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ESA3 > Urinary > Flashcards

Urinary Flashcards

1
Q

State the four sites of potential glomerular injury

A

Supepithelial - affecting podocytes
Within basement membrane
Subendothelial - inside basement membrane
Mesangial - supporting capillary loop

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2
Q

What affect will a blocked glomerular basement membrane have?

A

Renal failure

Decrease GFR

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3
Q

What affect will a leaky glomerular basement membrane have?

A

Proteinuria

Haematuria

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4
Q

Define proteinuria

A

Presence of excess serum proteins in urine

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5
Q

What is the cause of proteinuria?

A

Due to podocyte or subepithelial damage

Widened fenestration slits allow protein to leak through

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6
Q

Define nephrotic syndrome

A

Over 3.5g of protein in urine in 24hrs

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7
Q

What is a systemic symptom of nephrotic syndrome? Why?

A

Generalised oedema

Protein is lost in urine
Reduced oncotic pressure

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8
Q

State three causes of primary nephrotic syndrome

A

Minimal change glomerulonephritis
Focal segmental glomerulonephritis (FSGS)
Membranous glomerulonephritis

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9
Q

State secondary causes of nephrotic syndrome

A

Diabetes mellitus

Amyloidosis

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10
Q

Describe the pathogenesis of minimal change glomerulonephritis

A

Podocytes damaged

Widened fenestration slits

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11
Q

Describe the epidemiology of minimal change glomerulonephritis

A

Presents in childhood/adolescence

As age increases incidence reduces

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12
Q

Describe the treatment of minimal change glomerulonephritis

A

Steroids

No progression to renal failure

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13
Q

Describe the pathogenesis of FSGS

A

Circulating factor damages the podocytes, which become scarred

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14
Q

What is the most common form of nephrotic syndrome in adults?

A

Membranous glomerulonephritis

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15
Q

Describe the pathogenesis of membranous glomerulonephritis

A

Immune complex deposits in subepithelial space - IgG

Autoimmune

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16
Q

Describe the consequences for patients of membranous glomerulonephritis

A

1/3rd get better
1/3rd have proteinuria but are fine
1/3rd progress to renal failure

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17
Q

Define nephritic syndrome

A

Haematuria
Hypertension
AKI

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18
Q

What is IgA Nephropathy?

A

Deposition of circulating IgA in the glomerulus
Mesangial proliferation and scarring occurs
Haematuria

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19
Q

State two hereditary nephropathies

A

Thin GBM Nephropathy

Alport syndrome

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20
Q

Describe Thin GBM Nephropathy

A

Isolated haematuria

No renal failure

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21
Q

Describe Alport Syndrome

A 
X linked
Abnormal collagen IV
deafness
Abnormal GBM
Progresses to renal failure
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22
Q

What happens in Goodpasture syndrome?

A

Acute onset glomerulonephritis
Association with Pulmonary haemmorhage
IgG to collagen IV

Treated by immunosuppression and plasmapheresis

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23
Q

How does vasculitis affect the kidney?

A

Inflammation of blood vessels

Nephritic

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24
Q

What are the symptoms and signs of prostate cancer?

A 
Nocturia
Frequency
Hesitancy
Haematuria 
ED

Prostate hardness

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25
Q

Where are the most common sites for a prostate cancer metastasis?

A

Bone

Lymph nodes

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26
Q

Where are most prostate cancers found?

A

Adenocarcinoma in the peripheral zone

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27
Q

What are the risk factors for prostate cancer?

A

Old age
Family history
BRCA2 gene
Black or white ethnicity

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28
Q

What are the symptoms and signs of bladder cancer?

A

Painless Haematuria
Dysuria
Frequency

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29
Q

What type of cancer are most bladder cancers?

A

Transitional cell carcinomas

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30
Q

What are the risk factors for bladder cancer?

A

Age
Smoking - polycyclic aromatic hydrocarbons
Occupational exposure to aromatic amines - paint, dye, metals

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31
Q

What is a radical cystectomy?

A

Removal of the urinary bladder

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32
Q

What are the symptoms and signs of renal cancer?

A 
Haematuria
Loin pain
UTI 
Mass in flank
Varicocoele 
Ankle oedema
Paraneoplastic syndromes
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33
Q

Where do renal cancers spread?

A 
MOST COMMON = lungs
Adrenal glands
Liver 
spleen
Colon
Pancreas
Renal vein then IVC
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34
Q

What is the most common kind of renal cancer?

A

Renal cell carcinoma

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35
Q

What are the risk factors for renal cancer?

A

Smoking
Obesity
Hypertension
Dialysis

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36
Q

Describe the signs and symptoms of testicular cancer

A

Change in shape or texture of testis - usually painless
Painful
Hydrocoele
Gynacomastea from beta-hCG
Back pain from para-aortic lymph node metastasis

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37
Q

What kind of cells do most testicular cancers arise from?

A

Germ cells

Two types:
Seminoma
Non-Seminoma

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38
Q

When is testicular cancer most common?

A

Between 15 and 40

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39
Q

What are the risk factors for testicular cancer?

A 
Cryptorchidism - absence of testes from the scrotum
Klinefelter's syndrome - XXY
Male infertility
Low birth weight
Young parental age
Infantile hernia
Tall
TGCT1 gene on X chromosome
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40
Q

What are the tumour markers for testicular cancer?

A

Alpha-fetoprotein - not produced by Seminomas, but by yolk sac tumours

Beta-hCG - elevated in teratomas and Seminomas

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41
Q

Define clearance

A

the volume of plasma that is completely cleared of a substance per unit of time

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42
Q

how can clearance be calculated?

A

concentration in plasma

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43
Q

How can renal clearance rate be calculated?

A

concentration in plasma

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44
Q

How is the filtration fraction calculated?

A

renal plasma flow

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45
Q

When does renal clearance = GFR?

A

If the substance is
freely filtered
non reabsorbed
non secreted

46
Q

What can GFR be used to assess?

A

kidney function

the filtration process

47
Q

Describe tubular glomerular feedback

A

change in flow rate -> change in GFR ->change in amount of NaCl reaching distal tubule
macula densa cells take up NaCl via NaK2Cl cotransporter which is concentration dependant

if NaCl increases, adenosine is released
vasoconstriction of afferent arteriole

if NaCl decreases, prostaglandins are released
vasodilation of afferent arteriole

48
Q

Which transporter do loop diuretics act on?

Which segment of the nephron is this in?

A

NaKCC2

thick ascending limb

49
Q

Which transporter do thiazide diuretics act on?

Which segment of the nephron is this in?

A

NCC

DCT

50
Q

Which transporter do potassium sparing diuretics act on?

Which segment of the nephron is this in?

A

ENaC

Collecting duct

51
Q

How is chronic kidney disease seen histologically?

A

glomerulosclerosis

tubular interstitial fibrosis

52
Q

In CKD, what is functioning renal tissue replaced by?

What does this cause?

A

extra-cellular matrix

progressive loss of excretory and hormone functions of the kidney

53
Q

Why does CKD result in anaemia?

A

decreased erythropoietin

decreased RBC survival

54
Q

Why does CKD result in renal bone disease?

A

Decreased GFR
less Phosphate is excreted, increasing its serum concentration.
Phosphate forms complexes with free Calcium, reducing calcium’s effective serum concentration.
Parathyroid gland stimulated to produce PTH, causing over activity of Osteoclasts, leading to Osteitis Fibrosa Cystica.

55
Q

Why does CKD result in osteomalacia?

A

Damage to the kidneys means less Vitamin D undergoes its 2nd Hydroxylation to its active form

56
Q

Describe the conservative management of CKD

A 
To prevent oR delay progression
o	Stop smoking
o	decrease obesity
o	Exercise
o	Treat Diabetes (If present)
o	Treat Blood Pressure (If high)
o	ACE Inhibitors / Angiotensin Receptor Blockers in proteinuria
o	Lipid Lowering (Diet / Statins)
57
Q

When is renal replacement therapy initiated?

A

When native renal function declines to a level that is no longer adequate to support health, usually when GFR is

58
Q

What are the options for renal replacement therapy?

A

transplant
haemodialysis
peritoneal dialysis

59
Q

What GFR indicates Stage 1 CKD?

What are the signs and symptoms?

A

GFR >90+

Normal kidney function but urine findings or structural abnormalities or genetic trait point to kidney disease

60
Q

What GFR indicates Stage 2 CKD?

What are the signs and symptoms?

A

GFR 60-89

Mildly reduced kidney function, and urine findings or structural abnormalities or genetic trait point to kidney disease

61
Q

What GFR indicates Stage 3a CKD?

What are the signs and symptoms?

A

45-59

Moderately reduced kidney function

62
Q

What GFR indicates Stage 3b CKD?

What are the signs and symptoms?

A

30-44

Moderately reduced kidney function

63
Q

What GFR indicates Stage 4 CKD?

What are the signs and symptoms?

A

15-29

Severely reduced kidney function

64
Q

What GFR indicates Stage 5 CKD?

What are the signs and symptoms?

A
65
Q

What are the treatment option for the stages of CKD?

A

Stages 1, 2 and 3: Observation, control of blood pressure and risk factors

Stage 4: plan for endstage renal care

Stage 5: renal replacement therapy

66
Q

Describe haemodialysis

A

creation of a Ateriovenous (AV) Fistula
The difference in pressure means that blood moves from the artery to the vein, causing it to dilate and develop a muscular wall.
Using this vascular access, the patient is connected up to a dialysis machine, which contains highly purified water across a semi-permeable membrane. This allows for ‘filtering’ of the patient’s blood.
Anti-coagulation is also needed to prevent the patient’s blood from clotting in the machine.

67
Q

What are the advantages of haemodialysis?

A

Effective (Survivors > 25 years)
4/7 days free from treatment
Dialysis dose easily prescribed

68
Q

What are the disadvantages of haemodialysis?

A 
Fluid/Diet restrictions
Limits holidays
Access problems
CVS instability
High cost
69
Q

Describe peritoneal dialysis

A

Peritoneal Dialysis Fluid is put into the peritoneal cavity, and the dialysis occurs across the peritoneal membrane (semi-permeable membrane). The fluid is then drained away and disposed of.

70
Q

What are the advantages of peritoneal dialysis?

A 
Low Technology
Home technique
Easily learned
Allows mobility
CVS stability
71
Q

What are the disadvantages of peritoneal dialysis?

A 
Frequent exchanges (~4/day)
Frequent treatment failures
Peritonitis
Limited dialysis dose range
High revenue costs
72
Q

Where is a transplanted kidney located?

A

iliac fossa - connected to iliac vessels

73
Q

What are the advantages of kidney transplantation?

A 
Restores near normal renal function
Allows mobility and “rehabilitation”
Improved survival
Good long term results
Cheaper than dialysis
74
Q

What are the disadvantages of kidney transplantation?

A 
Not all are suitable
Limited donor supply
Operative morbidity and mortality
Lifelong immunosuppression
Still left with progressive CKD
75
Q

Define acidaemia

A

blood pH

76
Q

What are the effects of acidaemia?

A 
increased [K+]
reduced enzyme function
Reduced cardiac and skeletal muscle contractility
Reduced glycolysis 
Reduced hepatic function
77
Q

Define alkalaemia

A

blood pH >7.45

78
Q

What are the effects of alkalaemia?

A

reduces the solubility of calcium salts, causing them to come out of solution,
decreased concentration of free calcium ions

This increases neuronal excitability
paraesthesia
tetany

79
Q

What causes respiratory acidaemia?

A

Hypoventilation leads to hypercapnia (rise in pCO2)

leads to a fall in pH

80
Q

What causes respiratory alkalaemia?

A

Hyperventilation leads to hypocapnia (fall in pCO2),

so pH increases.

81
Q

How is respiratory acidaemia compensated for by the kidneys?

A

[HCO3-] rises proportionately to restore pH

82
Q

How is respiratory alkalaemia compensated for by the kidneys?

A

[HCO3-] falls proportionately to restore pH

83
Q

Why does metabolic acidosis occur?

A

Metabolically produced H+ ions react with HCO3- to produce CO2 in venous blood.
This CO2 is then breathed out through the lungs.
there is a reduction in [HCO3-]
as the pCO2 is unchanged, there is a fall in pH.

84
Q

What do the central chemoceptors detect?

A

pCO2

85
Q

What do the peripheral chemoceptors detect?

A

pCO2

plasma pH

86
Q

Why does metabolic alkalosis occur?

A

plasma [HCO3-] rises, for example after persistent vomiting, (due to H+ ions being lost in vomit, hence increasing the [HCO3-]
the [HCO3-] : pCO2 ratio will be increased,
causing a pH increase.

87
Q

How is metabolic acidosis compensated for by the respiratory system?

A

peripheral chemoreceptors detect changes in plasma pH increase ventilation rate to decrease pCO2,
which will correct the pH

88
Q

How is metabolic alkalosis compensated for by the respiratory system?

A

By decreasing ventilation rate,
increasing pCO2,
this can be PARTIALLY compensated for.

89
Q

Where in the kidney can HCO3- be made?

A

proximal cells

alpha-intercalated cells in distal tubule

90
Q

How is HCO3- made in proximal tubule cells?

A

Glutamine is converted to α-ketoglutarate and NH4+
α-ketoglutarate splits to give 2HCO3-
The HCO3- enters the ECF by a sodium cotransporter in the basolateral cell surface membrane
NH4+ enters the lumen of the PCT.

91
Q

How is HCO3- made in alpha-intercalated cells in the distal tubule?

A

CO2 produced by metabolism
CO2 reacts with water to form HCO3- and H+.
The HCO3- enters the plasma by Cl- antiporter
H+ enters the lumen of the DCT via H+ ATPase

92
Q

How is HCO3- reabsorbed in the PCT?

A

H+ enters lumen via NHE
HCO3- in lumen reacts with H+ to produce CO2 and H2O which diffuse into cell
carbonic anhydrase in tubular cell converts back
HCO3- enters ECF by Na cotransporter

93
Q

How is H+ excreted in the DCT?

A

If the ECF [HCO3-] is low, more HCO3- moves out of the cells to the ECF, so there will be more H+ in the cells.
low pH inside cells detected
increased activity of H+ ATPase on luminal membrane

94
Q

How is H+ excreted in the PCT?

A

If the ECF [HCO3-] is low, more HCO3- moves out of the cells to the ECF, so there will be more H+ in the cells.
low pH inside cells detected
increased activity of the Na+/H+ exchanger on luminal membrane

95
Q

Why does Metabolic acidosis lead to hyperkalaemia?

A

H+ uptake by cells to increase pH

K+ out of cells

96
Q

Why does Metabolic alkalosis lead to hypokalaemia?

A

H+ moves out of cells to decrease pH

K+ into cells

97
Q

Why can vomiting lead to hypokalaemia?

A

[HCO3-] increases after persistent vomiting, so the body stops actively secreting H+, as it would make metabolic alkalosis worse.

As H+ secretion has stopped, so has K+ reabsorption

98
Q

How is the anion gap calculated?

A

([Na+] + [K+]) – ([Cl- ] + [HCO3-])

99
Q

How does insulin lead to a fall in serum [K+]?

A

Insulin increases the amount of Na-K-ATPase, as it provides the drive for the Na-Glucose transporter.

The increase in Na-K-ATPase results in uptake of K+ by the muscle cells and liver.

100
Q

How do catecholamines lead to a fall in serum [K+]?

A

Beta 2 adrenoceptors stimulate Na-K-ATPase.

101
Q

How does aldosterone lead to a fall in serum [K+]?

A

increases the transcription of Na-K-ATPase in the basolateral membrane
increases transcription of ENaC / K+ channels in the apical membrane.
increased K+ excretion.

102
Q

Which components of the blood cannot be filtered by the glomerular basement membrane?

A

RBCs
plasma proteins
Mr 5200

103
Q

What are the layers of the filtration barrier in the glomerulus?

A

capillary endothelium
basement membrane
podocyte layer

104
Q

How are proteins prevented from moving through the basement membrane?

A

-ve ly charged glycoproteins repel protein movement

105
Q

What determines the size of molecule that can fit through the filtration barrier?

A

filtration slits between the podocyte pseudopodia

106
Q

How much of the blood in the glomerulus is filtered?

A

20%

107
Q

Describe the sympathetic innervation f the bladder

A

T10-L2
Hypo gastric nerve

Innervates detrusor and internal sphincter

108
Q

Describe the parasympathetic innervation of the bladder

A

S2-S4

Innervates detrusor

109
Q

What provides the sensory innervation of the bladder?

A

Pelvic nerve

S2-S4

110
Q

Describe the neural mechanism for storage of urine in the bladder

A

Stretch receptors in bladder - APs along Pelvic nerve

Inhibition pre synaptic parasympathetic neurones - no stimulation M3 receptors in detrusor by pelvic nerve. No contraction

Stimulation hypogastric nerve
Internal sphincter contracts, Detrusor relaxed

Conscious contraction of external sphincter - pudendal nerve to Nicotinic receptor

111
Q

Describe the neural mechanism of voiding of the bladder

A

Voluntary relaxation external sphincter - micturition centre in pons to inhibit pudendal nerve

Increased stretch in bladder wall

Stimulation parasympathetic pelvic nerve M3 - detrusor contracts

Inhibition sympathetic hypogastric - internal sphincter relaxed

ESA3 (5 decks)

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