

–Confounded by diet, catabolic state, GI bleeding (bacterial breakdown of blood in gut), drugs, liver function etc

122
Q

Evaluate the use of Creatinine as a method for assessing GFR

A

–Affected by muscle mass, age, race, sex etc. Need to look at the patient when interpreting the result

123
Q

Evaluate the use of Creatinine clearance as method for estimating GFR

A

–Difficult for elderly patients to collect an accurate sample

–Overestimates GFR at low GFR (as a small amount of creatinineis also secreted into urine)

124
Q

Evaluate the use of Inulin for estimating renal clearance

A

–Laborious - used for research purposes only

–> very difficult to make

125
Q

Evaluate the Radionuclide studies for assessing GFR

A

–EDTA clearance etc

–Reliable but expensive

–> Gold standart that is used today!

126
Q

Why does hyperaldosteronism lead to increased thirst and polyuria?

A

Becuause more ions are reabsorbed –> Blood has a highter osmolarity

–> thirst to try and reduce osmolarity

Year 1 LSS (12 decks)

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