Urinary Flashcards

Question

What does the nephron contain?

Answer 1

Renal corpuscles - glomerulus & bowman's capsule Proximal convoluted tubule Loop of Henle Distal Convoluted Tubule

Answer 2

Vascular pole - afferent/ efferent arterioles, glomerulus Urinary pole - bowman's capsule

Answer 3

Ureteric bud

Answer 4

The ureteric bud covers the growing glomerulus, resulting in a double-layered cover

Answer 5

Capillary endothelium and podocytes (visceral layer of bowman's capsule)

Answer 6

Capillary endothelium is fenestrated, with podocytes investing in them

Answer 7

Parietal layer of Bowman’s capsule makes a ‘funnel’ to collect the ultrafiltrate and drain into PCT

Answer 8

Simple cuboidal epithelium with a pronounced brush border membrane is the longest, most convoluted section of the tubule

Answer 9

o Pars recta o Thin descending limb o Thin ascending limb o Thick ascending limb

Answer 10

Simple squamous epithelia The thin limb dips down into the medulla. There is no active transport, and no brush border.

Answer 11

Simple cuboidal epithelium, no brush borders Best seen in the medulla, interspersed with thin limbs, vasa recta and collecting duct. Active transport takes place here.

Answer 12

Simple cuboidal epithelium, no brush borders, larger lumen than PCT The DCT is Cortical (in the cortex), and makes contact with its ‘parent’ glomerulus. It contains numerous mitochondria.

Answer 13

Macula Densa - Dense staining region of the DCT Juxtaglomerular Cells - Cells of afferent arteriole of the glomerulus Extraglomerular Mesangial Cells (aka lacis cells)

Answer 14

It is similar in appearance to the thick limbs of Henle’s loop, but the lumen is larger, and tends to be more irregular rather than circular. The collecting duct is a continuation of the DCT via the collecting tubule.

Answer 15

Progressively larger ducts merge together and empty at the renal papilla, forming a pyramidal shape

Answer 16

The ureter is a tube running from the renal pelvis to the bladder. It has two layers of muscle, with a third appearing in the lower third.

Answer 17

Lined by a specialised epithelium, transitional epithelium

Answer 18

The urinary bladder, like the lower third of the ureter, has three layers of muscle. Its internal epithelium is transitional, and it is surrounded by an outer adventitia. “Urothelium” is a stratified epithelium, the “umbrella cells” on the surface layer making it impermeable.

Answer 19

3Na-2K-ATPase

Answer 20

* Na-H Antiporter | * Na-Glucose Symporter (SGLUT)

Answer 21

• Na-K 2Cl Symporter

Answer 22

• Na-Cl Symporter

Answer 23

Na+ travels down its concentration gradient set up by 3Na-2K-ATPase from the tubule lumen into the Intersticium using a symporter sometimes, allowing reabsorption of organic substances. These then move on through cells via diffusion and/or other transport processes.

Answer 24

In the PCT using the Na-Glucose Symporter SGLUT. This moves glucose against its concentration gradient into the tubule cells. Glucose then moves out of the tubule cell on the basolateral side by facilitated diffusion. The renal threshold for glucose is 200mg/100ml.

Answer 25

The maximum capacity that is able to be reabsorbed. If the plasma concentration exceeds Tm, the rest spills over into the urine. If this happens, water follows into the urine, causing frequent urination (polyuria).

Answer 26

The volume of plasma from which a substance (X) can be completely cleared to the urine per unit time (Amount in urine × Urine flow rate)/(Arterial Plasma Concentration)

Answer 27

The volume of plasma from which any substance (X) is completely removed by the kidney in a given amount of time (usually 1 minute) (Amount in urine × Urine flow rate)/(Arterial Plasma Concentration) Measure of the kidney’s ability to filter a substance, thus overall function. It is an indication of how well the kidney works

Answer 28

Means kidney disease is progressing

Answer 29

Substance (X) must be freely filtered across the glomerulus. This substance must not be reabsorbed, secreted or metabolised by the cells of the nephron. It must pass directly into the urine.

Answer 30

Creatinine and Inulin

Answer 31

605ml/min of plasma

Answer 32

Proportion of a substance that is actually filtered | Glomerular Filtration Rate)/(Renal Plasma Flow

Answer 33

Autoregulation Myogenic Response Tubular Glomerular Feedback (TGF)

Answer 34

Keep GFR within normal limits when arterial BP is within physiological limit

Answer 35

Arterial BP rises → Afferent Arteriole Constriction | Arterial BP falls → Afferent Arteriole Dilation

Answer 36

Change the amount of NaCl reaching distal tubule. Macula densa cells respond to these changes. If NaCl increases: - Response is GFR needs to decrease - Adenosine released, causes vasoconstriction of afferent arteriole If NaCl decreases: - Response is GFR needs to increase - Prostaglandins released causing vasodilation of afferent arteriole

Answer 37

All AA’s present in the urine. This is normally due to inadequate deamination in the liver, or an increased GFR. It is often seen in early pregnancy.

Answer 38

Only a specific AA is present in the urine. This is usually due to a genetic inability to break down one AA, e.g. phenylalanine in PKU

Answer 39

Renal aminoaciduria is mainly confined to the dibasic acids, and it due to a genetically determined lack of the specific transport protein(s). For some reason cysteine is an abnormally insoluble amino acid, especially in acidic urine, and cystinuria may be associated with stone formation.

Answer 40

The diameter of each afferent arteriole is slightly greater than the diameter of the associated efferent arteriole. This diameter difference increases the pressure of the blood inside the glomerulus. This increased hydrostatic pressure helps to force the below components out of the blood in the glomerular capillaries. However, only 20% of the delivered blood is actually filtered, 80% exits via the efferent arteriole.

Answer 41

o Most of the water o Most/All of the salts o Most/All of the glucose o Most/All of the urea

Answer 42

Proteins | RBC

Answer 43

Size is too big Basement membrane and podocytes glycocalyx have negatively charged glycoproteins, so proteins are repelled

Answer 44

1. Hydrostatic pressure in the capillary 2. Hydrostatic pressure in Bowman’s capsule 3. Osmotic pressure difference between the capillary and tubular lumen

Answer 45

1. Capillary endothelium o Water, salts, glucose o Filtrate moves between cells 2. Basement Membrane o Acellular gelatinous layer of collagen/glycoproteins o Permeable to small proteins o Glycoproteins (-‘ve charge) repel protein movement 3. Podocyte Layer o Pseudopodia interdigitate to form filtration slits

Answer 46

Neutral Molecule – The bigger it is, the less likely to get through Anions – Negative charge also repels, more difficult to get through Cations – Positive charge allows slightly bigger molecules through

Answer 47

Only about 1% of glomerular filtrate actually leaves the body, the rest is reabsorbed into the blood as it passes through the renal tubules via three mechanisms: osmosis, diffusion and active transport.

Answer 48

1. Na+ is pumped out of tubular cells across the basolateral membrane by 3Na-2K-ATPase. 2. Na+ moves across the apical (luminal) membrane down its concentration gradient o This movement of Na+ utilises a membrane transported or channel on the apical membrane. 3. Water moves down the osmotic gradient created by the reabsorption of Na+

Answer 49

1. Entry by passive carrier Mediated diffusion across the basolateral membrane down favourable concentration and electrical gradients, created by the 3Na-2K-ATPase pump. 2. Secretion into the lumen H+-OC+ exchanger that is driven by the H+ gradient created by the Na+-H+ Antiporter.

Answer 50

``` For solutes to enter the tubular fluid. This is useful as only 20% of plasma is filtered each time the blood passes through the kidney. It also helps to maintain blood pH (7.38 – 7.42). The substances secreted into the tubular fluid are: o Protons (H+) o Potassium (K+) o Ammonium ions (NH¬4+) o Creatinine o Urea o Some hormones o Some drugs (e.g. penicillin) ```

Answer 51

``` Extracellular fluid (ECF) Intracellular fluid (ICF) ```

Answer 52

regulating the excretion of NaCl

Answer 53

If Na+ excretion is less than intake, water is drawn out of nephron. Increase in volume BP and arterial pressure increases Oedema may follow

Answer 54

If Na+ excretion greater than intake, Na+ in ECF decreases. Less water drawn out of nephron ECF volume decreases Blood volume and arterial pressure decreases

Answer 55

If Na+ excretion is less than intake (patient is in positive balance), it is retained in the bodily – primarily in the ECF. Water is drawn out of the nephron causing a corresponding increase in volume. Blood volume and arterial pressure increases, and oedema may follow.

Answer 56

If Na+ excretion is greater than intake (patient is in negative balance), the Na+ content of the ECF decreases. Less water is drawn out of the nephron, so ECF volume decreases, as does blood volume and arterial pressure.

Answer 57

67% is reabsorbed in the PCT This is a proportion of Na+ that is always reabsorbed, regardless of the actual amount that is filtered. Na+ reabsorption is mainly active, driven by 3Na-2K-ATPase pumps on the basolateral membrane. Different segments of the tubule have different types of Na+ transporters and channels in the apical membrane. Section 1 – Na+ Reabsorption o Co-Transported with glucose o Na-H exchange Section 2/3 – Na+ and Water Reabsorption o Na-H exchanger

Answer 58

The PCT is highly water permeable. This allows reabsorption to be isosmotic with plasma. The reabsorption of water is driven by: o Osmotic gradient established by solute reabsorption o Hydrostatic force in Intersticium o Oncotic force in the peritubular capillary due to the loss of 20% filtrate at the glomerulus, but cells and proteins remained in the blood.

Answer 59

The balance between Glomerular Filtration Rate and the rate of reabsorption of solutes. It must be kept as constant as possible, so if GFR increases, the rate of reabsorption must also increase.

Answer 60

If ECF volume increases, cardiac output will increase causing an increase in arterial blood pressure. This in turn will increase GFR.

Answer 61

Descending limb reabsorbs water but not NaCl Ascending limb reabsorbs NaCl but not water • Known as the diluting segment (Dilutes the NaCl in the filtrate) • Tubule fluid leaving the loop is therefore hypo-osmotic (more dilute) compared to plasma

Answer 62

The increase in intracellular concentrations of Na+ set up by the PCT allows for paracellular reuptake of water from the descending limb (No tight junctions). This concentrates the Na+ and Cl- in the lumen of the descending limb, ready for active transport in the ascending.

Answer 63

o NaCl transported from the lumen into cells by NaKCC2 channel. o Na+ then moves into the Intersticium due to the action of 3Na-2K-ATPase. o K+ ions diffuse back into the lumen via ROMK o Cl- ions move into the Intersticium o NaKCC2 is the target of loop diuretics • Increased loss of K+ in the urine → hypokalaemia This region uses more energy than any other region of the nephron, and is particularly sensitive to hypoxia.

Answer 64

Water permeability of the early DCT is fairly low, and the active reabsorption of Na+ results in dilution of the filtrate. o Hypo-osmotic fluid enters from the loop and ~5-8% of Na+ is actively transported by the NaCC transporter, driven by 3Na-2K-ATPase. o The NCC transporter is sensitive to Thiazide Diuretics o The DCT is also a major site of calcium reabsorption via PTH. This further dilution means the fluid that leaves is more hypo-osmotic.

Answer 65

Principle cells | Intercalated cells

Answer 66

o 70% of CD cells o Reabsorb Na+ by Epithelial Na+ Channel (ENaC) • Driven by 3Na-2K-ATPase o Produces lumen charge • Electrical gradient for paracellular Cl- reabsorption • Potassium secretion into the lumen o Variable water uptake through Aquaporin 2 • Dependent on ADH o Have a more distinct membrane than Intercalated cells

Answer 67

o Active reabsorption of Chloride | o Secrete H+ ions or HCO3-

Answer 68

1. Renin-angiotensin-aldosterone system 2. Sympathetic nervous system • Vasoconstriction by α1-adrenoceptors • Inc. force/rate of heart contraction β1-adrenoceptors o Decreased Renal Blood flow • Decreased GFR and Na+ excretion • Activates Na/H exchanger in PCT o Stimulates renin release from juxtaglomerular cells • Increased Angiotensin II/Aldosterone levels 3. Antidiuretic hormone (ADH) 4. Arial Natriuretic Peptide (ANP) o Acts in the opposite direction to the others o Synthesised and stored in atrial myocytes o Promotes Na+ excretion • Vasodilation of afferent arteriole o High BP → Stretch Atrial Cells • Increased release • Increased Na+ excretion, volume decreases, BP decreases o Low BP → Atrial Cells less stretched • Reduced release • Reduced Na+ excretion, volume increases, BP increases o Inhibits Na+ reabsorption along the nephron

Answer 69

Reduced perfusion pressure in the kidney detected by baroreceptors in the afferent arteriole, causes the release of renin from the granular cells of the juxtaglomerular apparatus. Decreased NaCl Concentration at the Macula Densa cells (Due to low perfusion and therefore low GFR) causes Sympathetic stimulation to the JGA. This also increases the release of renin. (Also causes Macula Densa cells to release Prostaglandins → Afferent Vasodilation) Renin cleaves Angiotensinogen → Angiotensin I, which is in turn cleaved by Angiotensin Converting Enzyme (ACE) to form the active hormone Angiotensin II. Angiotensin II There are two types of Angiotensin II receptors, AT1 and AT2. They are both G-protein coupled receptors. Angiotensin II’s main actions are via the AT1 receptor

Answer 70

o Vasoconstriction • Works on vascular smooth muscle cells, increases TPR thus BP • Vasoconstriction of afferent and efferent arteriole o Aldosterone • Stimulates the adrenal cortex to synthesise and release Aldosterone • Aldosterone stimulates Na+ and therefore water reabsorption • Acts on principal cells of CD • Activates ENaC and apical K+ channels • Increases basolateral Na+ extrusion via 3Na-2K-ATPase o Sympathetic Activity o Increase Na+ reabsorption • Stimulates Na-H exchanger in the apical membrane of PCT o Thirst • Stimulates ADH release at hypothalamus o Breaks down Bradykinin • Bradykinin is a vasodilator

Answer 71

The baroreceptor reflex works well to control acute changed in BP. It produces a rapid response, but does not control sustained increases as the threshold for baroreceptor firing resets. A 5-10% drop in blood pressure causes low-pressure baroreceptors in the atria and pulmonary vasculature to send signals to the brainstem via the vagus nerve. This activity modulates both sympathetic nerve outflow, secretion of the hormone ADH and reduction of ANP release. A 5-150% change in blood pressure causes high-pressure baroreceptors (carotid sinus/aortic arch) to send impulses via the vagus and glossopharyngeal nerves. A decrease in blood pressure will increase sympathetic nerve activity and the secretion of ADH.

Answer 72

o Addition of Aquaporin to Collecting Duct • Reabsorption of water • Forms concentrated urine • Release stimulated by increases in plasma osmolarity or severe hypovolemia o Thick Ascending Limb • Stimulates apical Na/K/Cl co-transporter • Less Na+ moves out into the medulla, reduced osmotic gradient for water to exit the lumen into the peritubular capillaries from the thin descending limb

Answer 73

Prostaglandins are vasodilators. Locally acting prostaglandins (mainly PGE2) enhance glomerular filtration and reduce Na+ reabsorption. They therefore may have an important protective function by acting as a buffer to excessive vasoconstriction by the sympathetic nervous system and the RAAS.

Answer 74

Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) inhibit the cyclo-oxygenase (COX) pathway that is involved in the formation of prostaglandins. As prostaglandins help to maintain renal blood flow and GFR in the presence of vasoconstrictors, if NSAIDs are administered when renal perfusion is compromised (e.g. in renal disease) GFR can be further decreased, leading to acute renal failure. In heart failure or hypertensive patients, NSAIDs can exacerbate the condition by increasing NaCl and water retention.

Answer 75

Hypertension is a sustained increase in blood pressure.

Answer 76

In around 95% of cases, the cause is unknown. This is known as Essential Hypertension. Genetic and environmental factors may both be involved and the pathogenesis is unclear.

Answer 77

``` Where a cause can be defined, hypertension is referred to as secondary hypertension. Here it is important to treat the primary cause. Examples include: o Renovascular disease o Chronic Renal Disease o Aldosteronism o Cushing’s syndrome ```

Answer 78

``` Conn’s Syndrome o Aldosterone secreting adenoma o Hypertension and hypokalaemia Cushing’s Syndrome o Excess cortisol o At high concentrations acts on aldosterone receptors • Na+ and water retention Pheochromocytoma o Tumour of the adrenal medulla o Secretes noradrenaline and adrenaline ```

Answer 79

Renovascular Disease is caused by an occlusion of the renal artery, causing a fall in perfusion pressure in that kidney. Decreased perfusion leads to that kidney releasing renin and activating RAAS. Vasoconstriction and Na+ retention will then take place at the other kidney.

Answer 80

o ACE Inhibitors • Prevent the production of Angiotensin II from Angiotensin I • Angiotensin II receptor antagonists o Thiazide Diuretics • Inhibit NaCC co-transporter on apical membrane of DCT • May cause hypokalaemia (more K+ lost in urine) o Vasodilators • Ca2+ channel blockers, reduce Ca2+ entry into smooth muscle cells • α1 receptor blockers, reduce sympathetic tone o Beta Blockers • Block β1-receptors in the heart • Reduces heart rate and contractility Non-pharmacological approaches to the treatment of hypertension include diet, exercise, reduced Na+ intake, reduced alcohol intake.

Answer 81

Water Intake Excretion → Plasma osmolarity decreases The more urine is produced, the less concentrated it is. Body fluid osmolarity is maintained by osmoregulation at about 275-295 mOsm/kg Disorders of water balance manifest as changes in body fluid osmolarity. In contrast, problems with Na+ balance causes changes in volume.

Answer 82

When a change in plasma osmolarity is sensed, it coordinates responses via two different efferent pathways, which work to concentrate urine and increase thirst respectively. You only feel thirsty at ~10% dehydration. ADH effects the kidneys by affecting renal water excretion Thirst has an affect on the brain and controls water intake

Answer 83

Hypothalamic Osmoreceptors located in the organum vasculoum of laminae terminalis (OVLT)

Answer 84

If plasma osmolarity increases (1% change) due to a predominant loss of water, osmoreceptors in the hypothalamus (OVLT) initiate the release of ADH from the POSTERIOR Pituitary. Similarly, decreased osmolarity inhibits ADH secretion. It acts on the kidney to regulate the volume and osmolarity of the urine. It achieves this by increasing the permeability of the kidneys to water and urea. ADH causes the addition of the water channel Aquaporin-2 to the apical membrane of the nephron’s collecting duct. This allows for the reabsorption of water to decrease plasma osmolarity.

Answer 85

In the absence of ADH, apical membranes do not contain Aquaporin 2. When ADH is released it is inserted into the membrane and when ADH is removed the channel is retrieved from the apical membrane via endocytosis. The basolateral membrane always contains Aquaporin 3 and 4, so is constantly permeable to water. This means any water that enters across the apical membrane is able to pass into the peritubular blood.

Answer 86

ADH also increases the permeability of the medullary part of the collecting duct to urea, causing its reabsorption. This in turn causes water to follow. The rise in urea concentration in the tissues causes it to passively move down its concentration gradient into the ascending limb, which is permeable to Urea but impermeable to H2O. Urea then passes back into the collecting duct, where it is reabsorbed in the medullary portion and more water follows. Urea is therefore recycled.

Answer 87

In SIADH the secretion of ADH is not inhibited by the lowering of blood osmolarity (negative feedback is removed). This means that excessive amounts of water is retained, causing blood osmolarity to drop and cause hyponatremia (Low blood Na+ concentration). Symptoms of hyponatremia include nausea and vomiting, headache, confusion, lethargy, fatigue, appetite loss, restlessness and irritability, muscle weakness, spasms, cramps, seizures and decreased consciousness or coma. If hypernatremia comes about because of SIADH the condition may be treated with ADH Receptor Antagonists.

Answer 88

At the cortico-medullary border, there is no osmotic gradient. However the medullary Intersticium is hyperosmotic up to 100 mOsmol/Kg at the papilla. There is a gradient of increasing osmolarity as you descend. The active transport of NaCl out of the TAL and the recycling of urea sets up the osmotic gradient. The action of the TAL is crucial, removing solute without water, diluting the filtrate and increasing Intersticium osmolarity. If you block the NaK2Cl transporters in the TAL with a loop diuretic (E.g. Furosemide) the medullary Intersticium becomes isosmotic and large amounts of dilute urine is produced.

Answer 89

The Loop of Henle acts as a counter current multiplier, to set up the osmotic gradient: Tubule filled initially with isotonic fluid Na+ ions are pumped out of the ascending loop (Na/K/2Cl co-transporter), raising the osmotic pressure outside the tubule and lowering it inside. (Max concentration difference is 200 mOsmol/L) Fresh fluid enters from glomerulus, and enters the descending limb. As the descending limb is permeable to water, it leaves via osmosis to raise the osmotic pressure inside the descending tubule to 400mOsmol/L. More fluid enters from the glomerulus, pushing the concentrated (400mOsmol/L) fluid into the ascending limb. The Na+ pump then produces another 200 mOsmol/L gradient across the membrane. But it started with a more concentrated solution (400mOsmol/L). So external osmolarity rises to 500mOsmol/L. This happens again, rising the external osmolarity to 700mOsmol/L. The final gradient will be limited by the diffusional process.

Answer 90

The concentration gradient that the loop of Henle sets up would not last long though without the Vasa Recta. These are blood vessels that run alongside the loops, but with opposite flow direction. This counter-current flow allows for the maintenance of the concentration gradient. Isosmotic blood in the descending limb of the vasa recta enters the hyperosmotic milieu of the medulla, where there is a high concentration of ions (Na+, Cl-, Urea). These ions therefore diffuse into the vasa recta and water diffuses out. The osmolarity of the blood in the vasa recta increases as it reaches the tip of the hairpin loop, where it is isosmotic with the medullary Intersticium. Blood ascending towards the cortex will have a higher solute content than the surrounding Intersticium, so solutes move back out. Water will also move back in from the descending limb of the loop of Henle. Therefore, although there is a large amount of fluid and solute exchange across the vasa recta, there is little net dilution of the concentration of the interstitial fluid because of the U shape of the vasa recta allowing it to act as a counter current exchanger. The vasa recta therefore do not create the medullary hyperosmolarity, but do prevent it from being dissipated.

Answer 91

Calcium plays a critical role in many cellular processes: ``` ◦Hormone secretion ◦Nerve conduction ◦Inactivation/activation of enzymes ◦Muscle contraction ◦Exocytosis ``` Therefore, the body very carefully regulates the plasma concentration of free ionised calcium ([Ca2+]), the physiologically active form of the metal, and maintains free plasma [Ca2+] within a narrow range (1.0 - 1.3mmol/L). In plasma, calcium exists as: ◦Free ionised species – 45% (Active Form) ◦Protein Bound – 45%(80% to Albumin) ◦Complexed– 10% (Citrates, phosphate etc)

Answer 92

The absorption of Calcium is under the control of Vitamin D. About 20-40% of dietary calcium (25mmol) is absorbed and some is excreted back into the gut (2-5mmol). Absorption increases in growing children, pregnancy, lactation and decreases with advanced age. Complexing calcium (e.g. with oxalates) reduces its absorption.

Answer 93

The kidneys filter 250mmol of Calcium per day, 95-98% of which is reabsorbed, giving a urinary calcium excretion of

Answer 94

Vitamin D is absorbed in the gut or synthesised in the skin in the presence of sunlight. However it has a short half-life, so is converted to Calciferol in the Liver to extend it.

Answer 95

Approximately 20% of men and 5-10% of women will develop renal stones in their lifetime, and 70-80% of all renal tract stones are made of Calcium. Factors involved in their formation include low urine volume, hypercalcuria and low urine pH (

Answer 96

Conservative management of renal stones includes increasing fluid intake, restricting dietary oxalate and sodium, and considering the dietary restriction of calcium and animal protein.

Answer 97

◦Primary hyperparathyroidism ◾~ 1/1,000 of the general population ◦Haematological malignancies ◦Non-Haematological malignancies Hypercalcaemia of malignancy comes about due to the production of Parathyroidhormone-Related Peptide (PTHrP). This peptide has AA homology with the active portion of PTH and works to increase plasma Ca2+ concentration

Answer 98

``` ◦Gastrointestinal ◾Anorexia ◾Nausea/Vomiting ◾Constipation ◾Acute pancreatitis (rarely) ``` ``` ◦Cardiovascular ◾Hypertension ◾Shortened QT interval on ECG ◾Enhanced sensitivity to digoxin ◾Renal ◾Polyuria and polydipsia ◾Occasional nephrocalcinosis ``` ◦Central Nervous System ◾Cognitive difficulties and apathy ◾Depression ◾Drowsiness, coma

Answer 99

◦General measures ◾Hydration – Increase Ca2+ excretion ◾Loop diuretics – Increase Ca2+ excretion ◦Specific Measures ◾Bisphosphonates – Inhibit the breakdown of bone ◾Calcitonin – Opposes the action of PTH ◦Treat underlying condition

Answer 100

Parathyroid Hormone (PTH) regulates the conversion of Calciferol in the kidney to its active form, Calcitriol. Calcitriol is the active form of Vitamin D and works by binding to Calcium in the gut to increase its absorption. PTH also affects calcium levels directly; by increasing it’s release from bone and its reabsorption in the PCT of the kidney. It also decreases the reabsorption of phosphate and bicarbonate, as if they are present in the blood with Calcium stones will form. Calcium levels regulate PTH via negative feedback.

Answer 101

The normal range of plasma pH is 7.38 – 7.46. This is a concentration of between 37-43 nmol/L of H+.

Answer 102

The effects of Acidaemia are severe below pH 7.1, and life threatening below pH 7.0. They include: ◦Reduced enzyme function ◦Reduced cardiac and skeletal muscle contractility ◦Reduced glycolysis ◦Reduced hepatic function ◦Increased plasma potassium

Answer 103

Alkalaemia reduces the solubility of calcium salts, which means that free Ca2+ leaves the ECF, binding to bone and proteins, resulting in hypocalcaemia. This increases the excitability of nerves. ◦pH > 7.45 ◾Paraesthesia ◾Tetany (uncontrolled muscle contractions) ◦pH > 7.55 ◾45% Mortality ◦pH > 7.65 ◾80% Mortality

Answer 104

The H+ ion concentration in the ECF is very low, so the addition of small amounts of acid changes the concentration and therefore pH dramatically. To prevent this, H+ ions are buffered by binding to various sites. The most important bugger is the Carbon Dioxide/Hydrogen Carbonate system. The extent the reversible reaction proceeds is determined by the ratio of pCO2 of plasma (controlled by the lungs) to [HCO3-] (largely created by RBCs, but concentration is controlled in the kidneys). The normal ratio, which gives a normal pH is 20 : 1, [HCO3-] : pCO2. Anything that alters this ratio will also alter pH.

Answer 105

As hyperventilation leads to hypocapnia (fall in pCO2), the ratio is altered and pH will rise. There is more than 20x the amount of HCO3- than CO2, so relatively more H+ ions are buffered, causing the pH increase. (pH > 7.45)

Answer 106

Hypoventilation leads to hypercapnia (rise in pCO2). The ratio is altered and pH will fall. There is less than 20x the amount of HCO3- than CO2, so relatively less H+ ions are buffered, causing the pH decrease. (pH

Answer 107

The kidney controls [HCO3-] via variable renal excretion/production. ◦If pCO2 rises, [HCO3-] rises proportionately to restore pH ◾(Compensates for Respiratory Acidaemia) ◦If pCO2 falls, [HCO3-] falls proportionately to restore pH ◾(Compensates for Respiratory Alkalaemia)

Answer 108

Metabolically produced H+ ions (e.g. from the metabolism of amino acids or the production of ketones) react with HCO3- to produce CO2 in venous blood. This CO2 is then breathed out through the lungs, giving a directly proportional (1 mmol acid: 1 mmol HCO3-) reduction in arterial HCO3-. This alters the [HCO3-] : pCO2 ratio, meaning that there is less than 20x the amount of HCO3- than CO2. Relatively less H+ ions are buffered, causing a pH decrease. (pH

Answer 109

If plasma [HCO3-] rises, for example after persistent vomiting, the [HCO3-] : pCO2 ratio will be altered. More than 20x the amount of HCO3- than CO2 will be present, so relatively more H+ ions are buffered, causing a pH increase. (pH > 7.45)

Answer 110

pH depends on the ratio of [HCO3-] : pCO2, these changes may be compensated for by altering pCO2. pCO2 is normally kept within tight limits by the Central Chemoreceptors. Changes in plasma pH drive changes in pCO2 via the Peripheral Chemoreceptors. ◦If [HCO3-] falls, pCO2 is lowered proportionately by increasing ventilation ◾Compensates for Metabolic Acidosis ◦If [HCO3-] rises, pCO2 may be slightly raised by reducing ventilation ◾Can only partially compensate for Metabolic Alkalosis

Answer 111

Hypoventilation has raised pCO2. Hypercapnia → low pH [HCO3-] unchanged.

Answer 112

Kidneys have increased [HCO3-]. | This increases the buffering of H+ ions caused by increased pCO2.

Answer 113

Hyperventilation has lowered pCO2. Hypocapnia → high pH [HCO3-] unchanged

Answer 114

Kidneys have decreased [HCO3-] | Decreased buffering of H+ ions

Answer 115

Decreased [HCO3-] → less buffering of H+ ions | Increase in unmeasured anions (Anion associated with the increase in H+ has taken [HCO3-]’s place)

Answer 116

Increased respiratory rate → hypocapnia → Raised pH | Anion gap still increased (see above)

Answer 117

Increased [HCO3-] → buffering of H+

Answer 118

Decreased respiratory rate → hypercapnia → Decreased pH | Can only partially compensate

Answer 119

A large fraction of HCO3- is reabsorbed in the PCT. o 3Na-2K-ATPase sets up a Na+ concentration gradient in PCT cells. o H+ ions pumped out of the apical membrane up their concentration gradient in exchange for inward movement of Na+ down its concentration gradient. o The H+ reacts with filtered HCO3-, producing CO2, which enters the cell and reacts with water to produce H+ ions. o The H+ is quickly exported, recreating HCO3-, which crosses the basolateral membrane to enter the plasma. 80-90% of filtered HCO3- is reabsorbed in the PCT, and up to 15% is also reabsorbed in the TAL of the loop of Henle by a similar method.

Answer 120

By the DCT most/all of the filtered HCO3- has been recovered. The Na+ gradient is also insufficient to drive H+ secretion, so H+ pumped across the apical membrane by a H+-ATPase. When cells export H+, K+ is absorbed into the blood. So if you export a lot of H+, you will also absorb a lot K+. This relationship means that blood pH is linked to [K+].

Answer 121

The minimum pH of urine is 4.5 ([H+] of 0.04mmol/L). There is no HCO3- however, so H+ is buffered by phosphate.

Answer 122

Phosphate is a Titratable acid, meaning that it can freely gain H+ ions in an acid/base reaction. The rest of the H+ in the urine is attached to ammonia as ammonium.

Answer 123

Metabolic acidosis is associated with hyperkalaemia. As [K+] rises, the kidney’s ability to reabsorb and create HCO3- is reduced. Hyperkalaemia makes intracellular pH alkaline, favouring HCO3- excretion. Metabolic alkalosis is associated with hypokalaemia. Hypokalaemia makes intracellular pH acidic, favouring H+ excretion and HCO3- recovery.

Answer 124

[HCO3-] increases after persistent vomiting, alongside dehydration. When this occurs the kidneys cannot excrete HCO3- as they are trying to compensate for the dehydration. HCO3- and Na+ recovery is favoured to increase the osmolarity of the plasma and cause the osmotic movement of water. In this case you cannot rely on the kidneys to correct the [HCO3-], however if you correct the dehydration by giving fluids, HCO3- will be excreted very rapidly.

Answer 125

[HCO3-] increases after persistent vomiting (metabolic alkalosis), so the body stops actively secreting H+, as it would make metabolic alkalosis worse. As H+ secretion has stopped, so has K+ reabsorption (Antiporter, Intercalated cells). This means that a dangerous side effect of persistent vomiting is hypokalaemia, which causes paraesthesia, tetany and CVS problems.

Answer 126

Metabolic acidosis will occur if there is excess metabolic production of acids, (lactic acidosis, ketoacidosis) acids are ingested, HCO3- is lost or there is a problem with the renal excretion of acid. If excess acid is produced, the associated anion (e.g. lactate in lactic acid) will replace HCO3- in the plasma. This will influence the anion gap.

Answer 127

The anion gap is the difference between the sum of the measured concentrations of Na+ and K+ and the sum of the measured concentrations of Cl- and HCO3-. If HCO3- is replaced in the plasma by another anion (see above), which is not included in the calculation, the gap will increase. If the problem causing metabolic acidosis lies with the renal excretion of H+, this will change the [HCO3-] directly without replacement by an unmeasured ion, so the anion gap is less likely to change.

Answer 128

Low [K+] outside cells is necessary for maintaining the steep K+ ion gradient across cell membranes that is largely responsible for the membrane potential of excitable and non-excitable cells. o increase ECF [K+] depolarises the cell membrane o decrease ECF [K+] hyperpolarises the cell membrane Therefore, changes in extracellular [K+] can cause severe disturbances in excitation and contraction. The potentially life threatening disturbances of cardiac rhythm that are a result of hyperkalaemia are particularly important.

Answer 129

3.5-5.3 mmol/L

Answer 130

``` High [K+] inside cells and inside mitochondria is essential for: o Maintaining cell volume o Regulating intra-cellular pH o Controlling cell-enzyme function o DNA / Protein synthesis o Cell Growth ```

Answer 131

o Inability of the kidney to form concentrated urine o A tendency to develop metabolic alkalosis (see above) o Large enhancement of renal ammonium excretion

Answer 132

K+ secretion in the DCT and Cortical CD o Principal cells o Passive processes - Driven by electro-chemical gradient for K+ between the principal cell & lumen o Na+ is reabsorbed via ENaC o This favours K+ secretion through the SEPARATE K+ channel, by creating a negative charge in the lumen. o This process is driven by Na-K-ATPase in the basolateral membrane - Creates the gradient for Na+ absorption Aldosterone is a steroid hormone, that increases the transcription of Na-K-ATPase in the basolateral membrane and ENaC / K+ channels in the apical membrane. This increased amount of these channels gives increase K+ excretion. ECF [K+] Hyperkalaemia – Stimulates aldosterone secretion (Inc. K+ secretion) Acidaemia decreases [K+] in principal cells, thus decreasing secretion Alkalaemia increases [K+] in principal cells, thus increasing secretion K+ absorption in the DCT and Cortical CD o Intercalated cells o Active process o Mediated by H+-K+-ATPase in the apical membrane

Answer 133

Tubular Factors – Aldosterone, ECF [K+], Acid base status Luminal Factors – increase Distal tubular flow rate = increase K+ loss – increase Na+ delivery to distal tubule = increase K+ loss

Answer 134

Two homeostatic mechanisms keep the ECF [K+] tightly controlled, External and Internal balance. External Balance o Regulates the total body K+ content, which depends on dietary intake, and excretion (renal/GI). o Responsible for the long-term control of K+ o Controlled by renal excretion Internal Balance o Regulates K+ movement between ECF and ICF o Responsible for moment to moment control • Quick, within minutes, acts as a K+ buffer o If ECF/Plasma [K+] , K+ moves into cells • ECF → ICF • Na-K-ATPase o If ECF/Plasma [K+] , K+ moves out of cells • ICF → ECF • K+ channels

Answer 135

If ECF/Plasma [K+] increase Insulin K+ in splanchnic blood stimulates insulin secretion from the pancreas. 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+. Catecholamines (β2 Agonists) β2 adrenoceptors stimulate Na-K-ATPase. Exercise and trauma increases K+ exit from cells, but also increases catecholamines to help offset the ECF [K+] rise. Aldosterone Aldosterone is a steroid hormone, that increases the transcription of Na-K-ATPase in the basolateral membrane and ENaC / K+ channels in the apical membrane. This increased amount of these channels gives increase K+ excretion. Alkalosis (decrease ECF/Plasma [H+])

Answer 136

If ECF/Plasma [K+] decrease Exercise Skeletal muscle contraction gives a net release of K+ (during recovery phase of action potential K+ exits the cell). Increase in plasma [K+] is directly proportional to the intensity of the exercise. Uptake of this K+ from the blood by non-contracting tissues is important in preventing hyperkalaemia (release of Catecholamines). ``` Cell lysis (Trauma) With cell lysis K+ is released from the ICF into the ECF. Possible causes include trauma to skeletal muscle, intravascular haemolysis and cancer chemotherapy. ``` Plasma Hyperosmolarity Increase in plasma osmolarity causes water to move from the ICF → ECF via osmosis. This increases the [K+] of the ICF, and K+ leaves down its concentration gradient. Acidosis (increase ECF/Plasma [H+])

Answer 137

Changes in the ECF pH cause reciprocal shifts in K+ between the ECF and ICF, and changes in the ECF [K+] can cause changes to the ECF pH.

Answer 138

Hypokalaemia hyperpolarises cardiac cells • More fast Na+ channels available in active form • Heart more excitable

Answer 139

Hyperkalaemia depolarises cardiac cells • More fast Na+ channels remain in inactive form • Heart less excitable

Answer 140

``` External Balance Problems o Inadequate intake o Excessive loss • GI – Diarrhoea / Vomiting • Renal – Diuretic drugs / osmotic diuresis (Diabetes) • High aldosterone levels Internal Balance Problems o Shift of potassium ECF → ICF • Alkalosis ```

Answer 141

o Heart • more excitable o GI • Neuromuscular dysfunction → paralytic ileus o Skeletal Muscle • Neuromuscular dysfunction → muscle weakness o Renal • Dysfunction of CD cells → Unresponsive to ADH → Nephrogenic diabetes

Answer 142

o Treat cause o K+ replacement – IV/Oral o If due to high aldosterone • K+ sparing diuretics that block action of aldosterone on principal cells • K+ sparing – Amiloride • Aldosterone Antagonist - Spironolactone

Answer 143

``` External Balance Problems o Inadequate renal excretion • (Increased intake only causes hyperkalaemia in the presence of renal dysfunction) o Acute kidney injury o Chronic kidney injury o Reduced mineralocorticoid effect • Drugs which reduce/block aldosterone action ➢ K sparing diuretics ➢ ACE Inhibitors • Adrenal insufficiency Internal Balance Problems o Shifts of K+ from ICF → ECF • Acidaemia (Ketoacidosis / Metabolic Acidosis) • Cell Lysis ```

Answer 144

``` o Heart • less excitable o GI • Neuromuscular Dysfunction → Paralytic ileus o Acidosis ```

Answer 145

``` Emergency o Reduce K+ effect on heart • IV Calcium Gluconate o Shift K+ into ICF via glucose and insulin IV • Remove excess K+ o Dialysis ``` ``` Longer Term o Remove excess K+ • Dialysis • Oral K+ binding resins to bind K+ in the gut o Reduce Intake o Treat cause ```

Answer 146

Most important is the regular flushing during voiding, which removes organisms from the distal urethra. Between voiding such organisms may ascend the urethra, therefore infection in commoner in females because the urethra is comparatively short. Other defence factors include antibacterial secretions into the urine and urethra.

Answer 147

Shorter urethra - More infections in female Obstruction - Enlarged prostate, pregnancy, stones, tumours Neurological - Incomplete emptying, residual urine Ureteric reflux - Ascending infection from bladder, especially in children

Answer 148

Faecal flora - Potential urinary pathogens colonise periurethral area Adhesion - Fimbriae and adhesins allow attachment to urethral and bladder epithelium K Antigens - Allow some E. coli to resist host defences by producing polysaccharide capsule Haemolysins - Damage membranes and cause renal damage Urease - Produced by some bacteria e.g. proteus. Breaks down Urea for energy.

Answer 149

Bacterial cystitis - Frequency and dysuria, often with pyuria and haematuria Abacterial cystitis - As above but without ‘significant bacteriuria’ Prostatitis - Fever, dysuria, frequency with perineal and low back pain

Answer 150

Acute pyelonephritis - Symptoms of cystitis plus fever and loin pain Chronic interstitial nephritis - Renal impairment following chronic inflammation – infection one of many causes

Answer 151

Covert bacteriuria - Detected only be culture. Important in children and pregnancy

Answer 152

The commonest pathogens in the community (80%) are Gram –‘ve rods, particularly Enterobacteriaceae (‘Coliforms’, especially E. coli). Young women and hospitalised patients may also develop a UTI due to coagulase-negative staphylococci, e.g. Staph. Saprophyticus. This is due to increased risk factors, such as catheterisation (biofilms).

Answer 153

Healthy women There is no need to culture urine in Uncomplicated UTIs, infection is indicated by Nitrite/Leukocyte esterase dipstick testing.

Answer 154

pregnancy, treatment failure, suspected pyelonephritis, complications, males, paediatric

Answer 155

o A mid-stream specimen is collected, as we do not want to culture the urethra’s normal flora. o Adhesive bag can be placed over young childrens genitals. This gives a false positive rate of 20%. o Catheter samples can be taken, not from the bag but by using a needle up a special tube in the catheter. o Supra-Pubic aspiration can be used to get a sample of bladder urine, by using a needle through the abdominal wall, but this is rare.

Answer 156

Collected samples are transported at 40C, with a small amount of boric acid in the collection tube. This stops bacterial division to keep the sample representative of the collection time.

Answer 157

Turbidity • Look to see if the sample is cloudy. Cloudy urine is indicative of UTI. Dipstick Testing • Leukocyte esterase – Indicates presence of WBCs • Nitrite – Indicates presence of Nitrate reducing bacteria • Haematuria – Many reasons, can’t diagnose UTI • Proteinuria – Many reasons, can’t diagnose UTI

Answer 158

``` o Kidney disease o Lion pain, nephritis, hypertension, toxaemia, renal colic, haematuria, renal TB, casts o Suspected endocarditis o Children under 6 o Schistosomiasis o Suprapubic aspirates o When requested ```

Answer 159

A number of colony forming units > 100,000 per ml (105 cfu/ml) distinguishes bacteriuria/contamination. o A single urine specimen is 80% predictive. o Used to investigate complicated UTI’s o Increased sensitivity (down to 102 cfu/ml) o Epidemiology of isolates o Sensitivity testing o Control of specimen quality o Can differentiate between properly collected and contaminated samples (poorly collected samples may contain epithelial cells).

Answer 160

Reasons for this include the patient having already been treated with antibiotics, or infected with bacteria that are difficult to isolate or culture (e.g. chlamydia). Can also be due to tuberculosis, or appendicitis (appendix stuck on the bladder)

Answer 161

General – Increase fluid intake, address underlying disorders. Bacteria may be present asymptomatically - only treat once symptoms appear. Uncomplicated o 3 Day course of antibiotics o 3 day course reduces the selection pressure for resistance Complicated o 7 Day course of antibiotics. o Amoxicillin not appropriate as 50% of isolates are resistant Pyelonephritis/Septicaemia o 14 day course of antibiotics o Use more potent agent with systemic activity ``` Prophylaxis o Three or more episodes in one year o No treatable underlying condition o Single, low, nightly dose of antibiotics to prevent bacteria build up in static urine o All breakthrough infections documented ```

Answer 162

block the reabsorption of Na+ and therefore water by the kidney.

Answer 163

Loop diuretics are the most powerful, capable of causing the excretion of 10-25% of filtered Na+ ions. They work by blocking the Na-2Cl Symporter in the apical membrane. E.g. Furosemide, Bumetanide

Answer 164

Thiazide Diuretics act on the early DCT. They are less potent than loop diuretics, inhibiting only 5% of Na+ reabsorption. They are ineffective in the treatment of renal failure. They work by blocking the Na-Cl Symporter. E.g. Bendroflumethiazide

Answer 165

Both types act on the late DCT to reduce Na+ channel activity. They are both mild diuretics, inhibiting only 2% on Na+ reabsorption. Both reduce the loss of K+ and are called K+ sparing diuretics, and can both produce life threatening hyperkalaemia, e.g. in renal failure. K+ Sparing Example - Amiloride Aldosterone Antagonist Example – Spironolactone

Answer 166

Loop and Thiazide diuretics increase the loss of Potassium in urine. This may cause Hypokalaemia. K+ sparing diuretics and Aldosterone antagonists reduce the loss of Potassium in urine. This may cause Hyperkalaemia. As diuretics reduce ECF volume, they will also cause the activation of RAAS. This increase aldosterone secretion, increasing Na+ absorption and K+ secretion, helping to contribute to hypokalaemia. Hypovolaemia o Decreased ECF volume due to excessive loss of Na+ and water o Monitor weight, signs of dehydration and BP (Look for postural hypotension) Hyponatraemia Increase Uric acid levels in blood o Can precipitate attack of Gout Metabolic effects o Glucose intolerance o Increased LDL levels Carbonic Anhydrase Inhibitors Diuretics which act in the PCT by inhibiting the enzyme carbonic anhydrase to interfere with Na+ and HCO3- reabsorption. Not used as a diuretic now, as HCO3- loss leads to metabolic acidosis.

Answer 167

Symptom – Polyuria (More than 2.5L urine/day) ``` Some Causes: o Diabetes Mellitus • Glucose in filtrate → Osmotic Diuresis o Diabetes Insipidus (Cranial) • decrease ADH release from posterior pituitary → Diuresis o Diabetes Insipidus (Nephrogenic) • Poor response of Collecting ducts to ADH → Diuresis o Psychogenic polydipsia • Increase intake of fluid ```

Answer 168

o Conditions with ECF expansion and Oedema • Congestive Heart failure • Nephrotic syndrome • Kidney failure (loop diuretic) • Ascites and oedema due to cirrhosis of the liver (spironolactone) o Acute Pulmonary Oedema • IV Furosemide • Due to left heart failure o Hypertension • Thiazide diuretics • Spironolactone in primary hyperaldosteronism (Conn’s syndrome) Other uses: ``` o Hypercalcaemia • Loop Diuretics promote calcium excretion by the Loop of Henle o Osmotic diuretics • E.g. Mannitol • Used in cerebral oedema o Carbonic anhydrase inhibitors • Acetazolamide useful in Glaucoma ```

Answer 169

``` o Alcohol • Inhibits ADH release o Coffee • increase GFR and decrease Tubular Na+ reabsorption o Other drugs – Lithium, demeclocyline • Inhibit ADH action on Collecting ducts ```

Answer 170

``` Body Trigone Neck Detrusor Urinae muscle Internal urethral muscle External urethral muscle ```

Answer 171

o Made from a meshwork of muscle fibres in roughly 3 layers • Inner longitudinal • Middle circular • Outer longitudinal o This arrangement of muscle fibres gives the bladder strength, irrespective of which direction it is being stretched in. o Supplied by the autonomic nervous system, not under voluntary control o Spinal nerve supply is bilateral.

Answer 172

o Continuation of the Detrusor muscle and made of smooth muscle. o Physiological sphincter at the bladder neck • Physiological Sphincter – no muscle thickening, action due to structure o Primary Muscle of continence

Answer 173

o Anatomical sphincter • Localised circular muscle thickening to facilitate action o Derived from pelvic floor muscles o Skeletal muscle, under somatic, voluntary control o Contracts to constrict urethra and “hold in” urine

Answer 174

``` Parasympathetic o Pelvic Nerve (S2-S4) o Ach →M3 Receptors o Contraction Sympathetic o Hypogastric Nerve (T10-L2) o NA → β3 Receptors o Relaxation ```

Answer 175

Sympathetic o Hypogastric Nerve (T10-L2) o NA → α1 Receptors o Contraction

Answer 176

``` Somatic o Pudendal Nerve (S2-S4) o Spinal motor outflow from Onof’s Nucleus of the ventral horn of the cord o Ach → Nicotinic Receptor o Contraction ```

Answer 177

When the bladder is full (threshold at 400ml), an urge to urinate arises. Brain Micturition Centres → Spinal Micturition Centres → Parasympathetic Neurones The increase in parasympathetic stimulation to the bladder via the Pelvic nerve causes the Detrusor to contract and increase intravesicular pressure. The Cerebral Cortex then makes a conscious, executive decision to urinate, reducing somatic stimulation to the External Urethral Sphincter. The contraction of the Detrusor coupled with the relaxation of the External Urethral Sphincter results in the bladder emptying through the urethra.

Answer 178

The ureters, urinary bladder, internal and external urethral sphincters work together to pass urine into the urinary bladder and store it over many hours (e.g. at night). The walls of the bladder have many folds, which distend when filling with urine. Because of this, as the bladder fills intravesicular pressure hardly changes. The increase in sympathetic stimulation to the bladder via the hypogastric nerve (see above) causes the Detrusor to relax and the Internal Urethral Sphincter to contract. The Cerebral Cortex then makes a conscious, executive decision not to urinate, increasing somatic stimulation to the External Urethral Sphincter. This causes it to contract, constricting the urethra. The relaxation of the Detrusor, coupled with the contraction of the Internal and External Urethral sphincters reduces intravesicular pressure and constricts the urethra, preventing micturition.

Answer 179

Stress Urinary Incontinence (SUI) - Involuntary leakage on effort or exertion, or on sneezing or coughing Urge Urinary Incontinence (UUI) - Involuntary leakage, accompanied by or immediately proceeded by urgency Mixed Urinary Incontinence (MUI) - Involuntary leakage, associated with urgency and exertion, effort, sneezing or coughing Overflow Incontinence - Retention of urine causing the bladder to swell. Can be low pressure and pain free. Stress Urinary Incontinence is by far the most common

Answer 180

The prevalence of urinary incontinence steadily increases with age.

Answer 181

Risk factors include anything that can weaken the pelvic floor muscles, e.g. childbirth. The support of the urethra by the muscles and ligaments of the pelvic floor are important for the efficiency of the sphincter mechanisms of the urethra that enable continence.

Answer 182

o Height/Weight o Abdominal exam to exclude palpable bladder o Digital rectal examination (DRE) Prostate (male) Limited neurological examination o Females External genitalia (stress test) Vaginal exam

Answer 183

Record the amount of fluid they pass for two or three days can assess frequency of micturition. Number of pads that the patient has to use per day to cope with the urine leakage. Is the leakage is continuous or intermittent and what precipitating factors there are, such as coughing and sneezing. Urgency and frequency of micturition will often be made worse if there is an intravesicular inflammatory condition. Previous surgery of the pelvic floor can be important as this may lead to denervation of parts of the bladder. Childbirth may also be an important factor in the development of SUI in women due to sphincter damage.

Answer 184

Mandatory o Urine dipstick – UTI, haematuria, proteinuria, glucosuria Basic non-invasive urodynamics o Frequency-volume chart o Bladder diary (~3 Days) o Post micturition residual volume (Patients with voiding dysfunction) Optional o Invasive urodynamics (pressure-flow studies +/- video) o Pad tests o Cystoscopy

Answer 185

``` Conservative Management General lifestyle interventions o Modify fluid intake o Weight loss o Stop smoking o Decrease caffeine intake (UUI) o Avoid constipation o Timed voiding – fixed schedule ``` Contained Incontinence For patients unsuitable for surgery who have failed conservative or medical management: o Indwelling Catheter Urethral or Suprapubic o Sheath device Analogous to an adhesive condom attached to a catheter tubing and bag o Incontinence pads ``` Specific Management of SUI o Pelvic floor muscle training 8 contractions, 3x a day At least 3 months duration Void bladder, stop stream ← use those muscles in pelvic floor training ``` Specific Management of UUI o Bladder training o Schedule of voiding Void every hour during the day Must not void in between – wait or leak Intervals increased by 15-30 minutes a week until interval of 2-3 hours o At least 6 weeks of training needed

Answer 186

Duloxetine - combined noradrenaline and serotonin uptake inhibitor. It increases the activity of the External Urethral Sphincter during the filling phase. Duloxetine is not recommended by NICE as a first line or routine second line treatment, but may be offered as an alternative to surgery. Anticholinergics - Act on muscarinic receptors, including the M3 receptors that cause the Detrusor to contract. There are many side effects though due to affects on M receptors at other sites. E.g. Oxybutynin Botulinum toxin - potent biological neurotoxin that inhibits Ach release. Prevents Detrusor muscle contraction, as the pelvic nerve cannot release Ach to act on the M3 receptors.

Answer 187

Permanent Intention Low-tension vaginal tapes are the commonest surgical intervention. It is a minimally invasive technique with a success rate of > 90%. They work by supporting the mid urethra with a polypropylene mesh. Open retropubic suspension procedures correct the anatomical position of the proximal urethra and improve urethral support. Classic fascial sling procedures support the urethra and increases bladder outflow resistance. It involves autologous transplantation of the fascia lata or rectus fascia. Temporary Intention Intramural bulking agents improve the ability of the urethra to resist abdominal pressure by improving urethral coaptation. This is achieved by injections of autologous fat, silicone, collagen or hyaluron-dextran polymers.

Answer 188

Artificial urinary sphincter is the gold standard treatment in urethral sphincter deficiency. The cuff is a mechanical (hydraulic) device that simulates the action of a normal sphincter to circumferentially close the urethra. Problems include infection, erosion and device failure. Male sling procedure corrects SUI in men, the cause of which is usually iatrogenic (radical prostatectomy, colorectal surgery, radical pelvic radiotherapy). It is an experimental/emerging treatment, using a bone-anchored tape. The long-term results are unknown.

Answer 189

There are four sites of glomerular injury: o Subepithelial - Anything that effects podocytes/podocyte side of glomerular basement membrane o Within Glomerular Basement Membrane o Subendothelial - Inside the Basement membrane o Mesangial/paramesangial - Supporting capillary loop

Answer 190

``` Filter can block o Renal failure • Hypertensive • Haematuria Filter can leak o Proteinuria (Albumin) o Haematuria o Separately or together, depending on damage ```

Answer 191

Proteinuria is the presence of excess serum proteins (

Answer 192

Over 3.5g of Protein is filtered in 24hrs is known as Nephrotic Syndrome. As a lot of protein is being filtered, oncotic pressure is reduced giving generalised oedema. Podocyte/Subepithelial damage is the likely site of injury.

Answer 193

Presents in childhood/adolescence with incidence reducing with increasing age. It causes heavy proteinuria or Nephrotic syndrome. The disease responds well to steroids, but may reoccur once weaned off treatment. There is usually no progression to renal failure and is normally purely protein loss from the kidney. Minimal Change Glomerulonephritis is named as such because when looking at the glomeruli under a light microscope they appear to be completely normal. However, under an electron microscope, the damage to podocytes is evident, widening fenestration slits and allowing protein to ‘leak’ through. Pathogenesis is unknown.

Answer 194

o Minimal Change Glomerulonephritis (GN) o Focal Segmental Glomerulosclerosis (FSGS) o Membranous Glomerulonephritis Common Secondary Causes of Proteinuria/Nephrotic Syndrome o Diabetes Mellitus (microvascular complications affect kidneys) o Amyloidosis

Answer 195

Focal – Involving less than 50% of glomeruli on light microscopy Segmental – Involving part of the glomerular tuft Glomerular Sclerosis – Scarring Presents in adulthood and is less responsive to steroids than minimal change glomerulonephritis. Podocytes undergo damage and subsequent scarring, so protein is present in the urine. A circulating factor is responsible for the damage, evidenced by the fact that transplanted kidneys undergo the same damage. Minimal change FSGS can progress to renal failure, but the pathogenesis is unknown.

Answer 196

The commonest cause of Nephrotic syndrome in adults. Results from immune complex deposits in the sub-epithelial space and probably has an autoimmune basis (autoantibody to podocytes). However there is also evidence that it may be secondary, as it is associated with other conditions, particularly malignancies e.g. lymphoma. Follows the rule of thirds: o 1/3 just get better o 1/3 ‘Grumble along’, proteinuria but are fine o 1/3 Progress to renal failure

Answer 197

Renal failure due to the blocking of filter.

Answer 198

The commonest Glomerular Nephropathy, which can occur at any age, characterised by the deposition of IgA antibody in the Glomerulus. It is classically present with visible/invisible haematuria and has been shown to have a relationship with mucosal infections (IgA protects mucosal surfaces). It has variable histological features and course. Some, but not all, patients have proteinuria, and a significant proportion of patients, but not all, progress to renal failure. It is unknown why this variation occurs. Mesangial proliferation and scarring may occur. There is no effective treatment.

Answer 199

There are two hereditary nephropathies, Thin GBM Nephropathy and Alport Syndrome. The two are not completely distinct however, with a grey area between them ``` Thin GBM Nephropathy: Nephropathy Benign Familial Nephropathy Isolated Haematuria Thin GBM Benign Course ``` ``` Alport Syndrome: X linked Abnormal collagen IV Associated with deafness Abnormal appearing GBM Progresses to renal failure ```

Answer 200

o Progressive proteinuria o Progressive renal failure o Microvascular (Damages glomerulus directly) o Mesangial sclerosis → nodules o Basement membrane thickening to 4-5x normal

Answer 201

Relatively uncommon, but clinically important as it is very rapidly progressing Glomerular Nephritis. The disease is brought about by an autoantibody to collagen IV in basement membranes, but only seems to affect the kidney for an unknown reason. It is treatable by immunosuppression and plasmaphoresis if caught early. Characterised by IgG deposition but no Extracellular Matrix deposit.

Answer 202

An inflammation of blood vessels that will therefore affect the highly vascularised kidney. Blood vessels are attacked directly in the glomerulus by Anti Neutrophil Cytoplasmic Antibody (ANCA), and is treatable if caught early.

Answer 203

Subepithelial Deposits Antigen abnormally recognised on podocytes, circulating IgG binds to it, forming immune complexes in the glomerulus. E.g. Membranous Glomerulonephritis Mesangial Deposits Immune complexes can be deposited directly in the mesangium, as there is no podocytes or basement membrane to act as a barrier. E.g. IgA Nephropathy

Answer 204

Most common cancer in men in the UK. Second most common cause of death from cancer in men. However, most men who are diagnosed with prostate cancer are more likely to die with it than of it.

Answer 205

Age o Correlation with increasing age. o Uncommon in men younger than 50. Family History o 4x increased risk o If one 1st degree relative is diagnosed with Prostate Cancer before age 60 o After age 60 any diagnosis was probably age related Race o Incidence in Asian

Answer 206

``` Usual o Vast majority asymptomatic o Urinary symptoms • Benign enlargement of prostate • Bladder over activity • +/- CaP o Bone pain • Advanced metastatic ``` Unusual o Haematuria • In advanced prostate cancer

Answer 207

A Digital Rectal Examination (DRE) and Serum PSA (Prostate specific antigen) are used to assess whether or not a biopsy of the prostate is necessary. If it is, it is carried out via a TRUS (TransRectal UltraSound) guided biopsy of prostate. Lower urinary tract symptoms (LUTS) are treated with a TransUrethral Resection of Prostate.

Answer 208

``` o Age o DRE • Localised (T1/2) • Locally advanced (T3) • Advanced (T4) o PSA Level o Biopsies • Gleason Grade o MRI scan and Bone scan • Nodal/Visceral Metastases ```

Answer 209

Established Prostate Cancers Surveillance – if the cancer is low risk, i.e. the Gleason score is quite low sometimes it is appropriate just to watch the cancer, as treatment may do more damage than good. Radical Prostatectomy – Open, laparoscopic or robotic Radiotherapy – External beam or low dose brachytherapy (implanted beads) Developmental Prostate Cancers High Intensity Focused Ultrasound (HIFU) Primary Cryotherapy – Freeze the prostate Brachytherapy – High dose

Answer 210

Hormones – Surgical castration, medical castration (LHRH agonists) Palliation – Single-dose radiotherapy, bisphosphonates, chemotherapy

Answer 211

o Surveillance o Hormones o Hormones & Radiotherapy

Answer 212

Haematuria is classified as Visible or Non-Visible. If Haematuria is visible, on investigated there is a 20% chance a malignancy is present (e.g. kidney, ureter). Non-Visible haematuria can be symptomatic or asymptomatic. It is detected via microscopy or urine dipstick (peroxidation of haem).

Answer 213

``` Urological o Cancer • Renal cell carcinoma (RCC) • Upper tract transition cell carcinoma (TCC) • Bladder cancer • Advanced prostate cancer o Other • Stones • Infection • Inflammation • Benign prostatic hyperplasia (large) o Nephrological (Glomerular) ```

Answer 214

Smoking, Occupation, painful or painless, other lower urinary tract symptoms and family history need to be asked about.

Answer 215

o BP o Abdominal mass o Varicocele – collection of veins in the scrotum o Leg swelling o Assess prostate by DRE (male) – Size, texture

Answer 216

Urine culture and cytology (abnormal cells), full blood count, ultrasound, flexible cystoscopy

Answer 217

7th most common cancer in the UK, but its incidence is decreasing. The male to female ratio is 2.5:1, and 90% are Transitional Cell Carcinomas (TCC)

Answer 218

o Smoking • 4x Increased Risk o Occupational exposure (20 year latent period) • Rubber or plastics manufacture (Arylamines) • Handling of carbon, crude oil, combustion (Polyaromatic hydrocarbons) • Painters, mechanics, printers, hairdressers o Schistosomiasis (e.g. Egypt)

Answer 219

o 75% of Cancers are superficial (Ta/T1) o 5% are Tis (In situ) o 20% are muscle invasive

Answer 220

``` High risk non-muscle invasive TCC o Check cystoscopies o Intravesical chemotherapy/immunotherapy Low risk non-muscle invasive TCC o Check cystoscopies Muscle Invasive TCC o Potentially curative • Radical cystectomy or radiotherapy (+/- chemotherapy) o Not curative • Palliative chemotherapy/radiotherapy o Radical Cystectomy ```

Answer 221

The removal of the urinary bladder. A piece of Ileum may be used to make a conduit from the ureters to the abdomen, where urine can be collected in a bag. May also attempt to reconstruct the bladder from a piece of small intestine.

Answer 222

8th most common cancer in the UK, making up 95% of all upper urinary tract tumours. The incidence and mortality are increasing. There is a Male to Female ratio of 3:2, and 30% of RCC have metastases on presentation.

Answer 223

o Smoking doubles risk o Obesity o Dialysis

Answer 224

Can spread to lymph nodes, up the renal vein and vena cava into the right atrium and into the subcapsular fat (Perinephric spread)

Answer 225

``` Established o Surveillance o Radical nephrectomy • Removal of kidney, adrenal, surrounding fat, upper ureter o Partial nephrectomy ``` ``` Developmental o Ablation (removal of tumour from the surface of kidney via an erosive process) ``` Palliative o Molecular therapies targeting angiogenesis o Immunotherapy

Answer 226

Only 5% of all malignancies of upper urinary tract (Rest are RCC). o 5% are due to the spread of cancer from the bladder up the ureter. o 40% of cancers of the upper urinary tract spread to the bladder.

Answer 227

``` o Ultrasound • Hydronephrosis – Swelling of kidney due to backup of urine o CT Urogram • Filling defect • Ureteric structure o Retrograde pyelogram – Inject contrast into the ureter o Ureteroscopy • Biopsy • Washings for cytology ```

Answer 228

Nephro-ureterectomy – Removal of the kidney, fat, ureter and cuff of bladder

Answer 229

o “Little urine” | o Less than 500ml of urine/day or less than 20ml/hour

Answer 230

o “No urine” o Less than 100ml of urine/day o Indicates blockage of urine flow

Answer 231

``` o Pre-Renal Disease • Decreased perfusion o Post-Renal Failure • Obstruction o Intrinsic Renal Failure • Damage to kidney ```

Answer 232

Caused by a reduction in renal perfusion. Unless the cause is recognised and treated promptly, Acute Tubular Necrosis (ATN) will develop. Causes of reduced renal perfusion include: ``` Reduced effective ECF volume o Hypovolaemia • Blood Loss • Fluid Loss o Systemic Vasodilation • Sepsis • Cirrhosis • Anaphylaxis o Cardiac Failure • LV dysfunction • Valve disease • Tamponade ``` ``` Impaired Renal Autoregulation Renal Autoregulation maintains a normal perfusion over a range of systemic BP. o Preglomerular vasoconstriction • Sepsis • Hypercalcaemia • Hepatorenal syndrome • Drugs – NSAIDS o Postglomerular vasodilation • ACE Inhibitors • Angiotensin II Antagonists ```

Answer 233

Obstruction to urine flow after the urine has left the tubules. It accounts for approximately 10% of AKIs. The obstruction can occur at three anatomical sites: 1. Ureters (bilateral) 2. Bladder 3. Urethra The obstructions can be further classified: Within the Lumen o Calculi (stones) • Both renal pelves/ureters • Neck of the bladder • Urethra • Stones > 10mm will not usually pass, pain and haematuria is common o Blood clot o Papillary necrosis o Tumour of renal pelvis, ureter, bladder Within the wall o Congenital • Pelviureteric neuromuscular dysfunction • Megaureter • Neurogenic bladder o Ureteric stricture o Usually cause Chronic not Acute Kidney Injury ``` Pressure from Outside o Prostatic hypertrophy o Malignancy o Aortic aneurysm o Diverticulitis o Accidental ligation of ureter (during surgery) ```

Answer 234

``` Intrinsic AKI accounts for 30% of all AKIs. It is direct injury to the kidney. o Acute Tubular Necrosis (ATN) o Severe Acute Ischaemia o Toxic Acute Tubular Necrosis o Glomerular and arteriolar disease o Immune disease affecting the glomerulus o Acute tubule-interstitial nephritis o Inflammation of kidney Intersticium ``` Acute Tubular Necrosis o Severe Acute Ischaemia • Pre-Renal Causes • If the fall in renal perfusion is not treated promptly, tubular necrosis results o Toxic Acute Tubular Necrosis • Nephrotoxins damage the epithelial cells lining the tubules, and cause cell death and shedding into the lumen. (endogenous or exogenous) • ATN is much more likely if there is reduced perfusion and a nephrotoxin • Muddy Brown casts and a Fractional Excretion of Na+ of ≥ 3% Nephrotoxic Drugs o Gentamicin o ACE Inhibitors o Angiotensin Receptor Blockers o NSAIDs • Prostaglandins normally cause vasodilation of afferent arterioles in Renal Autoregulation • NSAIDs inhibit Prostaglandin production (Inhibit COX enzyme) • Unopposed vasoconstriction of afferent arteriole → reduced glomerular perfusion pressure → AKI ``` Glomerular and Arteriolar Disease Acute Glomerulonephritis o Immune disease affecting the glomerulus o Primary o Disease only affects the kidneys o Secondary o Kidneys are involved as part of a systemic process o SLE, Vasculitis ``` ``` Acute Tubulo-Interstitial Nephritis Inflammation of the Kidney interstitium Infection o Acute pyelonephritis (Ascending bacterial infection) Toxin induced o Drugs ```

Answer 235

Pre-Renal Failure Volume Correction o Hypovolaemia → Fluid administration o Heart Failure → Diuretic Post-Renal Failure Urological intervention to re-establish urine flow Acute Tubular Necrosis Treatment is supportive, maintaining good kidney perfusion and avoiding nephrotoxins Dialysis - if the kidneys can no longer adequately excrete salt, water and potassium.

Answer 236

``` Detected incidentally by dipstick urinalysis, e.g. at a health check or life insurance medical. It may be detected as microscopy haematuria, proteinuria or both. Sometimes hypertension is detected at the same time. The first investigation carried out is a cystoscopy, with a renal biopsy not being mandatory. o Microscopic Haematuria • Renal Stones / Tumours • Arteriovenous malformations • Glomerular Disease o Microscopic Proteinuria • Non-nephrotic proteinuria ```

Answer 237

Episodic macroscopic haematuria associated with glomerular disease is often brown or smoky in colour rather than red. Clots are very unusual. It needs to be distinguished from other causes of red or brown urine, including haemoglobinuria, myoglobinuria and consumption of food dyes (e.g. beetroot). o Macroscopic Haematuria is usually painless. o Commonest glomerular cause is IgA nephropathy. o Requires urological work up.

Answer 238

A non-specific disorder, where the kidneys are damaged, leaking a large amount of protein into the urine ``` Classic Triad of Findings: o Proteinuria (>3.5g/24hrs) o Hypoalbuminaemia o Oedema • (+ Hyperlipidaemia) • (+ Muehrcke’s Bands) ```

Answer 239

o Minimal change Glomerulonephritis o Focal Segmental Glomerulosclerosis o Membranous Glomerulonephritis

Answer 240

Requires renal biopsy for diagnosis, using an ultrasound-guided needle. The biopsy is aimed at the bottom of the kidney, to try to make sure a piece of cortex is biopsied. As there are no glomeruli in the medulla, it would not be useful for diagnosis.

Answer 241

Collection of signs (syndrome) associated with disorders affecting the kidneys (specifically glomerular disorders), characterised by having small pores in the podocytes of the glomerulus large enough to permit proteins and red blood cells.

Answer 242

``` o Rapid onset o Oliguria o Hypertension o Generalised oedema o Haematuria with smoky brown urine o Normal serum albumin o Variable renal impairment o Urine contains blood protein and red blood cell casts ```

Answer 243

Typical Features Nephrotic Nephritic Onset Insidious ++ Blood Pressure - Increases JVP -/decrease increase Proteinuria ++++. ++ Haematuria May/not occur. +++ Red Cell Casts Absent. Present Serum Albumin decrease. -/slightly reduced

Answer 244

Clinical situation in which glomerular injury is so severe that renal function deteriorates over days. The patient may present as a uraemic emergency with evidence of extrarenal disease. It is associated with crescentic glomerulonephritis. A renal biopsy is required for diagnosis.

Answer 245

The natural course of many forms of glomerulonephritis is slowly progressive renal impairment, including hypertension, dipstick abnormalities and uraemic syndrome. It is often associated with small, smooth, shrunken kidneys. Biopsies are hazardous and unlikely to provide diagnostic material.

Answer 246

``` o Tiredness and lethargy o Breathlessness o Nausea and vomiting o Aches and pains o Sleep reversal o Nocturia o Restless legs o Itching o Chest pains o Seizures and coma ```

Answer 247

The progressive and irreversible loss of renal function over a period of months to years. Functioning renal tissue is replaced by extra-cellular matrix; histologically this gives rise to glomerulosclerosis and tubular interstitial fibrosis. As a result, there is a progressive loss of both the excretory and hormone functions of the kidney. Most Glomerular disease that lead to Chronic Renal Failure are characterised by the development of proteinuria and systemic hypertension.

Answer 248

``` o Immunologic • Glomerulonephritis o Infection • Pyelonephritis o Genetic • Polycystic Kidney Disease (PCK) • Alport’s Syndrome o Obstruction and reflux nephropathy o Hypertension o Vascular o Systemic Disease • Diabetes • Myeloma o Cause unknown ```

Answer 249

According to GFR Stage GFR Description 1 >90 Kidney damage with normal/increased GFR 2 60-89 Kidney damage with mild GFR fall 3 30-59 Moderate fall in GFR 4 15-29 Severe fall in GFR 5

Answer 250

85% of patients with CKD will be identified by looking in registries for diabetes, hypertension and ischaemic heart disease. More common in the Elder, Ethnic minorities and the socially disadvantaged.

Answer 251

Cardiovascular o Atherosclerosis o Cardiomyopathy o Pericarditis Haematology o Anaemia - Decreased or resistance to Erythropoietin Bone o Renal Bone Disease o Less Phosphate is excreted due to decreased GFR, increasing serum concentration. It then forms complexes with free Calcium, reducing its effective serum concentration. This stimulates the Parathyroid to produce PTH, causing over activity of Osteoclasts, leading to Osteitis Fibrosa Cystica. o Less Vitamin D undergoes its 2nd Hydroxylation to its active form due to kidney damage. This also causes hyperparathyroidism, but additionally causes Osteomalacia. o Non-Bone Calcification CNS o Neuropathy o Seizures o Coma

Answer 252

``` o Tiredness o Breathlessness o Restless legs o Sleep reversal o Seizure o Aches and pains o Nausea and vomiting o Itching o Chest Pain ```

Answer 253

Measuring Renal Function A normal GFR range is 80-120ml/min, and renal function can be expressed by a percentage of this. GFR can be measured via Inulin clearance or 24hr Creatinine clearance. If Creatinine is used to measure GFR, it needs to be modified to Estimated GFR (eGFR) by an equation to take into account age, sex, gender and ethnicity. Creatinine is not a perfect marker for renal function, as someone with a GFR of 40% of normal can still have a normal Creatinine level. Further to this it is only accurate in adults and only defines Chronic kidney disease (Not useful in acute renal failure).

Answer 254

``` o Auto-Antibody screen o Complement o Immunoglobulin o ANCA o CRP o SPEP/UPEP o Imagining of kidneys • Ultrasound for size and Hydronephrosis • CT • MRI ```

Answer 255

``` To prevent of delay progression, there are several potentially modifiable risks: o Lifestyle o Smoking o Obesity o Exercise o Treat Diabetes (If present) o Treat Blood Pressure (If high) o ACE Inhibitors / Angiotensin Receptor Blockers o Lipid Lowers (Diet / Statins) ```

Answer 256

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

Answer 257

Indications for the Initiation of Dialysis include uraemic symtoms, acidosis, pericarditis, fluid overload and hyperkalaemia. There are two types of dialysis, Haemodialysis and Peritoneal Dialysis.

Answer 258

Requires the creation of a Ateriovenous (AV) Fistula, a connection between an artery and vein. The difference in pressure means that blood moves from the artery → vein, causing it to dilate and develop a muscular wall. This provides vascular access. 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. Anti-coagulation is also needed to prevent the patient’s blood from clotting in the machine.

Answer 259

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

Answer 260

CVS instability | High capital cost

Answer 261

Peritoneal dialysis requires the peritoneal membrane, blood flow and peritoneal dialysis fluid. 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.

Answer 262

``` Low Technology Home technique Easily learned Allows mobility CVS stability Better for elderly and diabetics? ```

Answer 263

``` Frequent exchanges (~4/day) No long term survivors yet Frequent treatment failures Peritonitis Limited dialysis dose range High revenue costs ```

Answer 264

All patients with progressive CKD or end-stage renal failure should be considered from transplantation. ``` Sources of kidneys for transplantation: o Cadaver donors o Non-heart beating donors o Living related donors/friends o Autristic donors ``` When a kidney is transplanted, it is not to the normal anatomical location, but to the iliac fossa. This is because it can easily be connected both to the iliac vessels and the bladder.

Answer 265

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

Answer 266

``` Not all are suitable Limited donor supply Operative morbidity and mortality Life long immunosuppression Still left with progressive CKD ```

Urinary Flashcards

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