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
2
Q
What affect will a blocked glomerular basement membrane have?
A
Renal failure
Decrease GFR
3
Q
What affect will a leaky glomerular basement membrane have?
A
Proteinuria
Haematuria
4
Q
Define proteinuria
A
Presence of excess serum proteins in urine
5
Q
What is the cause of proteinuria?
A
Due to podocyte or subepithelial damage
Widened fenestration slits allow protein to leak through
6
Q
Define nephrotic syndrome
A
Over 3.5g of protein in urine in 24hrs
7
Q
What is a systemic symptom of nephrotic syndrome? Why?
A
Generalised oedema
Protein is lost in urine
Reduced oncotic pressure
8
Q
State three causes of primary nephrotic syndrome
A
Minimal change glomerulonephritis
Focal segmental glomerulonephritis (FSGS)
Membranous glomerulonephritis
9
Q
State secondary causes of nephrotic syndrome
A
Diabetes mellitus
Amyloidosis
10
Q
Describe the pathogenesis of minimal change glomerulonephritis
A
Podocytes damaged
Widened fenestration slits
11
Q
Describe the epidemiology of minimal change glomerulonephritis
A
Presents in childhood/adolescence
As age increases incidence reduces
12
Q
Describe the treatment of minimal change glomerulonephritis
A
Steroids
No progression to renal failure
13
Q
Describe the pathogenesis of FSGS
A
Circulating factor damages the podocytes, which become scarred
14
Q
What is the most common form of nephrotic syndrome in adults?
A
Membranous glomerulonephritis
15
Q
Describe the pathogenesis of membranous glomerulonephritis
A
Immune complex deposits in subepithelial space - IgG
Autoimmune
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
17
Q
Define nephritic syndrome
A
Haematuria
Hypertension
AKI
18
Q
What is IgA Nephropathy?
A
Deposition of circulating IgA in the glomerulus
Mesangial proliferation and scarring occurs
Haematuria
19
Q
State two hereditary nephropathies
A
Thin GBM Nephropathy
Alport syndrome
20
Q
Describe Thin GBM Nephropathy
A
Isolated haematuria
No renal failure
21
Q
Describe Alport Syndrome
A
X linked Abnormal collagen IV deafness Abnormal GBM Progresses to renal failure
22
Q
What happens in Goodpasture syndrome?
A
Acute onset glomerulonephritis
Association with Pulmonary haemmorhage
IgG to collagen IV
Treated by immunosuppression and plasmapheresis
23
Q
How does vasculitis affect the kidney?
A
Inflammation of blood vessels
Nephritic
24
Q
What are the symptoms and signs of prostate cancer?
A
Nocturia Frequency Hesitancy Haematuria ED
Prostate hardness
25
Where are the most common sites for a prostate cancer metastasis?
Bone
| Lymph nodes
26
Where are most prostate cancers found?
Adenocarcinoma in the peripheral zone
27
What are the risk factors for prostate cancer?
Old age
Family history
BRCA2 gene
Black or white ethnicity
28
What are the symptoms and signs of bladder cancer?
Painless Haematuria
Dysuria
Frequency
29
What type of cancer are most bladder cancers?
Transitional cell carcinomas
30
What are the risk factors for bladder cancer?
Age
Smoking - polycyclic aromatic hydrocarbons
Occupational exposure to aromatic amines - paint, dye, metals
31
What is a radical cystectomy?
Removal of the urinary bladder
32
What are the symptoms and signs of renal cancer?
```
Haematuria
Loin pain
UTI
Mass in flank
Varicocoele
Ankle oedema
Paraneoplastic syndromes
```
33
Where do renal cancers spread?
```
MOST COMMON = lungs
Adrenal glands
Liver
spleen
Colon
Pancreas
Renal vein then IVC
```
34
What is the most common kind of renal cancer?
Renal cell carcinoma
35
What are the risk factors for renal cancer?
Smoking
Obesity
Hypertension
Dialysis
36
Describe the signs and symptoms of testicular cancer
Change in shape or texture of testis - usually painless
Painful
Hydrocoele
Gynacomastea from beta-hCG
Back pain from para-aortic lymph node metastasis
37
What kind of cells do most testicular cancers arise from?
Germ cells
Two types:
Seminoma
Non-Seminoma
38
When is testicular cancer most common?
Between 15 and 40
39
What are the risk factors for testicular cancer?
```
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
```
40
What are the tumour markers for testicular cancer?
Alpha-fetoprotein - not produced by Seminomas, but by yolk sac tumours
Beta-hCG - elevated in teratomas and Seminomas
41
Define clearance
the volume of plasma that is completely cleared of a substance per unit of time
42
how can clearance be calculated?
concentration in urine x urine volume
---------------------------------------------
concentration in plasma
43
How can renal clearance rate be calculated?
concentration in urine x flow rate
---------------------------------------------
concentration in plasma
44
How is the filtration fraction calculated?
glomerular filtration rate
----------------------------------
renal plasma flow
45
When does renal clearance = GFR?
If the substance is
freely filtered
non reabsorbed
non secreted
46
What can GFR be used to assess?
kidney function
| the filtration process
47
Describe tubular glomerular feedback
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
Which transporter do loop diuretics act on?
| Which segment of the nephron is this in?
NaKCC2
| thick ascending limb
49
Which transporter do thiazide diuretics act on?
| Which segment of the nephron is this in?
NCC
| DCT
50
Which transporter do potassium sparing diuretics act on?
| Which segment of the nephron is this in?
ENaC
| Collecting duct
51
How is chronic kidney disease seen histologically?
glomerulosclerosis
| tubular interstitial fibrosis
52
In CKD, what is functioning renal tissue replaced by?
What does this cause?
extra-cellular matrix
progressive loss of excretory and hormone functions of the kidney
53
Why does CKD result in anaemia?
decreased erythropoietin
| decreased RBC survival
54
Why does CKD result in renal bone disease?
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
Why does CKD result in osteomalacia?
Damage to the kidneys means less Vitamin D undergoes its 2nd Hydroxylation to its active form
56
Describe the conservative management of CKD
```
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
When is renal replacement therapy initiated?
When native renal function declines to a level that is no longer adequate to support health, usually when GFR is
58
What are the options for renal replacement therapy?
transplant
haemodialysis
peritoneal dialysis
59
What GFR indicates Stage 1 CKD?
What are the signs and symptoms?
GFR >90+
Normal kidney function but urine findings or structural abnormalities or genetic trait point to kidney disease
60
What GFR indicates Stage 2 CKD?
What are the signs and symptoms?
GFR 60-89
Mildly reduced kidney function, and urine findings or structural abnormalities or genetic trait point to kidney disease
61
What GFR indicates Stage 3a CKD?
What are the signs and symptoms?
45-59
Moderately reduced kidney function
62
What GFR indicates Stage 3b CKD?
What are the signs and symptoms?
30-44
Moderately reduced kidney function
63
What GFR indicates Stage 4 CKD?
What are the signs and symptoms?
15-29
Severely reduced kidney function
64
What GFR indicates Stage 5 CKD?
What are the signs and symptoms?
65
What are the treatment option for the stages of CKD?
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
Describe haemodialysis
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
What are the advantages of haemodialysis?
Effective (Survivors > 25 years)
4/7 days free from treatment
Dialysis dose easily prescribed
68
What are the disadvantages of haemodialysis?
```
Fluid/Diet restrictions
Limits holidays
Access problems
CVS instability
High cost
```
69
Describe peritoneal dialysis
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
What are the advantages of peritoneal dialysis?
```
Low Technology
Home technique
Easily learned
Allows mobility
CVS stability
```
71
What are the disadvantages of peritoneal dialysis?
```
Frequent exchanges (~4/day)
Frequent treatment failures
Peritonitis
Limited dialysis dose range
High revenue costs
```
72
Where is a transplanted kidney located?
iliac fossa - connected to iliac vessels
73
What are the advantages of kidney transplantation?
```
Restores near normal renal function
Allows mobility and “rehabilitation”
Improved survival
Good long term results
Cheaper than dialysis
```
74
What are the disadvantages of kidney transplantation?
```
Not all are suitable
Limited donor supply
Operative morbidity and mortality
Lifelong immunosuppression
Still left with progressive CKD
```
75
Define acidaemia
blood pH
76
What are the effects of acidaemia?
```
increased [K+]
reduced enzyme function
Reduced cardiac and skeletal muscle contractility
Reduced glycolysis
Reduced hepatic function
```
77
Define alkalaemia
blood pH >7.45
78
What are the effects of alkalaemia?
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
What causes respiratory acidaemia?
Hypoventilation leads to hypercapnia (rise in pCO2)
| leads to a fall in pH
80
What causes respiratory alkalaemia?
Hyperventilation leads to hypocapnia (fall in pCO2),
| so pH increases.
81
How is respiratory acidaemia compensated for by the kidneys?
[HCO3-] rises proportionately to restore pH
82
How is respiratory alkalaemia compensated for by the kidneys?
[HCO3-] falls proportionately to restore pH
83
Why does metabolic acidosis occur?
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
What do the central chemoceptors detect?
pCO2
85
What do the peripheral chemoceptors detect?
pCO2
| plasma pH
86
Why does metabolic alkalosis occur?
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
How is metabolic acidosis compensated for by the respiratory system?
peripheral chemoreceptors detect changes in plasma pH increase ventilation rate to decrease pCO2,
which will correct the pH
88
How is metabolic alkalosis compensated for by the respiratory system?
By decreasing ventilation rate,
increasing pCO2,
this can be PARTIALLY compensated for.
89
Where in the kidney can HCO3- be made?
proximal cells
| alpha-intercalated cells in distal tubule
90
How is HCO3- made in proximal tubule cells?
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
How is HCO3- made in alpha-intercalated cells in the distal tubule?
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
How is HCO3- reabsorbed in the PCT?
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
How is H+ excreted in the DCT?
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
How is H+ excreted in the PCT?
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
Why does Metabolic acidosis lead to hyperkalaemia?
H+ uptake by cells to increase pH
| K+ out of cells
96
Why does Metabolic alkalosis lead to hypokalaemia?
H+ moves out of cells to decrease pH
| K+ into cells
97
Why can vomiting lead to hypokalaemia?
[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
How is the anion gap calculated?
([Na+] + [K+]) – ([Cl- ] + [HCO3-])
99
How does insulin lead to a fall in serum [K+]?
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
How do catecholamines lead to a fall in serum [K+]?
Beta 2 adrenoceptors stimulate Na-K-ATPase.
101
How does aldosterone lead to a fall in serum [K+]?
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
Which components of the blood cannot be filtered by the glomerular basement membrane?
RBCs
plasma proteins
Mr 5200
103
What are the layers of the filtration barrier in the glomerulus?
capillary endothelium
basement membrane
podocyte layer
104
How are proteins prevented from moving through the basement membrane?
-ve ly charged glycoproteins repel protein movement
105
What determines the size of molecule that can fit through the filtration barrier?
filtration slits between the podocyte pseudopodia
106
How much of the blood in the glomerulus is filtered?
20%
107
Describe the sympathetic innervation f the bladder
T10-L2
Hypo gastric nerve
Innervates detrusor and internal sphincter
108
Describe the parasympathetic innervation of the bladder
S2-S4
Innervates detrusor
109
What provides the sensory innervation of the bladder?
Pelvic nerve
| S2-S4
110
Describe the neural mechanism for storage of urine in the bladder
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
Describe the neural mechanism of voiding of the bladder
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
