1
Q
What are the actions of angiotensin II?
A
- Vasoconstriction of efferent arteriole of glomerulus - increases resistance to blood flow
- Stimulates aldosterone release from adrenal cortex
- Arteriolar vasoconstriction - increases blood pressure
- Stimulates release of ADH - increases aquaporin channels in collecting duct
- Breaksdown bradykinin (vasodilator) - causes vasoconstriction
2
Q
In response to what is renin released and from where?
A
Macula densa cells detect low Na in juxtaglomerular apparatus which stimulates renin release from juxtaglomerular cells
3
Q
What apical channels can be found in the PCT?
A
- Na+/Glu, AA or peptide cotransporter
- Na+/Glu cotransporter = SGLUT2
- Na+/H+ exchanger coupled with H+/organic cation exchanger
4
Q
What channels are present in the ascending loop of Henle?
A
- NaK2Cl cotransporter
- ROMK
- Chloride channel (basolateral membrane)
- Na/K-ATPase (basolateral membrane)
5
Q
What channels are present in the early DCT?
A
- Na/Cl cotransporter
- Calcium channel - under control of PTH
- NCX (basolateral membrane)
6
Q
What channels are present in late DCT/collecting duct?
A
Principle cells
- ENaC
- ROMK
- Aquaporin II - ADH controlled
Intercalated cells
- K+/H+ exchanger
- Cl- channel
- Cl/HCO3- exchanger (basolateral)
- Cl and K channels (basolateral membrane)
7
Q
At what channel do the following act? Give an example where indicated
- Loop diuretics
- Thiazides
- Aldosterone antagonists
- ADH
- Aldosterone
A
- Loop diuretics - NaK2Cl cotransporter (LoH) - Furosemide
- Thiazides - Na/Cl cotransporter (early DCT) - Bendroflumethiazide
- Aldosterone antagonists - Block action of aldosterone (late DCT/CD) - spironolactone
- ADH - Increase aquaporin channels (late DCT/CD)
- Aldosterone - Increases expression of ENaC, ROMK and Na/K-ATPase
8
Q
What spinal level do the kidney start and at what spinal level does the hilum sit?
A
T11/T12
L1/L2 = hilum
9
Q
What are the functions of the kidney?
A
- Regulation
- Excretion
- Endocrine
- Metabolism
10
Q
Describe the progression of blood vessels from renal artery to renal vein
A
- Renal artery
- Segmental artery
- Interlobar artery
- Arcuate artery
- Interlobular artery
- Afferent arteriole
- Glomerulus
- Efferent arteriole
- Peritubular capillaries
- Interlobular vein
- Arcuate vein
- Interlobar vein
- Renal vein
11
Q
Which muscle do the ureteres run anterior to?
A
Psoas major
12
Q
What are the common places for kidney stones to become lodged?
A
- Ureteropelvic junction
- Pelvic brim
- As ureters enter kidney
13
Q
What is the medial imbilical ligament a remanent of?
A
Urachus
14
Q
What is the difference between males and females with regards to urethral sphincters
A
Only males have the internal urethral sphincter
15
Q
Briefly describe main stages of embryonic development of the kidneys
A
- Pronephros
- Produces pronephric duct
- Mesonephros
- Mesonephric duct which sprouts ureteric bud (induces development of definitive kidney)
- Metanephros forms from ureteric bud as metanephric blastema
- Collecting system derived from ureteric bud
- Excretory component derived from intermediate mesoderm
16
Q
From which embryonic tissue do the kidney develop?
A
Intermediate mesoderm
17
Q
Describe a defect that can occur during migration of kidney during development
A
Kidney get caught going past the arterial fork (inferior mesenteric artery) then they can fuse to form a horseshoe kidney
18
Q
Briefly describe development of bladder
A
- Hindgut derivative
- Cloaca is split into two by urorectal septum
- Into urogenital sinus and anorectal canal
- Urogenital sinus is divided into 3 parts (bladder, pelvic part and phallic part)
- Allantois is a diverticulum of the hingut that extends into umbilical cord - becomes urachus that drains urinary bladder in utero
19
Q
Briefly describe development of openings into bladder
A
Males
- Mesonephric ducts reach urogenital sinus
- Ureteric buds sprout from mesonephric ducts
- Smooth muscle begins to develop from mesonephric ducts on bladder
- Ureteric buds and mesonephric ducts make independent openings into bladder
Females
- Same happens except that mesonephric ducts regress due to lack of androgens
20
Q
What is hypospadias?
A
Failure of urethral folds to fuse
Urethra opens onto ventral surface rather than end of glans
21
Q
What is the epithelial lining of:
- PCT
- Descending LoH
- Ascending LoH
- DCT
- Collecting duct
A
- PCT - simple cuboidal epithelium with brush border, active transport
- Descending LoH - Simple squamous, no active transport
- Ascending LoH - Simple cuboidal, active transport
- DCT - Simple cuboidal with few microvilli
- Collecting duct - suboidal epithelium
22
Q
What do the collecting ducts of kidney terminate to form?
A
Papillary ducts of Bellini which then connect to form minor calyx
23
Q
Describe muscularture of ureter
A
2 layers of smooth muscles
A third layer appears in lower third of ureter
24
Q
What is the epithelial layer of:
- Calyx of kidneys
- Ureters
- Bladder
- Inital part of urethra
A
All transitional epithelium
25
What is the epithelial layer of male and female urethra?
Male - Stratified columnar below ejaculatory ducts then becomes stratified squamous
Females - Stratified squamous
26
Decribe detrusor muscle
3 layers of muscle
Longitudinal-circular-longitudinal
Covers all areas except trigone
27
What feature of basement membrane and podocytes prevents proteins being filtered?
Negatively charged glycoproteins
28
What affects glomerular filtration rate?
1. Hydrostatic pressure in capillary
2. Hydrostatic pressure in Bowman's capsule
3. Osmotic pressure gradient between capillary and tubular lumen
29
Where does the majority of secretion occur in the nephron? And what is secreted?
Collecting duct
H+, K+, ammonium (NH4+), creatinine, urea, some hormones and drugs
30
Describe secretion of organic cations
1. OC enters through basolateral membrane via faciliated diffusion
* Down concentration and electrical gradients (Na/K-ATPase)
2. Secreted into lumen by H+/OC exchanger, driven by H+ gradient set by Na/H antiporter
31
What is the renal threshold for glucose?
200mg/100ml
32
Define clearance with regards to filtration
Volume of plasma from which a substance can be completely cleared to the urine per unit time
i.e. volume of plasma cleared of substance per minute
33
What is normal GFR for males and females?
Males = 115-125ml/min
Females = 90-100ml/min
34
What is the renal plasma flow?
* Kidney recieves ~1.1L/min of blood
* 45% is RBC, 55% is plasma = 605ml/min
* 20% of all plasma is filtered = 121ml/min
35
Describe the myogenic response
Mechanosensory channels are activated in response to stretch (e.g. increase in BP) causing influx of Ca2+ resulting in vasoconstriction
36
Describe tubular glomerular feedback
Macula densa cells detect amount of NaCl present in filtrate
If NaCl increases then adenosine is released causing vasoconstriction of afferent arteriole
If NaCl decreases then prostaglandins are released causing vasodilation of afferent arteriole
37
What is the difference between general overflow and specific overflow aminoaciduria?
General is all amino acids present in urine, normally due to inadequate deamination in liver or increased GFR
Specific is one amino acid present in urine, genetic inability to break down one amino acid - e.g. phenylalanine in PKU
38
What proportion and amount of fluid is found in the ICF?
25L
63% of total fluid
39
What proportion and amount of fluid is found in ECF?
15L
38% of all fluid
40
Describe glomerulotubular balance
Balance between GFR and rate of reabsorption must be kept constant
Therefore regardless of amount 67% of Na will always be reabsorbed in PCT
41
What are the four mechanisms that control BP?
1. RAAS System
2. Sympathetic Nervous System
3. Antidiuretic Hormone
4. Atrial Natriuretic Peptide
42
What is Conn's syndrome?
Aldosterone secreting adenoma of adrenal glands
Causes hypertension and hypokalaemia
43
What is pheochromocytoma?
Tumour of adrenal medulla causing secretion of NA and adrenaline
Increases sympathetic stimulation
44
How is osmolarity detected and what are the effects?
Detected by hypothalamic osmoreceptors in OVLT (organum vasculoum of the laminae terminalis)
Causes release of ADH from posterior pituitary and stimulates thirst (thirst is insensitive, requires \>10% change)
45
What is SIADH?
Syndrome of inappropriate ADH secretion
ADH not inhibited by lowering of blood osmolarity, and causing excessive water retension resulting in increased BP, dilutional hyponatreamia, lowered blood osmolarity
46
Explain how the corticopapillary osmotic gradient is set up and maintained
1. Counter-current multiplication
* Loop of Henle acts as counter current multiplier due to descending limb being permeable to water and ascending limb permabile to ions
* Sets up gradient
2. Counter-current exchange
* Vasa recta run alongside loop of Henle and flow in opposite direction
* They remove water and ion quickly to maintain gradient set by counter-current multiplication
47
How does PTH control serum calcium?
* Low serum calcium detected by parathyroid gland
* Releases PTH
* PTH increases osteoclast activity
* Also increases conversion of calcidiol to calcitriol and increases Ca2+ reabsorption but increases phosphate excretion in kidney
48
What are the causes of hypercalcinaemia?
1. Primary hyperparathyroidism
2. Haematological malignancies
3. Non-haematological malignancies - squamous cell carcinoma of lung producing PTHrP
49
What is normal blood pH?
7.38 - 7.42
50
What pH is severe and life threatening acidaemia?
Severe = \<7.1
Life threatening = \<7.0
51
What is the consequence of acidosis and alkalosis?
Acidosis = lethal denaturing of enzymes
Alkalosis = reduced solubility of calcium, so moves out of ECF (hypocalcaemia) making nerves more excitable
52
How do the kidneys produce new HCO3-?
* Metabolism of CO2 in intercalated cells of late DCT/CD - required carbonic anhydrase
* H+ pumped into lumen to react with hydrogen phosphate (HPO42- - titratable acid)
* HCO3- enters blood
53
How is H+ buffered in urine?
1. Titratable acid (HPO42-) - reacts with H+ to form HPO4- which limits rise in free H+ in tubule
2. Attach H+ to ammonia (NH3) which is synthesised by PCT metabolism of glutamine - also produces new HCO3- to go into blood
54
What are the pathophysiological factors that alter potassium concentrations?
1. Acid base balance - acidosis causes reciprocal shifts in K
2. Cell lysis - release of K into ECF
3. Exercise - net release of K during recovery phase of action potential of skeletal muscles, also skeletal muscle is damaged during exercise. Uptake of K by non-contracting tissues prevents dangerously high K. [K] proportional to exercise intensity
4. Plasma osmolarity - increased plasma osmolarity causes water to move into ECF, this increases ICF [K] due to less water so K moves from ICF into ECF
5. Drug related changes - diuretics, ACE inhibitors
55
What are the common causes of UTIs?
* Coliforms - E. coli
* Staphylococcus saprophyticus
56
Describe innervation of bladder
Parasympathetic = pelvic nerve (S2-S4) = M3 receptors = contraction
Sympathetic = hypogastric never (T10-L2) = B3 receptors = relaxation
Somatic (external urethral sphincter) = pudendal nerve (S2-S4) = relaxation to urinate
57
Define acute kidney injury
Decline in GFR that occurs during a period of less than 2 weeks with an increased urea and creatinine
58
What is difference between oliguria and anuria?
Oliguria - little urine (\<500ml per day)
Anuria - no urine (\<100ml per day)
Normal = 1.5L per day
59
Describe a pre-renal AKI
* Renal hypoperfusion
* Caused either by reduced effective circulating volume
* Hypovolaemia
* Systemic vasodilation e.g. sepsis, cirrhosis, anaphylaxis
* Cardiac failure
* Or impaired renal autoregulation
* Preglomerular vasoconstriction e.g. sepsis, hypercalcaemia, NSAIDs
* Postglomerular vasodilation e.g. ACE inhibitors, angiotensin II receptor antagonists
60
Describe intrinsic AKI
* Direct injury to kidney
* Causes:
* Nephrotoxic (damage epithelial cells causing cell death and shedding into lumen) - myoglobin, urate, bilirubin, NSAIDs, ACEi, aminoglycosides (gentamicin)
* Inflammatory - glomeruonephritis, acute tubule-interstitial nephritis
* Ischaemic - pre-renal cause or acute tubular necrosis (from ischaemic or nephrotoxic cause)
61
Describe a post-renal AKI
* Caused by obstruction in urinary tract (ureters, bladder, urethra)
* Ostruction can be:
* Within lumen - calculi, blood clot, tumour
* Within wall - congenital, ureteric stricture
* Pressure from outside - prostatic hypertrophy, mlaignancy, aortic aneurysm
62
Name some primary causes of nephrotic syndrome
Usually due to damage of podocyte/subepithelial layer
* Minimal change glomerulonephritis - fusion of podocyte foot processes
* Focal segmental glomerulosclerosis - circulating permability factor
* Membranous glomerulonephritis - immune complex deposition in sub-spithelial space (commonest cause in adults)
63
What are the 4 sites of glomerular injury?
1. Subepithelial - affects podocytes
2. Glomerular basement membrane
3. Subendothelial
4. Mesangial/paramesangial
64
Name common secondary causes of nephrotic syndrome
* Diabetic mellitus
* Amyloidosis
65
PPE Revision
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