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Leah URO > Week 5 > Flashcards

Week 5 Flashcards

1
Q

What are some roles of the kidney

A

Excretion of waste products

Control of body fluid volume & composition of this fluid

Regulation of body fluid osmolality & electrolyte concentrations

Regulation of acid-base

Regulation of arterial pressure

Erythropoietin

Regulation of 1,25-Dihydroxyvitamin D3 production

Gluconeogenesis

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2
Q

describe the location of the kidneys

A
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3
Q

Label

A
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4
Q

Label

A
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5
Q

Describe urine flow in kidney in cattle, pigs & primates

A

urine drains from tip of pyramids into minor calyx

2-3 minor calices then drain into a major calyx

major calices then drain into renal pelvis

renal pelvis drains into ureter

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6
Q

Describe urine flow in kidney in dogs, cats, sheep & horses

A

Medullary pyramids are fused and form renal crest

no calices

renal crest drains into renal pelvis

renal pelvis is located within renal sinus

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7
Q

Describe renal pelvis differences across species

A
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8
Q

Describe dog, cat, sheep & goat kidneys

A

kidney bean shaped

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9
Q

Describe equine kidneys

A
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10
Q

Describe porcine kidneys

A

long and flat

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11
Q

Describe bovine kidneys

A

oval & irregular shape
obvious lobes = reniculate

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12
Q

Describe these parts of the kidney

A
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13
Q

Describe unilobar kidneys

A

rodents & lagomorphs

single renal lobe
single pyramid
single papilla
- may extend through hilus in desert-adapted species

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14
Q

Describe cow, elephant, bear & aquatic animal multilobular kidney

A
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15
Q

Describe pig & primate multilobular kidney

A
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16
Q

Describe dog, cat, sheep & horse multilobular kidney

A
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17
Q

Fill in the kidney table

A
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18
Q

Give an overview of renal blood flow

A

Kidney receives 25% of cardiac output

basic flow is from hilus to cortex, then cortex to medulla

venous drainage is from medulla to cortex to join cortical venous drainage

outflow via hilus

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19
Q

Describe blockage in arcuate vs interlobulary arteries

A

doesn’t matter if an arcuate vessel gets blocked because they are anastomotic so blood can flow via different vessel

interlobulary arteries are end arteries so blockage causes infarcts and sections of kidney will die

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20
Q

Describe the renal blood flow circuit

A
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21
Q

Describe the capillary networks in the kidney

A
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22
Q

Describe the arterial portal system in kidneys

A
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23
Q

Describe blood flow in juxta-medullary nephrons

A
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24
Q

Describe the extra cortical venous drainage in carnivore kidneys

A
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25
Q

Describe what the ureter wall is made of

A
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26
Q

Describe how the ureter enters the bladder

A
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27
Q

Describe bladder anatomy

A
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28
Q

Describe bladder appearance when empty vs distended

A
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29
Q

label

A
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30
Q

Label the bladder ligaments

A
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31
Q

Describe the female urethra

A
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32
Q

Describe the general male urethra

A
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33
Q

Compare male urethra in different species

A
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34
Q

Label

A
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35
Q

Label

A
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36
Q

What supplies the renal pelvis, proximal ureter & distal ureter

A
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37
Q

What is the blood supply to the bladder and urethra

A
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38
Q

What is the lymphatic drainage of the kidney, ureter and bladder

A
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39
Q

Describe the kidney innervation

A
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40
Q

describe the bladder innervation

A
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41
Q

Describe the layers in the renal filter (glomerular capillary)

A
  1. Endothelial cells of the glomerulus
    - large fenestrations which allow many products to pass through
    - a lot of material that makes up pores is negatively charged & so there is charge-barrier as well as physical space restriction when passing through
    - Blood cells and most proteins are too large to pass
  2. Glomerular Basement Membrane (GBM)
    - Main filtration barrier to cells & large molecules
    - It is also negatively charged
  3. Podocytes of the visceral layer of Bowman’s capsule
    - Podocyte projections don’t completely cover GBM as there are some gaps
    - They therefore make a discontinuous layer on urinary space side of the GBM
    - Spaces between foot projections are called filtration slits
    - Filtration of smaller molecules is blocked by presence of thin negatively charged membrane within filtration slits
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42
Q

Label the glomerulus

A
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43
Q

Describe the juxtaglomerular apparatus

A

Region at vascular pole of the glomerulus. It is made up of 3 types of cells:

  1. Juxtaglomerular cells
    - modified smooth muscle cells in wall of afferent arterioles
    - contain renin
  2. Macula densa cells
    - specialised epithelial cells in wall of TAL of Loop of Henle &/or distal tubule
    - detect changes in luminal sodium chloride (NaCl) concentration
    - can signal changes in arteriolar resistance & so affect blood flow to glomerulus
    - signals release of renin
  3. Extraglomerular mesangial cells
    - bridge afferent & efferent arterioles & MD cells & help coordinate messages & effects of JGA
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44
Q

Describe the proximal convoluted tubule

A

This area of nephron is very coiled & these segments make up much of renal cortex

site where most solute reabsorption occurs

Cells here have a number of features that are suited to these roles:
- Cuboidal epithelial cells
- Apical intercellular tight junctions (try to stop “leakage” of molecules between cells but allow easy movement of water & some small ions)
- Intercellular gap junctions
- Layer of microvilli (brush border) – modification to increase surface area for absorption & intracellular transport of luminal material
- Basolateral intercellular interdigitations: increase surface area between cells to maximise transcellular transport of materials
- Lots of mitochondria

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45
Q

Describe the Loop of Henle

A

This part of tubule descends into medulla & then ascends back into cortex

It has several parts:

  1. The thick descending Limb
    - active in reabsorption
    - Simple cuboidal cells
  2. The thin descending and thin ascending limbs
    - Changes abruptly to flatter cells: simple squamous epithelium
    - No brush border or lateral interdigitations
    - Few organelles
    - important role in concentrating urine
  3. The thick ascending limb
    - Thicker again: simple cuboidal epithelium
    - Rises up towards cortex & ends up next to glomerulus & macula densa
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46
Q

Describe blood vessels associated with the Loop of Henle

A

Efferent arterioles in cortical nephrons go on to form peritubular capillaries – which surround rest of tubular system

Efferent arterioles from juxtamedullary nephrons:
- first form vascular bundles which give rise to peritubular capillaries & straight vessels that form vasa recta

Vasa recta are sole blood supply to medulla & are very important in creating concentration gradient

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47
Q

What are cortical vs juxtamedullary nephrons

A

Nephrons can be classified by location of their glomeruli. In cortex as superficial (near capsule), cortical, or juxtamedullary (near medulla)

Juxtamedullary nephrons are long & adapted to resorb lots of water back into blood

Useful in animals that need to minimise amount of water they lose in urine
- eg desert animals

Ability to produce very concentrated urine is associated with greater percentage of juxtamedullary nephrons

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48
Q

Describe the distal convoluted tubule

A

This part of the nephron is after the macula densa

It is shorter in length & has less developed microvilli than PCT

However, it has lots of basolateral interdigitations & even more mitochondria than PCT

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49
Q

describe the collecting ducts

A

This has 3 sections according to their depth in the kidney:
- Cortical collecting duct
- Outer medullary collecting duct
- Inner medullary collecting duct

Several nephrons join same collecting duct & several collecting ducts join to form papillary duct

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50
Q

Describe filtration process in the kidney

A
  1. blood carried to glomeruli is filtered
  2. ultrafiltrate is funnelled to PCT where glucose, amino acids, small proteins, vitamins, sodium & water are reabsorbed
  3. tubular fluid leaves cortex & enters descending loop of Henle where water is passively removed
  4. in the ascending LoH Na+ & Cl- are actively removed
  5. tubular fluid leaves medulla & enters DCT in cortex where salt & water balance between urine & blood is adjusted by juxtaglomerular apparatus & RAAS
  6. urine leaves nephron & enters collecting ducts that pass back through medulla
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51
Q

Label

A
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52
Q

Describe the function of the glomerulus

A

Selective filtration barrier that acts like sieve to filter blood based on size & charge of particles

No blood cells pass

Very little protein passes (albumin does)

Has a charge

Creation of an ULTRAFILTRATE:
- Water
- Electrolytes
- Glucose
- No cells, no/little protein

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53
Q

What is Glomerular Filtration Rate (GFR)

A

amount of fluid filtered from glomerular capillaries into Bowman’s Capsule per minute (across all nephrons)

GFR = Kf x net filtration pressure
- Kf is filtration coefficient – represents permeability of membranes

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54
Q

Why is GFR important

A

GFR is cumulative over all functional nephrons

Renal function is directly related to number of functional nephrons

so acts as an indirect measure of renal function

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55
Q

What GFR forces can be regulated and what cant be

A

Some forces can’t be regulated:
- Hydrostatic pressure in Bowman’s capsule
- The filtration coefficient

But some can:
- Hydrostatic pressure in the glomerular capillaries
- Renal blood flow

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56
Q

What factors can affect arterial blood pressure in afferent & efferent vessels

A

Autoregulation
- Stretch receptors
- Macula Densa

Angiotensin II
- Via renin release from JGA

Neural regulation
- SNS and PSNS

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57
Q

Define renal clearance

A

volume of plasma cleared of substance in unit of time

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58
Q

What substances are good candidates for measuring GFR

A

Urea
- From protein catabolism, easy to measure in blood
- Variable (protein meals (raw fed dog), GI bleeding, catabolic states)

Creatinine
- From muscle (& food) breakdown, easy to measure in blood
- Steady rate
- Affected by age, muscle mass
- Not very sensitive

Inulin
- Gold standard in human medicine
- Has to be administered & then measured (not practical in animals)

Cystatin-C
- Produced by all tissues
- Freely filtered, resorbed (PCT) and destroyed
- Good indicator of PCT damage

SDMA
- Produced by all cells
- More sensitive measure of GFR than creatinine

FGF-23

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59
Q

How can urinalysis be used to assess renal system function

A

We can use urinalysis to assess renal system function by knowing:

  • What concentration “normal” urine should be
  • What it should, and should not, normally contain
  • blood, haemoglobin, glucose, ketones, protein, Crystals (can occur if sample is old), casts, other cells
  • Other parameters
  • PH
  • Colour, turbidity, smell
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60
Q

What is nephrotic syndrome

A

Glomerulonephritis –> widespread inflammation, lots of causes

Glomerular disease often causes proteinuria

rare complication = nephrotic syndrome can result from extreme urinary protein loss

Nephrotic syndrome is defined as combination of significant protein loss in urine, high serum cholesterol & low serum albumin

Tissue oedema forms as a consequence of the low protein

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61
Q

What do these cause

A
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62
Q

Why is renal blood flow high?

A

Haemodynamic factors:
- lots of ‘push power’ to get blood to be adequately filtered

High resistance of afferent and efferent arterioles means the hydrostatic pressure beyond them is relatively low - helps promote resorption

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63
Q

Describe countercurrent exchange mechanism in kidney

A

Vasa recta amplifies concentrating ability of nephron

In the ascending limb:
- ions are pumped out of LoH
- water cannot follow
- makes interstitium salty

In the descending limb:
- water moves out
- concentrating tubular fluid

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64
Q

What is the vasa recta

A

Blood vessels that follow the LoH
Important in urine concentration

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65
Q

Which of these adaptations might desert mammals have to help them to live in such a water-depleted environment?

Ability to hyper-concentrate urine

Longer Loop of Henle

Proportionally more juxtamedullary nephrons

Reduced RBF so not as much water gets filtered or lost in urine

A

Ability to hyper-concentrate urine ✅

Longer Loop of Henle ✅

Proportionally more juxtamedullary nephrons ✅

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66
Q

Describe the autoregulation of renal blood flow

A

Myogenic reflex:
- high BP => stretches BV => reflex vasoconstriction and reduced blood flow

Tubuloglomerular feedback:
- Rise in glomerular pressure => increased GFR => increased tubular flow rate => less time for Na and Cl reabsorption => macula densa detects higher Na/Cl => JGA releases adenosis => afferent arteriolar vasoconstriction => reduces blood flow and GFR

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67
Q

What factors affect renal blood flow

A

Autoregulation
RAAS system
Vasoactive peptides

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68
Q

what are some vasoactive peptides that control renal blood flow?

A

Bradykinin

Natriuretic peptides (ANP, BNP and CNP)

Endothelin

Vasopressin

Adrenomedullin

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69
Q

What does myoglobin in urine indicate

A

muscle damage

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70
Q

What substances can be found in urine that indicate disease

A

Crystals (urolithiasis)
Myoglobin
Bilirubin
RBCs
Haemoglobin
WBCs

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71
Q

Describe the use of the gross appearance of urine in urinalysis

A

Colour:
- should be pale yellow-amber
- abnormal colour can be caused by diet, meds, environment or illness

Turbidity:
- should be clear
- cloudiness caused by suspended material e.g., bacteria

Smell:
- should be relatively odourless
- strong ammonia smell suggests infection

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72
Q

How is protein measured in urinalysis & what does it indicate

A

Dipstick

Should have no proteins in urine

Proteins present suggests poor filtration in glomerulus and/or poor reabsorption in the proximal tubules

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73
Q

How is urine pH used in urinalysis

A

Normal = 6-7.5

Increased pH may results from UTI

decreased pH may be due to diets high in animal protein or milk

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74
Q

How is glucose used in urinalysis

A

Glucose not normally present in detectable quantities on dipstick

Glucosuria occurs due to high blood glucose levels e.g., diabetes mellitus

If blood glucose is normal with glucosuria = renal tubular dysfunction

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75
Q

Describe urine ketones in urinalysis

A

Usually undetectable in urine

may suggest ketosis secondary to diabetes mellitus or starvation

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76
Q

How is occult blood used in urinalysis

A

Detects haem-containing substances e.g., haemoglobin

Red cells in sediment indicates haematuria is causing occult blood

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77
Q

Describe bilirubin in urinalysis

A

Should not be present (except small amount in healthy dogs)

Renal threshold for bilirubin is low in most animals

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78
Q

Describe what RBC, WBC & epithelial cells may suggest in urinalysis

A
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79
Q

What can casts suggest in urinalysis

A

can indicate:
renal disease
UTI
Dehydration
Neoplasia
& more

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80
Q

Define azotaemia

A
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81
Q

Why is azotaemia a useful marker in clinical practice and what are its limits

A
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82
Q

What are the types of azotaemia

A

Pre-renal azotaemia = azotaemia occurs because of systemic factors that result in inadequate renal perfusion

Renal azotaemia = due to reduced function of the kidneys

Post-renal azotaemia = caused by a problem after the kidneys (ureters, bladder or urethra)

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83
Q

What are the clinical signs of pre-renal azotaemia

A

Concentrated urine - high USG as kidneys working to reduce fluid loss

Azotaemia

Clinical signs of hypovolaemia and dehydration

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84
Q

What are the clinical signs of renal azotaemia

A
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85
Q

What are the clinical signs of post-renal azotaemia

A
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86
Q

What are the possible causes of renal azotaemia

A
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87
Q

What are the possible causes of pre-renal azotaemia

A
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88
Q

What are the possible causes of post-renal azotaemia

A
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89
Q

What is the result of failed excretion of waste products

A
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90
Q

What is the result of failed control of body fluid volume & composition

A
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91
Q

What is the result of failed regulation of acid-base

A
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92
Q

What is the result of failed erythropoietin

A
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93
Q

What urine sampling methods an be done at home?

A

Floor sampling
Litter tray sampling
Free catch

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94
Q

What are the pros and cons of free catch urine sampling

A
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95
Q

What are the pros and cons of litter tray sampling

A
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96
Q

What are the pros and cons of floor sampling (urine)

A
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97
Q

What urine sampling techniques can be done in practice

A

Expressed sample
Catheterised sample
Blind cystocentesis
Ultrasound guided cystocentesis

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98
Q

What are the pros and cons of expressed sampling (urine)

A
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99
Q

describe how to collect a catheterised urine sample from males

A
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100
Q

What are the pros and cons of catheterised sampling

A
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101
Q

Describe how to perform a blind cystocentesis

A
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102
Q

What are the pros and cons of blind cystocentesis

A
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103
Q

Describe how to perform an ultrasound guided cystocentesis

A
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104
Q

What are the pros and cons of ultrasound guided cystocentesis

A
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105
Q

Why should you not use cystocentesis on animals with a bladder mass?

A

Most common bladder neoplasia = transitional cell carcinoma (TCC)
Can ‘seed’ into abdomen if transabdominal needle sampling

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106
Q

What are the appropriate tubes for a urine sample?

A

Plain tube for biochemical and sediment analysis/imminent culture

EDTA - prevents degradation of cellular components

Boric acid - hold bacterial population and cellular components statis for 4 days

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107
Q

What levels are measured with a dipstick in urine?

A

Blood
Bilirubin
Ketones
Glucose
Protein
pH

108
Q

What USG is normal

A
109
Q

What might be seen in urine microscopy

A

Haematuria - blood cells
Transitional cells
Renal tubular cells
Squamous cells
Moulds of renal tubules
mucoproteins
Lipid droplets
Sperm
Pathogens
Contaminants

110
Q

In what situations might you find crystals in urine

A

Normal urine
Artefact from storage
Altered pH (UTI)
Liver disease
toxins or drugs

111
Q

What is this

A

Hyaline cast

112
Q

What is this

A

cellular cast

113
Q

What is this and when might we see it?

A

struvite crystal

e.g. in altered pH (UTI)

114
Q

What is this and when might we see it?

A

calcium oxalate dihydrate crystal

e.g. normal urine or artefact-storage

115
Q

What is this and when might we see it?

A

calcium oxalate monohydrate crystal

e.g. toxins or drugs

116
Q

What is this and when might we see it?

A

ammonium biurate crystal

e.g. liver disease

117
Q

What is this and when might we see it?

A

bilirubin crystal

e.g. liver disease

118
Q

What views can be used for urinary tract radiography

A

ventrodorsal and both laterals

119
Q

describe collimation & centring of VD radiography of urinary tract

A
120
Q

describe collimation & centring of lateral radiography of urinary tract

A
121
Q

Put the uroliths struvite, cystine, ammonium urate and calcium oxalate in order from least to most radiodense

A
122
Q

Label the kidneys and bladder

A
123
Q

What are the options of retrograde cystograms in contrast radiography of the lower urinary tract?

A

Pneumocystogram
Positive contrast cystogram
Double contrast cystogram

124
Q

What is the contrast used in a pneumocystogram and what are the possible uses?

A

Contrast = air
Use = assess bladder wall thickness

125
Q

What is the contrast used in a Positive contrast cystogram and what are the possible uses?

A

Contrast = dilute iodine
Used = bladder rupture

126
Q

What is the contrast used in a double contrast cystogram and what are the possible uses?

A

Contrast = air and dilute iodine
uses = improved detail of bladder wall, filling defects

127
Q

What is a retrograde vaginourethrogram

A
128
Q

What is a retrograde urethrogram

A
129
Q

What is this pointing at

A
130
Q

What is this pointing at

A
131
Q

Label this frontal/dorsal view of kidney

A
132
Q

label this sagittal view of the kidney

A
133
Q

What is the direction of a frontal view

A

lateral to medial

134
Q

What is the direction of a sagittal view

A

central to dorsal

135
Q

label the transverse view

A
136
Q

Label the bladder wall layers

A
137
Q

Label the bladder

A
138
Q

What is the technique for bladder endoscopy

A
139
Q

Label

A
140
Q

Label and what is abnormal?

A

Uterus contains fluid = pyometra

141
Q

What condition is present in this ultrasound of cat

A
142
Q

based on the mineralisation present radiographically, can you estimate how long this patient has been pregnant

A
143
Q

Label

A
144
Q

What conditions can cause an enlarged prostate

A

Benign prostatic hypertrophy
Prostatitis
Neoplasia
Abcesses
Paraprostatic cysts

145
Q

Label the male radiograph showing Benign prostatic hypertrophy

A
146
Q

What conditions cause urethral obstruction

A

Urolithiasis
Urethral spasm
Urethral plugs
Urethral inflammation
Neoplasia

147
Q

Identify the uroliths

A
148
Q

Identify the urolith and the organ is it in in this ultrasound of a dog

A
149
Q

Label the ultrasound

A
150
Q

Is this a transitional cell carcinoma or cystitis? why?

A
151
Q

Is this a transitional cell carcinoma or cystitis? why?

A
152
Q

Label the kidneys. what is abnormal?

A
153
Q

What pathology is present in this kidney

A
154
Q

What pathology is present in this kidney

A
155
Q

What is osmolarity

A

Conc of solute particles
Na+ extracellular
K+ intracellular
Water will move towards areas of high solute conc

156
Q

What are the components of extracellular fluid

A

Protein
Na+
Cl-
HCO3-
Capillary membrane freely permeable to water and electrolytes

157
Q

What are the components of intracellular fluid

A

K+
Cell membrane freely permeable to water only

158
Q

What are Starling’s forces

A

Hydrostatic pressure
Oncotic pressure
Osmotic pull
Permeability

159
Q

Define osmotic pull/force

A

Water diffuses from area of highest conc of water to area of lowest conc of water

160
Q

define hydrostatic pressire

A
161
Q

Define oncotic pressure

A
162
Q

define permeability

A
163
Q

Describe the balance of forces that balances water movement in and out of capillaries

A
164
Q

Define tonicity

A

osmotic pressure of solution relative to the plasma
isotonic = same osmotic pressure as plasma

165
Q

Define osmolarity

A

conc of particles dissolved in a fluid per L

166
Q

Define osmolality

A

Conc of particles dissolved in a fluid per kg

167
Q
A

into plasma

168
Q

What is a hypertonic solution

A

solution that is more concentrated than plasma

169
Q

Give an example of a isotonic, hypertonic and hypotonic solution

A
170
Q

What is an effective osmole and an ineffective osmole

A

effective osmole:
a solute that does not freely cross the membrane, e.g., Na+, K+

ineffective osmole:
a solute that freely crosses the membrane e.g., glucose, urea

171
Q

What is the formula for blood pressure

A

blood pressure = Heart rate x stroke volume x systemic vascular resistance

172
Q

What is pressure natriuresis

A

If perfusion to the kidneys is increased => more fluid is ‘pushed’ through the kidney => more excretion of sodium and water => lowers BP

Works with RAAS to maintain BP

173
Q

Normal dog blood pressure

A

Systolic = 110-160
Diastolic = 60-90

174
Q

Normal cat blood pressure

A

Systolic = 120-180
Diastolic = 70-90

175
Q

What is target organ damage

A
176
Q

What are the general treatment guidelines for hypertension

A
177
Q

List some drug groups that might be effective to manage hypertension

A

Angiotensin converting enzyme inhibitor (e.g. benazepril)

Angiotensin receptor blocker (e.g. telmisartan)

Calcium channel blocker (e.g. amlodipine)

A1 blocker (e.g. prazosin)

Direct vasodilator (e.g. hydralazine)

Aldosterone antagonist (e.g. spironolactone)

B blocker (e.g. propranolol)

Thiazide diuretic (e.g. hydrochlorothiazide)

Loop diuretic (e.g. furosemide)

178
Q

Where is erythropoietin produced

A

interstitial fibroblasts in renal cortex and outer medulla of kidney

179
Q

What is the function of erythropoietin

A

Stimulates production of RBCs in bone marrow when kidneys detect hypoxia

Binds to receptors on erythroid progenitor cells in bone marrow => proliferation and differentiation into mature RBCs

180
Q
A
181
Q

Why is Angiotensin converting enzyme inhibitor (drug) effective at managing hypertension

A

blocks conversion of angiotensin I to angiotensin II (vasoconstrictor) to help dilate blood vessels & decreases aldosterone (promotes sodium & water retention & thus increases volume & pressure) secretion

182
Q

Why is Angiotensin receptor blocker (drug) effective at managing hypertension

A

block action of angiotensin II

183
Q

Why is calcium channel blocker (drug) effective at managing hypertension

A

inhibits influx of calcium into vascular smooth muscle cells leading to dilation

184
Q

Why is A1 blocker (drug) effective at managing hypertension

A

block a1 adrenergic receptors on vascular smooth muscle cells to inhibit vasoconstrictive effects of catecholamines leading to vasodilation

185
Q

Why is aldosterone antagonist (drug) effective at managing hypertension

A

inhibit action of aldosterone by binding to mineralocorticoid receptors in kidneys to prevent water retention, potassium excretion & vasoconstriction

186
Q

Why is B blocker (drug) effective at managing hypertension

A

block action of catecholamines & inhibit release of renin

187
Q

Why is thiazide diuretic (drug) effective at managing hypertension

A

inhibit reabsorption of sodium & chloride ions in distal convoluted tubules of kidneys to reduce blood volume & thus pressure

188
Q

Why is loop diuretic (drug) effective at managing hypertension

A

inhibit sodium-potassium-chloride co-transporter in thick ascending loop of henle leading to increased secretion

189
Q

What is urinary incontinence

A

lack of voluntary control of bladder

190
Q

At what age would you expect a puppy to have developed urinary continence

A

16 weeks (4 months)

191
Q

What abnormality does this radiograph show

A
192
Q

Give some signs of each level of dehydration

A
193
Q

define isosthenuria

A

USG is same as plasma
Kidney is not concentrating or diluting urine

194
Q

What are some clinical signs of chronic kidney disease and why do they occur

A
195
Q

What is SDMA and how is it useful in diagnosing kidney disease?

A
196
Q

What is FGF-23 and how might it be useful in diagnosing kidney disease?

A
197
Q

Why can CKD result in anaemia

A
198
Q

Why can CKD result in hypertension

A
199
Q

Why can CKD result in calcium imbalance

A
200
Q

What clinical signs may you see in a cat with hypertension

A
201
Q

How can PU/PD, isosthenuria, dehydration be treated in CKD?

A

IV fluid therapy
Subcut fluid
Encourage water intake

202
Q

How can proteinuria be treated in CKD?

A

Reduced protein diet

PUFA - reduces inflammation, antioxidant

203
Q

What can be used to treat hyperphosphataemia in CKD?

A

reduced phosphate diet
phosphate binders

204
Q

What can be used to treat hypocalcaemia in CKD?

A

calcitriol (vit D)

205
Q

What can be used to treat nausea in CKD?

A

Gastroprotectants

Anti-nausea e.g., maropitant

206
Q

How can hypokalaemia be treated in CKD?

A

potassium supplementation

207
Q

Why does H+ concentration of body fluids need be kept constant

A

Avoid detrimental changes in proteins, enzyme structure and cellular structure

208
Q

What is the equation of removing H+ from the body by the lungs?

A
209
Q

Describe acid (H+) secretion by the kidneys

A

free H+ conc in urine is very low

Most H+ secreted bound to filtered buffers e.g., phosphate or ammonia

Must absorb all filtered HCO3- as loss = same effect as adding H+ to plasma

210
Q

What organs are involved in pH regulation

A

lungs
liver
kidney

211
Q

How does the liver remove H+

A

metabolises amino acids from protein catabolism to glucose or triglycerides, NH4+ released

212
Q

Describe bicarbonate reclamation in PCT cells

A

HCO3- is freely filtered into tubular lumen

H+ enters tubular lumen via Na/H pump

HCO3- and H+ react => CO2 (under influence of carbonic anhydrase)

Resulting CO2 diffuses into PCT cells, dissociates in H+ and HCO3-

HCO3- is reabsorbed into the blood via Na3HCO3- co transporter

H+ returns to tubular lumen to react with more HCO3-

213
Q

Describe acid secretion in PCT cells

A

Kidney has ability to excrete H+ as ammonium (NH4+)
New HCO3- generated in this process

214
Q

What factors control bicarbonate reabsorption in PCT

A

luminal HCO3- conc
Luminal flow rate
Arterial pCO2
Angiotensin II

215
Q

Describe acidification in distal tubule

A

H+ secreted in cortical and medullary collecting tubules by active secretion

H+ combine with phosphate buffers => secreted

216
Q

What factors cause increased H+ secretion and HCO3- reabsorption in the kidney?

A

Increased pCO2
Increased H+, decreased HCO3-
Decreased ECF volume
Increased angiotensin
Increased aldosterone
Hypokalaemia

217
Q

What factors cause decreased H+ secretion and HCO3-reabsorption in the kidney?

A

Decreased pCO2
Decreased H+, increased HCO3-
Increased ECF volume
Decreased angiontensin
Decreased aldosterone
Hyperkalaemia

218
Q

Describe the effect increased pCO2 has on hydrogen excretion in kidney

A

Tubular cells respond to increased pCO2 of blood by increased rate of H+ secretion

219
Q

What is the effect of decreased ECF volume on hydrogen excretion in kidney?

A

Decreased ECF vol stimulates sodium reabsorption => increased H+ secretion and HCO3- reabsorption:
- increased angiotensin II levels stimulates activity of Na+/H+ exchanger
- increased aldosterone levels stimulates H+ secretion by the cortical collecting tubules
- can cause alkalosis due to excess H+ secretion and HCO3- reabsorption

220
Q

How does plasma potassium effect hydrogen excretion in kidney

A

Hypokalemia stimulates H+ secretion in proximal tubule:
- decreased plasma K => increases H+ conc in renal tubular cells
- stimulates H+ secretion and HCO3- reabsorption
- => alkalosis

Hyperkalemia inhibits H+ secretion in proximal tubule:
- hyperkalemia decreases H+ secretion and HCO3- reabsorption => acidosis

221
Q

What are the uses of arterial & venous blood gas measurement

A

Arterial:
- assessing respiratory status
- may not reflect changes in periphery

Venous:
- used in metabolic scenarios
- low pH and higher pCO2
- may not be accurate in low flow states

222
Q

Fill in the table for changes in arterial pH

A
223
Q

What is you diagnosis and what would you do?

A

metabolic acidosis

give IV fluids so kidneys cant fix issue and then work out the cause

224
Q

What are salts vs electrolytes

A
225
Q

What are the transport mechanisms in the kidney

A
226
Q

Describe absorption in the proximal tubule

A
227
Q

Describe absorption in the Loop of Henle

A
228
Q

Describe absorption in the distal tubules

A
229
Q

Describe absorption in the collecting duct

A
230
Q

What is the effect of aldosterone on potassium in the collecting duct?

A

Increased activity of Na+/K+ pump - resorbs Na, secretes K

Increased number of K+ channels

231
Q

Describe the effect of insulin on potassium absorption in kidney

A

Used to shift K+ into cells

Increases activity of Na+/K+ pump

Can be used to treat hyperkalaemia

232
Q

Describe the passage of Ca through the kidney

A

Free ion - freely filtered

Passive reabsorption in proximal tubules and ascending limb of LoH - driven by Na+

Active transcellular reabsorption in distal tubules

PTH (parathyroid hormone) can increase Ca2+ reabsorption

233
Q

Describe the passage of phosphate in the kidney

A

Free ion - freely filtered

80% reabsorbed in proximal tubules

Transcellular process: co-transport with Na+ ions

PTH decreases phosphate reabsorption

234
Q

Describe the passage of magnesium in the kidney

A

Free ion - freely filtered

30% reabsorbed in proximal tubules - paracellular movement driven by Na+

65% reabsorbed in thick ascending limb of LoH due to transepithelial potential

5% reabsorbed in distal tubules via Mg ATPases

Regulated via PTH

235
Q

Describe the passage of glucose in the kidney

A

Freely filtered

Only reabsorbed in proximal tubule via secondary active reabsorption

As glucose conc increases more of the proximal tubule participates in reabsorption

236
Q

Why is urine concentration control important

A

Intracellular environments require tightly controlled extracellular environments

ECF is affected by substrate levels and amount of water that it is dissolved in

Body water volume affects circulating volume, tissue perfusion and blood pressure

237
Q

How do kidneys produce dilute urine

A

normal ion transport (so filtrate gets more dilute) but little ADH so water cannot follow out of lumen

238
Q

How does the kidney produce concentrated urine

A

kidney reabsorbs lots of water

239
Q

describe water handling in proximal convoluted tubule

A

High water permeability

Solutes resorbed and water follows by osmosis = isotonic change

Filtrate volume reduced by 65% but osmolality does not change

240
Q

describe water handling in LoH

A

Variable water permeability depending on location

Descending limb = water permeable

Ascending limb = ions actively pumped out

Produces dilute urine and hypertonic medullary interstitium at base of LoH

240
Q

Describe water handling in collecting ducts

A

Water permeability varies depending on ADH

Cells and tight junctions are impermeable to water

ADH increases water permeability through aquaporins

Allows water to leave down conc gradient => concentrated urine

241
Q

Describe water handling in distal convoluted tubule

A

Largely impermeable to water (some ADH effect)

Macula densa and DCT - lots of electrolyte active transport

Filtrate becomes dilute

242
Q

Where is ADH/vasopressin produced

A

Made in hypothalamus

Released from post. pit in response to osmoreceptors detecting rise in plasma osmolality

243
Q

What is the effect of low ADH levels

A

No water reabsorption in collecting ducts

Na and Cl continue to be resorbed

Urine gets even more dilute

244
Q

define hyposthenuria

A

Kidneys are actively diluting urine

Mainly occurs in LoH where water follows solutes out of tubule

245
Q

What is hypersthenuric urine and what does it require?

A

Concentrated urine (what we expect to find in most animals)

Requires:
- ADH
- DCT/collecting ducts to be responsive to ADH
- hypertonic medullary interstitium

246
Q

Define pollakiuria

A

frequent passing of urine (not the same as polyuria)

247
Q

define nocturia

A

urinating at night

248
Q

What factors affect water intake

A

Ambient temp
Respiratory evaporative loss
Exercise level
Water content of food
Faecal water content
Age
Physiological state e.g., pregnancy

249
Q

What is the exception to PD coming after PU?

A

psychogenic polydipsia (PP) - excess drinking is behavioural issue => secondary polyuria

250
Q

What are the most common causes of PU/PD in dogs and cats

A

Renal insufficiency, chronic renal disease
Diabetes mellitus
HAC (dog)
Hyperadrenocorticism (cats)

251
Q

What mechanisms is the production of concentrated urine dependent on

A
252
Q

What are the causes of primary polyuria

A

Central diabetes insipidus

Primary nephrogenic diabetes insipidus

Secondary nephrogenic diabetes insipidus

253
Q

describe central diabetes insipidus

A

the pit gland does not release enough ADH due to hypothalamus or pituitary problem

254
Q

what is the test for central diabetes insipidus

A

Synthetic ADH => urine concentration increases

255
Q

what is the treatment for central diabetes insipidus

A

Desmopressin = ADH agonist
maximises low levels of ADH

256
Q

What is nephrogenic diabetes insipidus

A

Kidney does not respond normally to ADH

Primary/congenital diabetes insipidus:
- aquaporin insertion defect

Secondary/acquired nephrogenic diabetes insipidus:
- variety of renal/metabolic conditions which interfere with normal ADH action
- affects renal tubular function
- or decreases hypertonicity of medullary interstitium => loss of conc gradient

257
Q

What are the mechanisms for renal insufficiency causing PU/PD

A

Osmotic diuresis in remnant nephrons

Disruption of medullary architecture

Loss of medullary hypertonicity

Decreased functional nephrons

258
Q

How does HAC cause diabetes insipidus

A

Causes PU/PD by defective ADH release - central diabetes insipidus

Impaired tubule response to ADH action - nephrogenic diabetes insipidus

259
Q

How does hypoadrenocorticism cause PU/PD?

A

loss of osmotic gradient in renal medulla due to chronic Na wasting => loss of renal medullary hypertonicity => inadequate urine conc

260
Q

How does hyperthyroidism cause primary polyuria

A

thyrotoxicosis => increased CO and GFR and increased renal medullary blood flow, has potential to decrease renal medullary hypertonicity and urine concentrating ability

Some cats with hyperthyroidism may have primary polydipsia secondary to the effects of high thyroid hormone concs on the thirst centre

261
Q

How does liver disease cause PU/PD?

A

due to loss of medullary hypertonicity

Liver disease => decreased production of urea => decreased renal medullary hypertonicity

Increased levels of corticosteroids inhibit the release of ADH => central diabetes insipidus

262
Q

How do you test for psychogenic polydipsia

A

Controlled water deprivation

Dangerous to do if you have not already looked for renal or endocrine causes as dehydration could exacerbate disease

263
Q

Define dysuria

A

pain associated with urination

264
Q

What are the likely clinical signs of UTIs and urolithiasis?

A

stranguria - straining to pee
Haematuria
Pollakiuria - frequent, small volume urinations

265
Q

What is the common clinical sign seen is prostatic hypoplasia?

A

flat poo
faecal tenesmus
stranguria
haematuria

Leah URO (8 decks)

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