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)
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
3
Q
To which structure does the kidney relate superiorly?
A
The kidney relates superiorly to the diaphragm
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
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)
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)
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
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
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
- Vein
- Artery
- The pelvis of Kidney (also inferior)
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
11
Q
What is the Calyx in the kidney?
A
Chambers of the kidney through which urine passes
12
Q
What is the renal papilla?
A
It is the junction of the site where urine from medullary pyramids enters the calyx
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
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
15
Q
How is urine transported down the ureters?
A
By peristaltic contraction of SM
16
Q
Where do the sphincters of the ureters sit?
What is their relevance?
A
3 sites of ureteric constriction:
- pelviuretericjunction
- where ureter crosses pelvic brim
- where ureter traverses bladder wall
–> often sites where renal stones get trapped and cause pain
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
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
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
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
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
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
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
24
Q
How is the lymph drainage of the urinary system organised?
A
Lymph basically follows arterial supply
25
What are the 5 main steps in urine production of the kidney?
1. Filtration
2. Reabsorption
3. Creation of hyper-osmotic extracellular fluid
4. Adjustment of ion content of urine
5. Concentration of urine
26
Of which components does the Renal corpuscle consist?
It consists of the
* Bowman's capsule (surrounding glomerulus)
* Glomerulus (capillary network)
* Podocytes (cells that wrap around glomerulus)
27
How does the blood supply of the renal corpuscle supports its function?
A big afferent and small efferent ateriole create a hypertonic environment for filtrate to leave capillaries
28
What structural components support the filtration of blood in the renal corpuscle?
1. Large surface area --\> many capillaries
2. Fenestrated epithelium
3. Modified basement membrane with many gaps
## Footnote
**--\> Allows plasma to leave blood**
29
Which substances are filtered out of the blood in the renal corpuscle?
Everything \<50.000 kDa
--\> Almost everything except blood cells and bigger proteins
30
Which components of the primary filtrate are reabsorbed in the proximal convoluted tubule?
What is the mechanism behind each?
* 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
31
Which structural components of the proximal convoluted tubule allow reabsorption of the filtrate?
* 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
32
Which structural component of the nephron creates the hyper-osmotic extracellular fluid?
What does it consist of?
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)
33
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?
•Passive osmotic equilibrium (aquaporins present)
--\> Water leaves the primary filtrate
•Simple squamous epithelium
34
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?
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
35
What is the vasa rectae and which role does it play in the creation of a hyperosmotic extracellular fluid?
* 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
36
Where does the adjustment of the ion-concentration in the urine occur?
In the Distal convulated tubules
37
How do the distal convoluted tubules in the kidney control the adjustment of ion concentration in the urine?
Which structural components support this?
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
38
Where does the concentration of the urine occur?
It occurs in the collecting tubule or duct in the medulla
39
How is the concentration of the urine in the collecting duct controlled?
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
40
Which structural components are present in the collecting tubule/duct to match their function?
* Tight, water impermeable junction (only aquaporins molecules can regulate water in/outflow)
* few mitochondria (passive process)
Aquaporin 2/3 controlled by vasopressin
41
Where is the juxtaglomerular apparatus located?
Which structures does it include?
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
42
What is the function of the juxtaglomerular apparatus?
To regulate blood pressure via hormone production
43
Explain the mechanism of blood pressure regulation via the juxtaglomerular apparatus
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
44
What is glomerular filtration?
It is the formation of an ultrafiltrate of plasma in the glomerulus
45
What is by definition renal disease/ renal failure?
The fall in glomerular filtration rate
46
Where does glomerular filtration take place?
In the glomerulus + Bowmans capsule of the kidney
47
Which concentration do solutes in the primary urine have?
The same as in the blood plasma (isotonic)
48
49
What are the pressures that influence/drive glomerular filtration rate?
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
50
What is the net ultrafiltration pressure?
By which factors is it influenced?
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
51
What happens in the proximal convoluted tubule?
Active reabsorption and secretion of important substances
52
How would you calculate the amount of a substance excreted by the kidney?
Have to consider everything that can happen to the substance:
Filtration
Absorption
Secretion
53
Which factors influence glomerular filtration rate?
Basically **pressure (Puf )** and ultrafiltration coefficient **(Kf)**(determined by **surface area** and membrane **permeability**)
GFR = Puf x Kf
54
How does taking out of a kidney influence glomerular filtration rate? (Which parameter does it inlfluence)
It reduces the surface area of the nephron which reduces **Kf**
**GFR = Puf x Kf**
55
What does the glomerular filtration rate actually show? (Verbalisation of formula)
Amount of fluid filtered from glomerulus in Bowmans capsule
Dependant on pressure and Koeficient
56
How much blood flows to the kidney a minute?
How much of this is plasma?
20% of CO --\> 1l/min
60% of this is plasma:
Renal plasma flow= 0.6 l/min
57
What is filtration fraction?
What is its value?
How much of the plasma is actually filtered by the kidney
--\> Normally 0.2 (20%) which means 120ml/min of plasmfilteredilterd
58
Hwo can you calculate glomerular filtration rate based on renal blood flow?
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
Explain the concept of myogenic autoregulation to control blood flow to the kidenys
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
What is the definition of renal clearance?
It is the volume of plasma that can be completely cleared of the substance per unit of time (normally ml/min)
61
How can you calculate reanal clearance?
**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
How can you estimate GFR using renal clearance?
By measuring a substance that is only filtered in the glomerulus (not modified (reabsorbed, excreted)) in the urine/blood plasma
63
Which substances can be used to measure glomerular filtration rate?
Why?
Inulin and Creatine (muscle metabolic product) normally measured
--\> Both are only filtered and not reabsorbed/secreted into primary urine
64
How can you measure renal plasma flow?
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
Explain where water is reabsorbed in the nephron
66
In which part of the nephron is the amount of water reabsorbtion regulated?
It is regulated in the collecting duct
67
Which two components in the collecting duct can be regulated to alter water reabsorption?
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
How can you establish the cortico-medullary gradient via the countercurrent mechanism?
* 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
Why doesn't medullary blood flow eliminate medullary osmotic gradient?
The osmolarity in the vasa recta also changes in a counter-current mechanism and has a very high osmolarity in the inner medulla
70
Which role does urea play in concentrating the urine?
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
When is ADH released?
* High Plasma osmolarity, sensed by osmoreceptors in the hypothalamus (\>300mOs)
* Low blood pressure (sensed by baroreceptors)
72
How does ADH increase water reabsorption in the collecting duct?
1. Causes the insertion of **Aquaporins 2** in the luminal membrane
--\> Allow water to flow into the medulla, following the concentration gradient
2. Stimulates **urea transport** from collecting duct to thin ascending loop via increasing the membrane position of urea transporters ---\> **increased osmolarity**
73
Where is sodium reabsorbed? (Percentages where?)
74
How does GFR influences Na+ reabsorption?
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
What are the target sides of sympathetic activity on the urinary system?
1. It increases GFR
2. Increases reabsorption in the proximal convoluted tubule
3. Stimulates the Juxtaglomerular apparatus
76
How does Angiotensin II control the reabsorption of Na+?
It
* Increases reabsorption in the proximal convoluted tubule (increased affinity of Na+/H+ cotransporters)
* Stimulates the production of Aldosterone
77
What effect does aldosterone have on the tubules of the nephron?
It increases Sodium reabsorption in the
* distal convoluted tubule
* and in the collecting duct
78
How and where does Atrial natriuretic peptide influence the reabsorption of Sodium?
It decreases Sodium reabsorption by
* Decreasing GFR
* Decreasing reabsorption in proximal convoluted tubule
* Decreasing Renin production
* Decreasing reabsorption in collecting duct
79
Which effect does Na+ in the distal convoluted tubule have?
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
What does an excess in aldosterone cause?
It leads to an hypokalaemic alkalosis
+ High BP:
81
What effects does aldosterone have on ion balance in the kidney?
* Increased Sodium reabsorption
(controls reabsorption of 35g Na/day)
* Increased Potassium secretion
* Increased hydrogen ion secretion (via activation of Na+/H+ exchanger)
82
What is the effect of hypoaldosteronism?
83
How does aldosterone increase Na+ reabsorption in the collecting duct?
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
What are the symptoms and reasons for Liddls Syndrome?
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
How do ACE inhibitors affect the urinary system?
REduction in Angiotensin II and Aldosterone leading to a decrease in Na+ reabsobrion--\> Decreased Extracellular Fluid --\> Lowered BP
86
Explain the mechanism of function of Carbonic anhydrase inhibitor diuretics
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
What is an example of a carbonic anhydrase inhibitor?
Acetazolamide
88
Explain the mechanism of action of an Osmo diuretic
Name examples
* 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
Explain the mechanism of action of Loop diuretics
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
Explain the target site and mechanism of action of Thiadize diuretics
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
Explain the mechanism of action of Potassium-Sparing Diuretics and the effects of Aldosterone on it
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
By which cells and where is Potassium secreted?
it is secreted by the principal cell in the collecting duct
93
How does aldosterone influence Potassium secretion?
Aldosterone stimmulates Na+/K+ ATPase
and also stimmulates K+ channels
--\> Stimmulates K+ excretion
94
How does tubular flow rate influence potassium secretion?
Increased flow= stimulates Ca2+ uptake which stimulates K+ channels and the excretion of K+
95
How are Potassium levels regulated?
It is taken up into the cell via Na+/K+ channels
And excreted into the lumen via K+ channels
96
What is a normal range for urine pH?
pH is normal aound 5-8
--\> huge range (in comparison to blood) because urine regulates the blood
97
What is the normal pH range for blood?
Which pH values are compatible with life?
Normal around **7.35-7.45**
Compatible with life are values around **6.8-7.8**
98
What are normal bicarbonate blood concentrations?
22-26 mEq/L
99
Where is how much bicarbonate in the nephron reabsorbed?
100
What is the Henderson-Hasselbach equastion?
How would it look like for Bicarbonate?
101
How is HCO3- reabsorbed in the proximal convoluted tubule?
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
5. **Bicarbonate uptake** via
* 3HCO3-/NA+ cotransport
* HCO3-/Cl- exchanger
102
What is the function of the alpha cell and beta cells?
What is their relation to one another?
Where are they located
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
Where does acid/base regulation in the kidney occur?
It occurs in the collecting duct via Alpha/beta cells
104
Hot do alpha cells in the kidney secrete H+?
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
5. Bicarbonate uptake via
* HCO3-/Cl- exchanger
105
How do beta cells in the collecting duct secrete bicarbonate?
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
5. **Bicarbonate excrete**d via
* HCO3-/Cl- exchanger
106
How Can Bicarbonate be generated by cells in the kidney?
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
How is Ammonium excreted?
It is transported across the membrane via an Na+/NH4+ exchanger and excreted into urine
108
How do phosphate and acid-base regulation intervolve?
Why is this relevant?
H+ excreted can form:
HPO42- + H+ = H2PO4-
These substances can be measured in a lab
109
Will a patient with low GFR always notice, that something is wrong with him?
What does it determine?
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
What is the problem with the loss of the excretory function of the kidney in renal failure?
Toxins will accumulate in the body
--\> could e.g. cause nausea, vomiting, intoxication
111
Which symptoms can be observed in a patient with kidney failure and why?
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
Why is it important to differentiate between blood sodium levels and total body sodium?
Because they can be very different:
CKD AND AKI (acute kidney injury) ARE OFTEN ASSOCIATED WITH **HYPONATRAEMIA**
113
How can renal failure disturb acid-base balance?
It often comes to a metabolic acidosis --\> Kidneys can't excrete enough H+
114
How can an acidosis lead to hyperkalemia?
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
How does renal failure lead to Hyperkalaemia?
Renal failure can lead to a failure to excrete potassium in the distal tubule
116
What does hyperkalaemia lead to?
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
How can a loss of the metabolic function of the kidney impact blood cells?
Kidney failure can lead to anaemia because of reduced erythropoietin levels
118
What do low 1-25VitD levels in renal failure lead to?
uLow 1-25 VitD levels result in poor intestinal calcium absorption, hypocalcaemia (short term) and hyperparathyroidism (longer term)
119
Why have patients with kidney disease an increased Cardiovascular risk?
Direct mechanism is unclear but it leads to:
* Hypertension
* Secondary cardiac effects
* Endothelial effects
* Lipid abnormalities
120
How can you differentiate between chronic and acute renal failure?
Barely any difference but: **History** and **Kidney size**
121
Evaluate the use of Urea as a method of assessing GFR
–Poor indicator
–Confounded by diet, catabolic state, GI bleeding (bacterial breakdown of blood in gut), drugs, liver function etc
122
Evaluate the use of Creatinine as a method for assessing GFR
–Affected by muscle mass, age, race, sex etc. Need to look at the patient when interpreting the result
123
Evaluate the use of Creatinine clearance as method for estimating GFR
–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
Evaluate the use of Inulin for estimating renal clearance
–Laborious - used for research purposes only
--\> very difficult to make
125
Evaluate the Radionuclide studies for assessing GFR
–EDTA clearance etc
–Reliable but expensive
--\> Gold standart that is used today!
126
Why does hyperaldosteronism lead to increased thirst and polyuria?
Becuause more ions are reabsorbed --\> Blood has a highter osmolarity
--\> thirst to try and reduce osmolarity
