Urology and Renal

Question 1

How is osmolarity calculated

Answer 1

concentration X number of dissociated particles (e.g glucose would be x1 but NaCl would be x2)

UNITS: osm/L if the solute is in mol/L, mOsm/L if solute i mmol/L

Question 2

What is the relationship between osmotic pressure and number of solute particles

Answer 2

directly proportional

Question 3

Describe body fluid distribution

Answer 3

2/3 Intracellular fluid
1/3 Extracellular fluid - 25% plasma, 75% (Interstitual fluid mostly and small amount of transcellular)

Question 4

What fluid loss is unregulated

Answer 4

sweat ,faecrs, vomit, water evaporation from respiratory lining and skin

Question 5

Describe the renal regulation of water loss

Answer 5

High water intake = increase in extracellular fluid, decreases Na+ conc and therefore osmolarity decreases (more water less particle). Produce hypoosmotic urine : pee more water than solute to normalise the osmolarity

Low water intake= decrease in extracellular fluid, so higher Na+ concentration, and increased osmolarity. Produce hyperosmotic urine (pee more solute than urine) to normalise osmolarity

Question 6

Where in the kidney is water reabsorbed, how is it reabsorbed

Answer 6

Passive- osmosis
most in proximal convuluted tubule
Some in thin descending limb
Thick ascending limb is impermeable to water
some in collecting duct

Question 7

For water to be absorbed the medullary interstitium needs to be what

Answer 7

Hyperosmotic in Loop of Henle and Collecting Duct

Question 8

How are concentration gradients formed in the loop of henle for water reabsorption

Answer 8

1- isoosmotic filtrate arrives
2- active salt reabsorption: thick ascending limb, salt actively transported into medullary interstitium so its osmolality rises . This causes
3- passive water reabsorption: water passively moves into the medullary interstitium to reduce osmolality
4- Fluid flow. As urine is continually being produced, new isoosmotic tubular fluid enters the descending limb, which pushes the fluid at higher osmolarity down the tube and an osmotic gradient begins to develop.

Question 9

How is urea recycled in the kidneys

Answer 9

Urea reaches the collecting duct and throught the UT-A1 on apical side and UT-A3 on basolateral is reabsorbed into the medullary interstitium. The urea here will then either enter the vasa recta through UT-B1 or into the thin descending limbs tubule through UT-A2. At the proximal convuluted tubule most urea and water is reabsorbed so by urea moving back into the TDL tubule the conc and osmolality increases. TAL is impermeable to water and urea so only reabsorbed when reach DCT and CD which it will move through aquaporins and UT-A1 back into the medullary interstitium because at that point osmolality of medullary interstitium is high from Na+ and Cl- but has low urea content so will move down conc gradient out the tubule. It means that less water is used to get rid of urea and urine can become concentrated still

Question 10

What effect does ADH/Vasopressin have on urea recycling

Answer 10

increases UT-A1 and UT-A3 numbers so in the DCT and CD urea can be passively absorbed just like water

Question 11

How is ADH stimulated and inhibited what factors

Answer 11

Change in plasma osmolality is detected by osmoreceptors in the hypothalamus (supraoptic and paraventricular nuclei then stimulate posterior pituitary to release). Change in blood pressure is detected by baroreceptors in carotid sinuses and the aortic arch and transmitted to hypothalamus

Inc plasma osmolality or hypovolaemia means we would want to conserve water so it stimulates ADH to open aquaporin-2 channels. Nausea, Angiotensin II and nicotine also stimulate ADH increase (retaining water)

If there’s decreases plasma osmolality or hypervolaemia aquaporins must be shut to get rid of water by inhibiting ADH. Ethanol and Atrial natriuretic peptide both cause ADH inhibiton too

Question 12

How does ADH affect the kidneys

Answer 12

Principal cells lining the CD and DCT, ADH will bind to the V2 receptor which starts G protein cascade (AC converts ATP to cAMP which then activates protein kinase A), so aquaporin 2 channels are secreted and inserted into the apical membrane, ad AQP3 channels on the basolateral membrane to reach the blood. can also enter blood through AQP4 but DH affects AQp3

Question 13

Describe how water moves through the kidney tubule

Answer 13

Isoosmotic when reaches TDT, water passively moves out, then at TAT Na+Cl- actively moved out, fluid becomes hypoosmotic

Question 14

How is Cl- and Na+ reabsorbed in the thick ascending limb

Answer 14

on apical/tubule lining : Na+/K+/2CL- symporter moving these into the cell, K+ is pushed back into the lumen by another channel.

on basolateral side: Na+/K+ ATPase pump moves 3Na+ out and 2K+ in. There is also a K+ and Cl- symporter

Question 15

How is diuresis achieved

Answer 15

Low ADH so AQP2 is absent so the hypoosmotic fluid (high water, low Na+/Cl-) when reaches DCT and CD no water can be reabsorbed so result is hypoosmotic fluid still flowing through.
At the principal cells of the collecting duct, further Na absorption occurs as it moves into the cell on the apical side. It is then transported through the basolateral side by a Na+/K+ Atpase pump (3 Na+ in blood and 2K out)
Hypoosmotic fluid is thus excreted

Question 16

How is antidiuresis achieved

Answer 16

High ADH level.
ADH inserts AQP2 in DCT for water reabsorption from the hypoosmotic fluid to make it hyperosmotic and low volume.
ADH also increases Na+ reabsorption in TAL (Na+/K+/2Cl- symporter), DCT (Na+/Cl- symporter), CD (Na channel)

Question 17

What are the three ADH related disorders, describe them

Answer 17

Central Diabetes Insipidus: decreased/ no release of ADh. get polyuria and polydypsia. Treat with external ADH

SIADH - Syndrome of inappropriate ADH secretion : increased production and release of ADH, lots of water reabsorbed so hyperosmolar urine, hypervolaemia, hyponatraemia. Treat with non-peptide inhibitor of ADH and its receptr (conivapatan and tolvaptan)

Nephrogenic Diabetes Insipidus: less/mutant AQP2 so ADH cannot wok, causes polyuria and polydipsia (lose a lot of water). Treat: Thiazide diuretics and NSAIDs to slow down filtration at Bowmans

Question 18

How does diet and metabolism affect acid-base balance

Answer 18

Lose base in faeces so becomes more acidic

Question 19

What is the role of kidneys in acid-base regulation

Answer 19

Secrete and excrete H+
Reabsorb HCO3-
Produce ner HCO3-

Question 20

Where does reabsorption of HCO3- occur in the kidney

Answer 20

80 in PCT: CO2 moves into the cells lining the PCT by diffusion from blood, carbonic anhydrase within the kidney converts this to H+ and HCO3-. Proton is transported into tubular fludi through NA+/H+ antiporter (NHE3) and H+ATPase pump (V-ATPase). Once in tubular fluid it binds with bicarb there to become water and Co2 again. Bicarbonate in the cells lining the PCT are pumped into the blood through NBC1 Na+/HCO3- symporter

10 in TAL,
minimal in DCT and CD: alpha-intercalated cells pump H+ into tubular fluid through H+ATPase pump (V-ATPase) and the H+/K+ ATPase = HCO3- REABSORP and H+ SECRETION. beta intercalated cells use Cl-/HCO3- antiporters to move HCO3 into the tubular fluid, and then V-ATPase H+/ATPase moves H+ into the blood. HCO3- SECRETION and H+ REABSORPTION

Question 21

What is the Henderson - Hasselbalch equation and how does it explain the cause of acid-base disorders

Answer 21

pH= pK (dissociation constant) + log (base conc/acid conc)

Aka : acid conc= (24 x PCO2)/(base conc)

shows that acid con/[H+] is directly proportional to the partial pressure of CO2.
IF CO2 is high then is a resp disorder
If base is disturbed then metabolic

Question 22

How do alkalosis and acidosis affect alpha and beta intercalated cells

Answer 22

Alkalosis = high bicarbonate, so beta intercalated cells work to increase HCO3- secretion into tubular fluid whilst reabsorbing H+

ACidosis= high H+, so alpha interCalated cells work to reabsorb HCO3- and secrete H+

Question 23

How do the kidneys produce bicarbonate ions

Answer 23

In PCT, glutamine molecules within the tubule linings cells give rise to two ammonium ions and one divalent ion (A2-). This divalent ion gives rise to two bicarbonate ions which are then reabsorbed. If the ammonium ions enter blood circulation they will go to the liver which will turn it into one urea and one proton per each ammonium. Since its two ammonias there will be two protons made, these protons will have to be neutralised by the two bicarbonates so it would be net zero.. THEREFORE the ammonia must be excreted to prevent this. This can be done through the sodium/proton antiporter (NEH3) on the apical membrane where oNa+ will be reabsobed and ammonia secreted into the tubular fluid OR by changing the ammonium ions into ammonia gas which is released into the tubular fluid and gotten rid of. Must get rid of ammonia ions to conserve bicarbonate ions.
We also produce bicarbonate ions int the DCT and CD area, along with the bicarbonate buffer system there are other systems too. The renal system has a phosphate buffer system, the phosphate neutralises the proton when it reached the tubular fluid so we gain a bicarbonate ion.

Question 24

General rule of metabolic and respiratory causes of alkalosis and acidosis

Answer 24

if metabolic then both pH and HCO3 will rise together or decrease together
If acidic then PCO2 and pH will be opposite

Question 25

Describe the compensatory response to metabolic acidosis, metabolic alkalosis

Answer 25

Metabolic acidosis : low HCO3- and low pH, will decrease ventilation slightly but mostly inc HCO3 reabsorption and production Metabolic alkalosis: high HCO3-, high pH= hyperventilation (reduces H+) and HCO3- excretion

Question 26

Describe the compensatory response to respiratory acidosis and respiratory alkalosis

Answer 26

Respiratory acidosis: high PCO2, low pH= if acute then intracellular buffering where CO2 will enter cells CA will hydrate and make bicarbonate and proton. Proton neutralised by proteins leaving a bicarbonate. If chronic then increase HCO3- reabsorption and production by working on alpha intercalated cells Respiratory alkalosis: low PCO2, high pH= intracellular buffering left shift as bicarbonate produces carbonic acid, reducing HCO3-. If chronic then decreased HCO3- reabsorption and production by working on beta intercalated cells

Question 27

Define osmolarity

Answer 27

measure of the solute (particle) concentration in a solution 1 osmole = 1mole of dissolved particles in 1 litre 1 osmole of NaCL= 2 dissolved particles SO 1 osmole of NaCl= 0.5molNaCl as 1 mole of NaCl is 2 osmoles

Question 28

What is the usual plasma osmolality

Answer 28

285-295mosmol/L

Question 29

What is the most prevalent solute in ECF

Answer 29

sodium

Question 30

How does sodium affect blood pressure

Answer 30

High dietary sodium= more water retention and intake = higher ECF volume so higher BP and BP. reverse is also true

Question 31

How is sodium intake regulated

Answer 31

If sodium is low lateral parabrachial nucleus increases appetite for Na+, the salty receptors are on the tip of tongue at sides if euvolemic sodium or low sodium then inhibit Na+ intake/ aversive.

Question 32

How does blood pressure affect sodium excretion

Answer 32

Renal Plasma Flow and GFR are proportional to blood pressure/mean arteriole pressure. This causes excretion of sodium as the amount of sodium going through increases and the time decreases so More sodium in DCT than normal as wasnt time to take out . Eventually after 100mmHg RPF and GFR plateau to conserve Na+

Question 33

When there is high sodium in the tubule what happens

Answer 33

Macula densa senses if there is high Na+ in the distal convuluted tubular fluid as it is in close proximity to the end part of the thick ascending limb, it therefore, senses increased sodium/cl/k triple transporter function. Increased tubular sodium is usually because blood pressure is high and it cannot absorb fast enough Macula densa then releases adenosine which the extraglomerular mesangial cells (between glomerulus and DCT) sense. Extraglomerular mesangial cells then interact with the smooth muscle cells to make the afferent arteriole contract which reduced GFR. Release of adenosine also leads to a reduction in renin, stopping further water reabsorption and higher blood pressure

Question 34

How is sodium retained/ sodium absorption increased

Answer 34

Increased sympathetic activity stimulates the juxtglomerular cells of the juxtaglomerular apparatus to release renin. Renin cleaves angiotensinogen made by the liver to angiotensin I. ACE from the lung cleaves Angiotensin I to Angiotensin II. Angiotensin II binds to the zona glomerulosa and stimulates the synthesis of aldosterone. Aldosterone works on the distal convuluted tubule and collecting duct to absorb more Na+. Angiotensin II also directly works on PCT to take up sodium Increased sympathetic stimulation contracts afferent arterioles smooth muscle cells which increases vascular resestance to reduce RBF/GFR. This means slower filtration of blood and less sodium lost Increased sympathetic activity directly acts on the proximal collecting duct to take up more sodium.

Question 35

How is sodium excretion regulated

Answer 35

Atrial naturietic peptide acts as a vasodilator of the afferent arteriole, increasing GFR so lowering sodium reuptake. Has effects on PCT, DCT and CT (entire system). It also suppressed production of renin by stopping juxtaglomerular cells from making

Question 36

Describe how the body will respond to a reduction in blood pressure and fluid volume

Answer 36

Will increase B1 sympathetic activation : contract afferent arteriole, stim juxtaglomerular cells to make renin which will result in aldosterone increasing Na+ uptake. water will follow.

Question 37

Describe how the body will respond to an increase in blood pressure and fluid volume

Answer 37

Decrease B1 sympathetic activation. B1 symapthetic system inhibits atrial naturietic peptide. By decreasing B1 sympathetic, ANP is made. ANP stops renin production and vasodilates (stops vasoconstriction of the afferent arteriole)

Question 38

What type of hormone is aldosterone

Answer 38

Steroid hormone

Question 39

When is aldosterone released

Answer 39

Angiotenin II levels Low blood pressure

Question 40

What does aldosterone do

Answer 40

Increases sodium reabsorption in principal cells Increases potassium secretion in principal cell H+ secretion in alpha intercalated cells

Question 41

How does aldosterone work

Answer 41

A steroid hormone so lipid soluble, moves through cell membrane and is bound to HSP90, it then binds to mineralcorticoid receptor and the HSP90 is removed. It will become a dimer and translocate into the nucleus . In the nucleus it binds to DNA and stimulates the production of mRNA for certain genes that code for sodium channels and the Na+/K+ ATPase. It also stimulates production of regulatory proteins to stimulate activity of the transporters it is making. For example, ENaC which stimulates activation of Na+ absorption from collecting duct

Question 42

How does hypoalsosteronism and hyperaldosteronism affect ECF, renin, ANP and BNP

Answer 42

Hypoaldosteronism: less reabsorption of sodium, ECF volume low, juxtaglomerular cells make renin, AGTII and ADH. Dizziness, Low BP, salt craving, palpitations Hyperaldosteronism : reabsorb sodium in DCT, water follows: ECF inc= hypertension. Hypertension= less renin from juxtaglomerular cells so less AGTII and ADH. Inc ANP and BNP to vasodilate afferent arteriole. high BP, muscle weakness, polyuria, thirst

Question 43

What syndrome has normal/low aldosterone levels but clinically appears to be hyperaldosteronism

Answer 43

Liddle's Syndrome: High BP due to a mutation in the ENaC sodium channel on the apical principal cells that aldosterone activates. Switches it to be constantly on causing sodium retention and thus hypertension

Question 44

How does spirinolactone work

Answer 44

Spironolactone is a potassium sparing diuretic like eplerenone that competitively inhibits mineralocorticoid receptors in the distal convoluted tubule to promote sodium and water excretion and potassium retention

Question 45

How will spirinolactone effect (1)hypertension (2) normal BP (3) Liddles Syndrome

Answer 45

(1) Blocks aldosterone and the MC receptors it binds to, reducing sodium uptake and water reabsorption to reduce blood pressure (2) Will cause a reduction in blood pressure (hypovolaemia) as more sodium and water is excreting. (3) No effect as mutation in the sodium channels, so aldosterone increase or blocking aldosterone with spirinolactone wont have an effect. Aldosterone increases channel expression and regulatory proteins to stimulate the channels so if channel faulty there will be no change

Question 46

Describe how the body detects low and high blood pressure

Answer 46

Heart lower pressure system includes right atrium, right ventricle and the pulmonary vasculature. This system detects both high and low pressure. If there is low pressure then theres reduced baroreceptor firing which sends afferent signals to the brainstem to increase sympathetic activity and ADH release. If there is high pressure then atrial stretch causes ANP and BNP to be released causing water loss Vascular system is a high pressure system composed of the carotid sinus, aortic arch and juxtaglomerular apparatus (pulmonary vasculature too). If there is low pressure then basoreceptors fire less, acts on juxtaglomerular cells to increase renin release, also sends afferent signals to brainstem to increase sympathetic activity and ADH release

Question 47

What is ANP

Answer 47

Arial Natriuretic peptide : peptide made in the atria (BNP made here too) in response to atrial stretch. ANP binds to guanlyl cyclase domain of GTP and converts to cyclic GMP which activates protein kinase G causing: - vasodilation of blood vessels - inhibition of sodium reabsorption in proximal tubule and in collecting ducts - inhibits renin and aldosterone release -reduces blood pressure

Question 48

How does the body respond to volume expansion and volume contraction

Answer 48

Volume expansion/increase: less sympathetic activity so less vasoconstriction, less sodium reuptake, less renin production (less ANGTII and aldosterone) increased sodium and water excretion. Heart also detects higher BP, increasing ANP and BNP. ANP and BNP work on brain to decrease AVP Volume depletion/contraction: more sympathetic activity, stimulates sodium uptake by increasing renin which increases aldosterone. Also works on the heart to decrease ANP and BNP so aldosterone and renin can be released, sodium can be uptaken, bp can increase and vasoconstriction may occur. Also works on the brain to stimulate AVP. net reduction in sodium and water excretion

Question 49

How does increase sodium levels reaching the collecting duct affect water secretion/ reabsorption

Answer 49

If there are increased sodium levels in the distal convuluted tubule then the osmotic gradient across the membrane is dampened. water moves from hypoosmolar regions into the medullary interstitial which is hyperosmolar SO by making both regions hyperosmolar then water cant move through so more excretion

Question 50

How does sodium affect ECF volume

Answer 50

More sodium excretion = less ECF/ less BP/ less Na+ Less sodium excretion = more ECF/more BP/more Na+

Question 51

What diuretic affects the renin angiotenin system

Answer 51

ACEi : leads to less angiotensin II which means vasodilation, higher vascular volume which lowers BP. It acts on the kidneys to decrease Na+ reuptake in the PCT which increases Na+ in the distal nephron so the DCT is hyperosmolar and water cant move across the gradient as both regions hyperosmolar. Also works on the adrenal glands to decrease aldosterone as less AGTII. This means less Na+ uptake in the DCT so more Na+ in the distal nephron: again water cannot move from hyperosmolar to hyperosmola

Question 52

Describe the other available diuretics

Answer 52

Carbonic anhydrase inhibitors: Carbonic anhydrase causes Na+ reabsorption and urinary acidity (as causes HCO3- reabsorption). Blocking it stops Na+ reabsorption in PCT so more Na+ in distal nephron so less water moves out. Reduces urine acidity as more bicarbonate and less protons will go into the urine. Loop Diuretic- furosemide: Blocks the triple transporter in the thick ascending limb of loop of henle. Reduces Na+ intake so more Na+ in the distal portion of the kidney so water cant be reabsorbed Thiazides: blocks Na+Cl- reuptake transporter in distal collecting tubule, less sodium uptake, increases sodium in distal tubule so less water reabsorption. Also increases calcium reabsorption. Havent blocked the Na+/K+ATPase on basolateral side which pumps 3 sodium out and 2 potassium in. Theres no sodium in the cells so then theres more potential for the 3Na+/Ca2+ antiporter to have to work to balance the sodium imbalance Potassium sparing diuretics- spironolactone- aldosterone inhibitor: binds to MC receptor on the DCT and CD to inhibit function. Aldosterone increases Na+ uptake and decreases K+ so by blocking less Na+ uptake and more K+ kept

Question 53

Enzyme released from the kidney into the plasma to stimulate Na+ reuptake is what

Answer 53

Renin from the juxtaglomerular cells

Question 54

Describe the overall effect of all the diuretics with their location

Answer 54

Block renin: acts on juxtaglomerular cells to block renin production ACEi: works on enzyme in lung affects entire nephron, decreases Na+ and water Carbonic Anhydrase Inhibitors: PCT, less Na+ reabsorbed and less acidic urine Loop Diuretics: Thick ascending limb, less Na+, Cl- and K+, less water Thiazides : DCT, less Na+ and water, Higher Ca2+ reabsorption Potassium Sparing Diuretics/Spironolactone: DCT and CD. More K+, less Na+

Question 55

Heart arrhythmia are caused by low concentrations of what

Answer 55

K+, since it depolarises membranes causing action potentials: makes it exciteable

Question 56

Is potassium low of high in ECF

Answer 56

ECF is high in sodium but LOW in potassium

Question 57

How does the body respond to dietary potassium

Answer 57

Potassium is in all cells. Once eaten then insulin stimulates K+ uptake by stimulating the Na+/H+ exchanger which pushes sodium into cells and H+ out. Sodium is then higher in the cell so K+/Na+ ATPase used to swap and increase intracellular K+

Question 58

Where in the kidney is potassium taken up

Answer 58

most in PCT (66%) 20% in thick ascending limb thru the Na+/2Cl-/K+ triple transporter then negligible amounts in DT and CD

Question 59

Where in the kidney is potassium stimulated to be secreted and what stimulates it

Answer 59

DCT and CD : principle cells, at basolateral side pushes K+ in from the blood and Na+ out through an ATPase. then K+ is pushed out through the cells excitability and concentration gradient into the tubular fluid. Stimulated by : High plasma K+, high aldosterone, high tubular flow rate and high plasma pH

Question 60

How does tubular flow stimulate K+ excretion

Answer 60

Distal cells have primary cilium that reach into the tubular fluid. If tubular low rate increases then the primary cilium is moved and stimulated PDK1 which increases Ca+ concentrations in the cell and stimulates K+ channels to open on the apical side so K+ flows into the tubular fluid

Question 61

What are the causes and symptoms of hypokalaemia and hyperkalaemia

Answer 61

Hypokalaemia : Low dietary intake (processed food), diuretics: increase tubular flow rate so more K+ secreted, vomiting, diarrhoea, genetics Hyperkalaemia: K+ sparing diuretics, ACE inhibitors, Elderly patients, severe diabetes and kidney disease

Question 62

What syndrome causes a mutation in the Na+/Cl- channel in the distal nephron and what does it cause

Answer 62

Gitelmans syndrome, leads to hypokalaemia because need Na+/Cl- channel to increase Na+ concentration in the cell and then Na+ moves out and K+ in

Question 63

Why do most diuretics increase potassium secretion

Answer 63

Increase flow rate which increases potassium excretion

Question 64

if a patient is dehydrated what part of the nephron have the highest osmolarity

Answer 64

if a patient is dehydrated the tip of the loop of henle will have the highest osmolarity

Question 65

Increase of what plasma solute will have no effect on ADH production

Answer 65

Urea

Question 66

How will glucose, alcohol/ethanol and potassium plasma concentrations affect ADH secretion

Answer 66

Ethanol- inhibits ADH production and release and increases flow rate Glucose: inc ADH to take up more water? Potassium: inc ADH to take up more water?

Question 67

One patient is given a thiazide diuretic, and one a loop diuretic, which one will have a higher urine osmolality

Answer 67

One with the loop diuretic will have a lower urine osmolality because loop diuretics take up Cl, K and Na, but thiazide diuretics only take up Na and Ca urine osmolarity : one with a loop diuretic will have Na, K and Cl still in urine as blocked uptake, thiazide will mean Na and Calcium is in the urine

Question 68

Why does potassium not have much of an effect on water reuptake

Answer 68

Amount of potassium in the plasma and extracellular is much lower so less likely to have and effect on water balance

Question 69

What are the four main functions of the kidney

Answer 69

Homeostatic function : electrolyte, acid-base and volume Excretory function: nitrogenous waste, hormones, peptides, salt and water Endocrine function: Erythropoeitin is made in kidney stimulates RBC to be made. Has 1-alpha-hydroxylase vitamin D which activates vitamin D Glucose metabolism: gluconeogenesis and insulin clearance

Question 70

How does kidney failure affect function

Answer 70

Homeostatic: higher potassium as cant be excreted, lower bicarbonate (not taken up), more acidic blood, higher phosphate in blood, salt and water imbalance Excretory: wont excrete urea, creatinine so higher in blood, will have a decreased insulin requirement as wont excrete it effectively Endocrine function: No EPO so lowers calcium and causes anaemia, PTH will increase as trying to stimulate vitamin D to become active but the kidney cant produce the enzyme required Glucose metabolism: insulin not cleared, and glucose not made Increased cardiovascular risk

Question 71

Why do kidney failure patients become tachypneic even with normal oxygen stats ad no lung problems

Answer 71

Kussmaul respiration: have an acidosis as not clearing H+, so clear it by breathing fastedr

Question 72

How will kidney failure affect : urea, creatinine, sodium, potassium and haemoglobin

Answer 72

Urea, creatinine and potassium will rise Haemoglobin and sodium will fall

Question 73

How will kidney failure affect : pH, pCO2, pO2, Bicarbonate and base excess

Answer 73

High pH low pCO2 high pO2 low bicarbonate low base excess

Question 74

What are the symptoms of a tubulointerstitial disorder

Answer 74

Lethargy, weakness, anorexia, volume depleted resulting in hypotension: loss of CRT and skin turgor as dehydrated. High plasma urea and creatine High K+, low Na+, acidosis and anaemia On ultrasound will see two shrunken kidneys

Question 75

How will the appearance of the kidneys on ultrasound differ between acute kidney failure, chronic kidney failure, Kidney failure due to diabetes or polycystic kidneys

Answer 75

Acute: kidney size wont be affected Chronic: small kidneys Due to diabetes/myeloma/amyloid: kidney size preserved Polycystic kidneys: Large with cyct

Question 76

How will the appearance of the kidneys on ultrasound differ between acute kidney failure, chronic kidney failure, Kidney failure due to diabetes or polycystic kidneys

Answer 76

Acute: kidney size wont be affected Chronic: small kidneys Due to diabetes/myeloma/amyloid: kidney size preserved Polycystic kidneys: Large with cyct

Question 77

What are the symptoms of acute or chronic kidney failure

Answer 77

high blood pressure, high urea, VERY HIGH creatinine, sodium, potassium and Hb will be normal Kidney failure usually reduces salt and water secretion leading to hypertension, oedema and pulmonary oedema

Question 78

Why is serum sodium not a good indicator of total sodium

Answer 78

May have a sodium concentration of 129 but severe oedema so they have extra ECF which would mean that if measured the actual sodium it would be much higher. Serum sodium is an indicator of ECF

Question 79

Why does kidney failure cause acidosis and what does this lead to

Answer 79

reduces excretion of H+ leading to anorexia and muscel catabolism Potassium compensates for the high H+ concentration by moving H+ into the cell and K+ out. Leads to hyperkalaemia

Question 80

What are the causes of hyperkalaemia and the symptoms

Answer 80

Lower distal tubule potassium secretion and acidosis Symptoms: cardiac arrhythmias, neural and muscular activity, vomiting

Question 81

how does hyperkalaemia change ECGs

Answer 81

peaked T waves, broad p wave, QRS widening, eventually asystole

Question 82

How does kidney failure affect metabolism in detail

Answer 82

Low EPO so anaemia GFR drops so leads to phosphate retension. Low 1 alpha hydroxylase so leads to low levels of 1-25 vitamin D. Phosphate binds to calcium in the blood so hypocalcaemia. Lack of Vitamin D also leads to less calcium reabsorption from the gut, bone and urine Low calcium leads to seconday hyperparathyroisidm because they detect low calcium and increase PTH to try to increase. 1-25 Vit D also acts as a PTH suppressor so both stimulate PTH. Overtime glands get larger and larger

Question 83

What cardiovascular risks does kidney failure put the patient at risk of

Answer 83

Hypertension, Diabetes, Lipid abnormalities Inflma, Oxidative stree and brittle bone/other bone problems

Question 84

How is kidney failure managed

Answer 84

CORRECT VOLUME FIRST If hypovolaemic: fluids If hypervolaemic: diuretics/dialysis TREAT HYPERKALAEMIA sodium bicarbonate or insulin dextrose : both drive K+ into cells, which also corrects acidosis diuretics/dialysis: drives K+ out of the body potassium binders: gut absorption

Question 85

What is the long term management of kidney failure

Answer 85

Acute then treat that, it may be reversible If CKD: end stage risk assessment. eythropoeitin injections, diuretics to correct salt-water, phosphate binders, 1,24 Vit D supplement, haemodialysis, periotoneal dialysis transplant is best

Question 86

How is kidney failure risk calculated

Answer 86

Kidney failure risk equation, only use if STABLE CKD not if eGFR is rapidly declining

Question 87

What are the negatives of urea, creatinine and creatinine clearance being used to assess GFR

Answer 87

Urea: diet, catabolic state, GI bleeding, drugs all affect Creatinine: muscel mass, age, race, sex affects, only the trend is useful Creatinine Clearance: elderly patients struggle to collect sample, at low GFR it overestimates as some creatinine is always secreted

Question 88

What are the two dialysis methods

Answer 88

Haemodialysis: run the patients blood next to a semipermeable membrane which is next to a dialyzer. Fresh dialysate will run the opposite way to which the patients blood comes in, required dialysis centre visits, 3-4.5 hours 3 times per week, strict dietary constraints, needs access Periotoneal dialysis: run dialysis in the peritoneal cavity which is next to abdominal cavity. At home, 7 days a week, lesser meal constraints, can travel with the machine, can do any time but chance of infection

Question 89

What factors influence whether someone can be a kidney donor

Answer 89

Age, mental health, comorbidities, future pregnancy Has to have two healthy kidneys: normal sized, normal GFR, no blood or protein in the urine. Kidney match: have to have blood type compatibility, HLA typing and a serum crossmatch

Question 90

In kidney transplantation what happens to the native kidney

Answer 90

Transplanted kidney is in a different anatomical location to native kidneys as the native kidney remains inside

Question 91

After kidney transplant surgery what precautions should the patient take

Answer 91

take flu jabs and immunosuppressive medications (not tacrolimus tho) , avoid live vaccines, alcohol, NSAIDs, drugs, alcohol, smoking low salt and sugar diet, avoid raw eggs/meat and unpasturised cheese, seville oranges, earl grey tea, grapefruit, Psychiatric disorders, Cancer CVD and diabetes are all risk factors so : seek help, check skin and breasts, use suncream, measure BP, active lifestyle

Question 92

How does kidney cancer present

Answer 92

Painless haematuria (if pain could be a kidney stone or UTI) May feel loin pain, a palpable mass, get boney mets, haemoptysis

Question 93

What investigations should be done if (1) patient presents with painless haematuria (2) persistant non-visible haematuria (3) kidney cancer is suspected

Answer 93

If painless and visible haematuria: Flexible cytoscopy, CT urogram then assess renal function persistant non visible haematuria: flexible cytoscopy, US of kidney ureter and bladder Kidney cancer: CT renal, staging chest CT, bone scan if symptomatic for bony mets same investigations for bladder and kidney cancer

Question 94

How is kidney cancer staged and graded

Answer 94

t1 smaller or euqal to 7cm, t2 over 7cm, t3 out kindey but not the fascia or adrenal, t4 beyond n1- met in one lymph node m1 distant Fuhrman grade: 1well differentiated ,2, 3+4 poorly

Question 95

How is kidney cancer managed

Answer 95

Partial nephrectomy - T1 tumours, one kidney Radial Nephrectomy Cryosurgery: if small tumours and unfit for surgery Receptor Tyrosine Kinase Inhibitors: mets

Question 96

What can cause kidney cancer

Answer 96

smoking, obesity, dialysis, high BP, genetics

Question 97

How would bladder cancer present

Answer 97

Painless haematuria, may get: suprapubic pain, UTI symptoms, mets- bone, swelling

Question 98

How is bladder cancer treated

Answer 98

cytoscopy and transurethral resection of the bladder lesion, cut out the tumour and test: can be curative

Question 99

How is bladder cancer managed

Answer 99

Non muscle invasive: if low grade cancer cells looking liek theyll grow then cystoscopic survaellence of intravesicula chemo. If invades the muscles: cystectomy, radiotherapy, chemo, palliative

Question 100

What are the risk factors for prostate cancer

Answer 100

Age, western-esp scandinavian, african americans

Question 101

How is prostate cancer investigated

Answer 101

asymptomatic so by chance as a met or in a screening exam Blood tests: PSA may be raised, but UTI, prostatitis can also cause MRI: image look at volume and PSA density Trans perineal prostate biopsy

Question 102

How is prostate cancer managed

Answer 102

Dependent on grade and comorbidities if young/fit: low grade would surveillance, high grade do radiotherapy/ radical prostatectomy Monitor PSA after every 6 months for both, should be undetectable, if over 0.2 then relapse if old/unfit and high grade then hormone therapy, if low grade just wait

Question 103

What risks does prostatectomy have?

Answer 103

removes proximal urethral sphincter and changes urethral length so urinary incontinence and bladder function affected may damage cavernous nerves which cause erectile dysfunction

Question 104

If painless visible haematuria what investigation

Answer 104

Cytoscopy and imaging

Question 105

What are the serum tumour markers for testicular cancer

Answer 105

1- Alpha-fetoprotein AFP: half life 4.5 days, high in pations with yolk sac component within a teratomatous germ cell tumour 2- Beta subunit of human chorionic gonadotrophin HCG: placental syncitiotrophoblastic cells secrete, half life of 1-1.5 days, elevated in germ cell tumours with syncitiotrophoblast cells 3- lactate dehydrogenase: general tumour marker

Question 106

How to manage suspected testicular cancer

Answer 106

Testicular ultrasound biopsy serum tumour markers

Question 107

How is testicular cancer diagnosed

Answer 107

serum tumour markers CT Testes ultrasound

Question 108

one possible treatment for testicular cancer

Answer 108

Radical orchidectomy

Question 109

What are the symptoms of penile cancer

Answer 109

Difficulty/pain on retracing foreskin spraying of stream

Question 110

If a patient had a prostatectomy and is experiencing bladder incontinence what is the treatment

Answer 110

building the pelvic floor muscles or artificial urinary sphincter device

Question 111

If a patient had a prostatectomy and is experiencing erectile dysfunction

Answer 111

PDE5 inhibitors, prostaglanding E1 injections and penile prosthesis devices

Question 112

What are the markers of a UTI on a blood test

Answer 112

nitrate and leukocyte positive

Question 113

Where do the left and right ureters drain in a female

Answer 113

left into para aortic nodes, right into right paracaval and interaortocaval lymph nodes

Question 114

What is the blood supply of the bladder

Answer 114

superior and inferior branches of internal iliac artery

Question 115

What is the difference between female and male venous drainage of the bladder

Answer 115

Female: vesical plexus into internal iliac vein Male: prstatic venous plexus into internal iliac

Question 116

Describe the process of micturition

Answer 116

start: when bladder is empties the stretch fibres are inactivated, T11-L2 sympathetic nervous system is stimulated and activates Beta3 receptors through release of NA to relax detrusor muscle filling phase: bladder fills and distends, no intravesical pressure. urethral sphincter contracts to close urethra. voiding: Bladder filling activates M3 receptors of parasympathetic S2-S3, will release ACh to bind and activate M3 receptors to inhibit internal urethral sphincter to relax it and open. Also causes detrusor to contract : bladder contracts and expels urine, internal urethral sphincter relaxes

Question 117

What types of urinary incontinence are there

Answer 117

Stress urinary incontinence: leakage in effort or exertion (sneeze or cough). Due to impaired bladder and urethral support, impaired urethral closure Overactive bladder- Urge urinary incontinence: urinary urgency, frequency and nocturia, with or without incontinence. Due to involuntary detrusor muscel contractions, Overflow incontinence: so full leaks, chronic retention due to obstruction or atonic bladder like underactive detrusor, bladder denervation, bladder neck stricture, faecal obstruction Continuous incontinence: leak all the time, vesicovaginal fistula, ectopic ureter Funtional incontinence: cognitive impairment or mobility limitation preventing use of toilet, bladder is normal just cant get to bathroom

Question 118

What are risk factors of stress urinary incontinence

Answer 118

ageing, obesity, smoking, pregnancy, delivery route

Question 119

How is stress urinary incontinence investigated

Answer 119

History and stress test urodynamics- urinary leakage during inc in intrabdominal pressure

Question 120

How is stress urinary incontinence managed

Answer 120

Physio or surgical mid urethral sling, periurethral bulking if due to sphincter

Question 121

What are risk factors of urge urinary incontinence

Answer 121

Age, prolapse, high BMI, IBS, bladder irritants like caffiene or nicotine

Question 122

What are the symptoms of urge urinary incontinence

Answer 122

urgency, frequency, nocturia, imapcts quality of sleep so anxiety and depression possible men would have large prostate (bladder outflow obstruction) women would have prolapse

Question 123

What are the investigations fo an overactive bladder

Answer 123

Dipstick (as may be infection) Voiding diary Asses post void residual via US scan urodynamics cystoscopy

Question 124

How is an overactive bladder managed

Answer 124

Lifestyle: less coffee or nicotine retrain bladder with physio Antimuscarinic drugs (M3 blocked so detrusor doesnt contract) Beta 3 agonist (keeps detrusor relaxed BOTOX in detrusor stops ACh release to make detrusor contract cystoplasty (make bladder bigger with bowel), urinary diversion

Question 125

What is benign prostatic hyperplasia

Answer 125

non malignant growth of prostate, UTI symptoms as will compress ureter and stop bladder outflow, usually older people Testosterone affecting prostate tissue is a risk factor

Question 126

What are the symptoms of benign prostatic hyperplasia

Answer 126

hesistancy of urination poor stream dribbling after micturition nocturia, high frequency acute retention

Question 127

What causes should be excluded if present with urination hesitancy, poor stream, nocturia etc

Answer 127

Bladder or prostate cancer Cauda equine High pressure chronic retention then : infections, prostatitis, neurogenic bladder, urinary stones

Question 128

How is benign prostatic hyperplasia investigated

Answer 128

urine dip, voidal diary, post void residual PSA antigen from bloods to predict prostate volume US of renal tracts urodynamics cytoscopy if think cancer

Question 129

How is benign prostatic hyperplasia managed and thr complications

Answer 129

weight loss, less caffiene and nicotine in evening alpha blocker alpha 1-AR is on prostate smooth muscle and bladder neck. Block to relax so can pee 5- alpha reductase inhibitor stops testosterone being converted to DHT which enlarges prostate, shrinks prostate to improve urinary flow transurethral resection of prostate (take some out) complications: progressive bladder distention, chronic painless retention and overflow incontinence. can lead to bilateral upper tract obstruction and renal impairment - renal disease