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Year 2 - Semester 2 > Renal - Week 1 > Flashcards

Renal - Week 1 Flashcards

1
Q

what are the functions of the liver

A
  • Filtration of blood
  • Detoxification (incl drugs)
  • Regulate blood pressure
  • Regulation of blood pH
  • Regulation of haematopoiesis
  • Making vitamin D
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2
Q

are the kidneys peritoneal or retroperitoneal?

A

retroperitoneal

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3
Q

which kidney is higher up

A

left due to the liver on the right

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4
Q

how much of the cardiac output goes to the liver

A

20%

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5
Q

what happens if you restrict afferent arteriole?

A
  • Blood pressure in capillaries drops

* Filtration rate drops

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6
Q

what happens if you restrict efferent arteriole?

A
  • Blood pressure in glomerular capillaries rises

* Filtration rate rises

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7
Q

what is the slit diaphragm?

A

the filter made of cells which get very close to one another and then connecting to each other with protein structures which leave a tiny gap
Only 3% is slit and the rest is diaphragm so this is a big resistance to fluid flow

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8
Q

why does the kidney need pressure from the heart?

A

to oppose osmosis (once the blood is filtered the water wants to dilute the unfiltered blood)

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9
Q

describe anticlogging in the kidney

A

• Pinocytosis of trapped proteins
o Vesicles which take proteins into the cell and either export them or break them down with lysosomes
o There is a LOT of this going on

• This only works for things small enough to pinocytose
o Big protein aggregates, bacteria, platelets can cause a problem
o For these there are fenestrae on the endothelial cells which let large proteins get to the basement membrane of the cell (the glomerular basement membrane)
o The GBM forms a finer filter but not as fine as the slit diaphragm

  • The fenestrae are cleaned by blood flow and phagocytes
  • The GBM is renewed by mesangial cells
  • And the slit diaphragm is cleaned by pinocytosis by podocytes
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10
Q

describe plasma flow to the kidney

A

Blood flow to the kidneys is about 1.2L/min
Plasma flow to kidneys is about 0.66L/min
Rate of filtration through glomeruli = 0.13l/min
~20% of plasma is removed as filtrate

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11
Q

what structural properties does the proximal tubule have

A

microvilli

tight junctions between cells are more leaky than other cells – some ions can get past them

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12
Q

what do nephron epithelia have to recover

A
  • Na+
  • K+
  • Ca2+
  • Mg2+
  • Cl-
  • HCO3-
  • PO42-
  • H2O
  • Amino acids
  • Glucose
  • Proteins
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13
Q

what channels do we have to recover things

A
  • Primary active transporter - Na/K ATPase, H ATPase
  • Solute carrier family – SLC proteins – about 300 – many are co-transporters powered by established conc gradients (“secondary active transporters”)
  • Aquaporins (water channels NOT pumps)
  • Ion channels
  • Protein endocytosis receptors
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14
Q

what is required to move things from the filtrate to the plasma

A

ATP – lots of mitochondria in the kidney cells

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15
Q

what are some channels involving sodium

A

Na/K ATPase sends 3 Na out for 2 K in which uses ATP.

There is an SLC which moves one proton out for one Na in – does NOT use ATP

Another SLC brings a Na and a Cl into the cell

Another co-transports one Na, one K and two Cl into the cell

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16
Q

how does K move out of the cell

A

There are regulatable K channels which can leak K out of the cells so they can be co-transported back in

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17
Q

how can amino acids be transported

A

Some channels bring in Na, 2 Cl and a particular type of amino acids – different channels for different amino acids

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18
Q

how is glucose transported

A

Glucose can be brought in along with Na - one channel needs one Na and another needs 2 but is better at bringing in Glucose from a low concentration

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19
Q

what happens to glucose in diabetes

A

there is excessive amount of glucose in the blood and therefore primary filtrate – the cells cannot reabsorb all of it and therefore it is excreted

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20
Q

describe OCTs

A

Organic Cation Transporters

can pump cations out of the cell in exchange for protons, pump them out at the cost of ATP (multiple drug resistance – chemotherapy agents being pumped out) or allow cations in

The cytoplasmic cation concentration should never exceed that of the plasma

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21
Q

describe OATs

A

Anions, on the other hand, push in and drift out
Alpha ketoglutarate moves in along with Na and then an OAT antiporter transports alpha ketoglutarate out in exchange for anions. Passive channels on the apical side to allow them out.
This is dangerous as if there is an organic anion which is toxic and does not have an efficient passive channel then there can be high concentrations in the cell. This is often the cause of drugs damaging kidney cells – methotrexate, furosemide and penicillin
Probenecid stops the OAT uptake, allowing penicillin to stay in circulation and not be excreted rapidly like normal

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22
Q

describe bicarbonate uptake

A

we have the SLC which pumps protons out for Na in. The proton can combine with any bicarbonate to make carbonic acid which can be hydrolysed by carbonic anhydrase to make water and CO2 which can cross the membrane. Once in the cell, carbonic anhydrase will turn it back into carbonic acid which will naturally dissociate into a proton and bicarbonate. Another SLC can then transport it back into the body from the cell along with a Na. this takes up bicarbonate without messing up body pH – no net loss of bicarbonate or H.

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23
Q

what happens to H in acidosis

A

If there are remaining protons but no bicarbonate (acidosis), the protons combine with hydrogen phosphate and leave the body as H2PO4. This DOES effect acid base balance as it results in a net loss of protons
Ammonia can also take up protons and be excreted as ammonium – net secretion of H. ammonia comes from the catabolism of glutamine. This not only leads to H excreted but also generates bicarbonate which can enter the body so very powerful at restoring acid base balance.

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24
Q

what are type A and B cells

A

The H ATPase expels H from the cell and there is also a transporter which takes up K and expels H from the cell – type A cell
Type B cell has the same H ATPase but on the basal side not the apical side. Bicarbonate goes out into the urine in exchange for Cl and H gets pumped into the body – corrects alkalosis

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25
Q

how can Ca move

A

The leaky tight junctions allow for Ca to move into the plasma if its concentration gets too high in the urine

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26
Q

how is water taken up

A

recovered passively through aquaporins

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27
Q

how can proteins be taken up

A

Proximal tubule cells take up proteins via receptors such as Megalin – endocytosis

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28
Q

how is phosphate taken up

A

recovered along with one Na and then actively exported from the cell into the basal side.

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29
Q

what is the primary filtrate like as it leaves the renal corpuscle

A

iso-osmotic to the plasma and has approximately the same concentration of small molecules

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30
Q

what happens in the proximal tubule

A
  • A lot of sodium recovered. – through basal pump
  • Glucose, amino acids etc are pulled through by sodium conc gradient
  • Chloride, phosphate pulled through by sodium gradient
  • Potassium pushed in at basal side by Na/K ATPase and can be pushed out or brought in at apical side
  • HCO3 is recovered and H cycled, powered by the Na gradient
  • All of this solute movement would lower the osmolarity of the tubule if water didn’t also flow passively from the tubule to counteract this
  • Chloride also leaves passively to stop its conc increasing in the tubule
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31
Q

what is the structure of the proximal tubule to achieve all its functions

A

a lot of surface area from villi and packing a long length into a small space

32
Q

what has been achieved once the filtrate leaves the proximal tubule

A
  • 65% of calcium, sodium, chloride and phosphate recovery and more of glucose
  • Recovery of some water
  • No concentration of the urine
  • No control of acid/base
33
Q

what creates the hypertonic area in the medulla

A

only proximal tubule has leaky tight junctions
descending thin limb allows water out but not ions
this makes the ion conc increase in the filtrate

on the ascending thin limb, water is not allowed out but ions are, making the ion conc in the plasma increase and pulling more water out from the descending limb

then in the ascending thick limb, ions are actively recovered,

This mechanism recovers about 10% of water and 25% of NaCl, giving a total of 75% of water an 90% of Na, Cl

34
Q

how is the high osmolarity of the medulla maintained

A

All the loops of henle being in the medulla stops the high osmolarity of the area being washed away by capillaries etc
The anatomy of the capillaries also helps. The capillary comes down alongside the ascending limb where water is drawn out of it and ions enter, and as it ascends alongside the descending thin limb it gains back the water and loses ions. This isolates the osmotic environment of the cortex from the environment of the medulla

35
Q

what has been recovered by the start of the collecting duct?

A

In the distal tubule there is more recovery of salt but no water transport which dilutes the urine even further. At the start of collecting ducts, 75% of water recovered and 95% of Na, Cl.

36
Q

what happens in the collecting duct?

A

The collecting duct (full of dilute urine) flows through the hypertonic zone in the medulla to the renal pelvis. – up to 24% of the water in the dilute urine can be drawn out into the hypertonic plasma concentrations. More (2-5%) of NaCl recovered in collecting duct

37
Q

what regulates the water reabsorption in the collecting duct

A

Water does not necessarily all want to be reabsorbed which is regulated by changing the numbers of aquaporins in the membrane. When they are not on the membrane they are in vesicles which is regulated by vasopressin

38
Q

how is urea reabsorbed

A

The duct can also choose to leak urea back into the plasma – again regulated by vasopressin

39
Q

how many times does the filtrate go through the loop of Henle?

A

3x

40
Q

what does the countercurrent exchange of oxygen mean

A

much of the oxygen gets shunted from the arteries to veins before it reaches the capillaries.

this makes the kidneys especially sensitive to ischaemia

41
Q

whats happens in low renal oxygen?

A

erythropoietin release which causes more red blood cells to be made in the bone marrow

42
Q

what can be done to control pressure in the kidney

A

Between about 80-180mmHg the kidneys can hold a constant flow rate
Mechanisms which control this pressure include:
• Stretch activated cation channels depolarize the membrane and cause smooth muscle to contract: fast and protective against acute surges – the myogenic mechanism
• Monitoring the performance of the nephron – tubuloglomerular feedback
o We need this control nephron by nephron
 The end of the distal tubule makes “kissing contact” with the arterioles entering the glomerulus
 This zone is the macula densa and together with the cells they influence they are the juxtaglomerular apparatus

43
Q

what happens in elevated glomerular blood pressure?

A

filtrate flows faster
less time for solute recovery
more NaCl remains in distal tubule
macula densa cells pump out more than usual
juxtaglomerular cells release adenosine
afferent arteriole restricts in response to this

44
Q

what happens when macula densa cells are not pumping out lots of NaCl

A

renin is released by juxtaglomerular cells.

this is because the lack of NaCl in the distal tubule could be due to low blood pressure

if macula densa cells are pumping enough NaCl, they inhibit renin release

45
Q

what does angiotensin II act on

A

angiotensin receptors on the kidney cells which increase the activity of the proton sodium antiporter (Na in, protons out).

Angiotensin 2 also acts on the adrenal gland which produces aldosterone.
Aldosterone has two functions here:
• Acts on the gene transcription of the H ATPase in alpha-intercalated cells in the collecting ducts which pumps protons out
• Acts on the transcription of a gene which codes for ASC (amiloride sensitive channel) in principal cells in the collecting duct which allows for the recovery of Na

Also acts on the pituitary gland which produces AVP – Arginine Vasopressin – causes aquaporins to be moved into the cell membrane from storage vesicles.

All of this has a positive effect on water and salt retention and increases blood pressure and therefore juxtaglomerular perfusion

46
Q

what does ANP do

A

atrial naturietic peptide from the heart blocks the Na reuptake channel in collecting ducts and causes more sodium loss

47
Q

what happens in low calcium

A
  • Parathyroid glands signal with parathyroid hormone
  • This has receptors on renal cells

o Distal convoluted tubule
 Increases activity of a Ca uptake channel
 This Ca is shuttled across the cell by calbindin – need vit D
 The export channel into the blood is also increased by parathyroid hormone – need vit D

o Proximal tubule
 Also blocks Phosphate/sodium symporter to prevent phosphate uptake
 This is because if you want lots of free calcium in the blood you don’t want phosphate mopping it up – makes insoluble calcium phosphate

48
Q

how is acid base controlled

A

• Removal of acid created by the oxidation of food
• If the pH inside the cell falls, apical Na/H exchangers become more active
o Protons excreted into urine

49
Q

where is most reabsorption done

A

For most substances, reabsorption happens early on in the kidney with little regulation. This is why most of the control is focused on the last 10%, usually in the collecting duct cells.

50
Q

what cells are in the collecting ducts

A 
•	Intercalated cells
o	Less common
o	Constantly reabsorb potassium
•	Principal cells
o	More common
o	Have a regulated excretion of potassium
51
Q

what happens in changes in potassium

A

If there is high tissue potassium, then there is a lot to flow into the cells and then out into the urine

If you give animals low potassium diets, the regulated principal cell channels are removed from the membrane to lose less potassium into the urine
The opposite is true for high potassium diets

52
Q

what happens in alkalosis

A

• H out-pumping by intercalated cells reduced
o Therefore less potassium re-uptake
• The apical K channel activity in principal cells is also increased which is very unhelpful
o More K loss
• This causes hypokalaemia

53
Q

what happens in acute acidosis

A

H out-pumping by intercalated cells increased
o Therefore more potassium re-uptake
• Principal cells less active so K secretion falls
• Hyperkalaemia
• In chronic acidosis Na pump less efficient in proximal convoluted tubule so urine more copious and helps flush K away

54
Q

describe loop diuretics

A

 furosemide
 bumetanide

  • Block the SLC which moves Na, 2 Cl and K into the cell
  • Prevents salt recovery in the loop of henle
  • This prevents water recovery
  • Increase fluid excretion to 20% from about 0.4%
  • They result in the loss of Na, K and Cl
  • They can result in hypercalcuria – less pull for Ca recovery – kidney stones
  • More Na getting to collecting ducts means more uptake there and more K loss
  • The main effect on BP is NOT fluid loss (the patient will just drink more) but to keep NaCl in the distal tubule. This will make the macula densa cells pump out more NaCl which prevents the production of renin – lowering BP

25% of Na and Cl ions

• Indications
o Heart failure – acute and chronic
o Renal failure - including nephrotic syndrome
o Liver cirrhosis with ascites

• Adverse effects
o Hyponatraemia, Hypokalaemia, Metabolic alkalosis
o Fluid depletion – dehydration, hypovolaemia, Incontinence
o Ototoxicity

Loop diuretics have higher natriuretic efficacy than thiazides. However, thiazides require lower doses so are more potent

55
Q

describe thiazides

A

 Bendroflumethiazide
 Hydrochlorothiazide

thiazide like
 Chlortalidone
 Indapamide

  • Very powerful – often a good idea to prescribe something else if poss
  • Operate in the distal tubule
  • Block sodium and chlorine co transporter

5-10% of NaCl

• Indications
o Hypertension

• Adverse effects
o Hypokalaemia, hyponatraemia, hypomagnesaemia, alkalosis
o Hyperuricaemia, hyperglycaemia
o Fluid depletion, incontinence, erectile dysfunction

56
Q

describe potassium sparing diuretics

A

o Aldosterone receptor antagonists:
 Spironolactone
 eplerenone

o Sodium channel blockers:
 Amiloride
 Triamterene

  • Act on collecting duct cells on the amiloride sensitive channel – blocks sodium reuptake
  • This reduces the action of Na/K ATPase which in turn prevents K being pumped into the cell and then into the urine

inhibit 2-3% of Na reabsorption

• Indications
o Chronic heart failure, liver failure with ascites, primary hyperaldosteronism (Conn’s syndrome), resistant hypertension
o Combined with loop and thiazide diuretics to reduce risk of hypokalaemia

• Oral dosage

• Adverse effects
o Hyperkalaemia – potentially fatal - no potassium supplements
o Must have plasma electrolytes, urea and creatinine monitored regularly
o Can causes gynecomastia, testicular atrophy and menstrual disorders

57
Q

describe spironolactone

A
  • Interferes with the signalling of aldosterone
  • Aldosterone increases production of amiloride sensitive channel
  • So blocking it reduces sodium uptake
  • This reduces the action of Na/K ATPase which in turn prevents K being pumped into the cell and then into the urine
  • Also antiandrogenic – can lead to gynaecomastia
58
Q

describe carbonic anhydrase inhibitors

A

 Acetazolamide
• More bicarbonate in the lumen
• Water does not follow the solutes
• More water excreted

 Reduces production of hydrogen and bicarbonate ions which are responsible for some of the reabsorption of sodium and chloride in the proximal convoluted tubule

• Indications
o Glaucoma
o Altitude sickness

• Adverse effects
o Metabolic acidosis
o Can be rashes and interstitial nephritis

59
Q

describe osmotic agents e.g. mannitol

A

• Stay in lumen and resist water egress osmotically
o Also stops Na, Cl, and K reabsorption
• Indications
o Raised intracranial pressure due to cerebral oedema
o Raised intra-ocular pressure

• IV administration

• Adverse effects
o Initial fluid overload
o Hypernatraemia

• Care needs to be taken in patients with uncontrolled diabetes, where glucose also acts as an osmotic drag into the lumen

60
Q

what can happen in diabetes

A

Very high plasma glucose can exceed recovery capacity and keep water in the lumen, water lost so thirst but Na not lost as much – can lead to hypernatraemia

61
Q

what do we call an upper urinary tract infection

A

pyelonephritis

62
Q

what do we call an lower urinary tract infection

A

cystitis

63
Q

who gets uncomplicated UTIs

A
  • Females
  • Those with previous UTI
  • Sexually active
  • Vaginal infection
  • Diabetes
  • Obesity
  • Genetic susceptibility

• Older age
o Oestrogen deficiency
o Cognitive impairment

64
Q

who gets complicated UTIs

A
  • Urinary obstruction e.g. prolapse, prostatic enlargement
  • Urinary retention – neurological diseases
  • Immunosuppression
  • Renal failure
  • Renal transplantation
  • Pregnancy

• Foreign bodies e.g. catheters or other drainage devices
o THESE ARE THE MOST COMMON CAUSE OF SECONDARY BLOODSTREAM INFECTIONS

65
Q

what causes UTIs

A
  • E. coli - 75% uncomplicated and 65% complicated
  • K. pneumoniae
  • Enterococcus spp.
  • Staph saprophyticus
66
Q

what can happen once bacteria are in the urinary tract

A

Can invade bladder wall with type 1 pilli
Multiply to form intracellular bacterial communities (IBC)
These exfoliate or bury deeper into the wall to form quiescent intracellular reservoirs (QIR

67
Q

what are host factors in the urinary tract

A
  • Extremes of osmolarity
  • Low pH and high urea concentration
  • Urine flow
  • Urinary tract mucosa – bactericidal activity, cytokines
  • Urinary inhibitors of bacterial adherence – Tamm-horsefall protein
  • Inflammatory response
68
Q

where can UTIs come from

A
  • From the gut
  • Intracellular bacterial communities/QIRs
  • Hematogenous – rare
69
Q

what is an infection of the urethra called

A

Urethritis

70
Q

what infections can men get

A

Prostatitis

Epididymo-orchitis

71
Q

what can UTIs lead to

A
  • Bacteraemia common in pyelonephritis
  • Perinephric abscesses
  • Can rarely lead to remote, deep seated infection
72
Q

what is the presentation in UTIs

A 
•	Cystitis
o	Dysuria
o	Frequency
o	 Suprapubic tenderness
o	Urgency

• Pyelonephritis
o Loin pain/flank tenderness
o Fever/rigors
o Sepsis

73
Q

how do you diagnose UTIs

A 
•	Dipstick only under 65s – often have harmless bacteria in the urine	
o	Indicate a possible diagnosis
•	Urine culture
o	Midstream urine culture
o	Clean catch urine 
o	Catheter sample urine – FROM THE PORT NOT THE BAG
o	Others – urostomy, cystoscopy, pad
•	Generally significant if >105 CFU/ml
74
Q

what is important to note about the use of antibiotics in UTI

A

Use of antibiotics for UTIs without diagnosis can limit treatment further on

Cystitis is self limiting so antibiotics are only to ameliorate symptoms
Antimicrobial use increases risk of recurrent UTIs and antimicrobial resistance
E coli has 60-70% amoxicillin resistance and 30% trimethoprim resistance
Some organisms only have IV options

Only give IV antibiotics AFTER a blood culture – Gentamycin

75
Q

what are special cases in UTIs

A

• Men – prostate involvement – requires longer treatment and certain antibiotics to penetrate prostate
• Pregnant women – certain Abx contra-indicated
o Treat asymptomatic bacteriuria as it can lead to pyelonephritis which can lead to pre-term labour
• Children – all with confirmed UTI need investigation for vesico-ureteric reflux

Year 2 - Semester 2 (8 decks)

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