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Renal Flashcards

1
Q

How much filtrate does the kidney produce each day?

A

150 litres

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2
Q

the kidneys require what % of the cardiac output?

A

20%

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3
Q

the nephron is composed of what major parts?

A

renal corpuscle and the tubule (but not the collecting duct)

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4
Q

the renal corpuscle is composed of what major parts?

A

the glomerulus and the bowmans capsule

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5
Q

the glomerulus is made up of what?

A

capilaries and podocytes plus the BM

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6
Q

the kidneys lie is what position in the abdominal cavity?

A

the kidneys are retroperitoneal

they lie approx T12 - L3 with the left slightly higher, more narrow and closer to the midline

10-11 cms long,

6cm wide,

3cm deep 1

50g in weight each

1.2 million nephrons each

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7
Q

what nerves innervate the kidneys?

A

the splanchic nerve and the aortic plexus

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8
Q

how long are the ureters?

A

25-30 cms long about 3mm in diameter

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9
Q

what vasculature supplies the ureters?

A

Proximal - renal arteries

middle - branches of the aorta, ovarian/testes arteries

distal - common and internal illiac arteries

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10
Q

what innervates the ureters?

A

several plexus from surrounding vasculature. sympathetic from T10-L1

parasympathetic from S2-S4

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11
Q

what makes up the juxtoglomerular aparatus

A

granular cells - release renin

macula densa - detect NaCl - release PGE’s to stim renin release

mesangial cells

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12
Q

Describe the gomerular basement membrane and what it does?

A

The GBM is a non-cellular three layered structure which restricts the passage of medium to large neg chanrged anions (eg albumin)

it is composed of glycogen and collagen

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13
Q

describe podocytes structure and function

A

Podocyte makes up the visceral layer of the bowmans capsule prevents the passage of RBC and plasma proteins/platelets

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14
Q

What are granular cells?

A

specialised smooth muscle cells in the media of the AFFERENT arteriole

Release renin upon sympathetic stimulation, plus stimulation from PGE’s from macula densa

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15
Q

Which has the most control when it comes to BP regulation, baro or osm receptors?

A

Baro overrides osmo

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16
Q

What are the main factors that balance sodium levels?

A

GFR - ↑ GFR = ↑ Na delivered = ↑ loss in urine

Pressure naturesis - ↑ pressure transmitted across interstitium = ↑ Na excretion = ↑ urine output = ↓ BP

ANP - released by cardiac myocytes due to stretching = ↑ Eff resistance, ↓ Aff resistance = ↑ GFR, ↓ Na reab, ↓ renin release.

RAAS

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17
Q

How do nsaids effects the kidney?

A

Decrease PG release from macula densa = ↓ renin production from granular cells.

Plus the shift to the AA pathway away from PGE production = more leukotrienes = vasoconstriction

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18
Q

What is the triple whammy when it comes to renal failure?

A

ACE’s

nsaids

diuretics/dehydration

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19
Q

State in % the sodium reabsorption through the nephron

A

PCT 65%

LoH 25%

DCT 5%

CD 3%

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20
Q

State in % the bicarb reabsorption through the nephron

A

PCT 80-90% by facilitated diffusion

LoH 10-20%

CD - the intercalated cells can reabsorb if required

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21
Q

State in % the urea reabsorption through the nephron

A

PCT 50% by diffusion but can also be secreted

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22
Q

How and how much of organic molecules (glucose, AA’s) are reabsorbed in the PCT?

A

100% in PCT by Na/X symporters

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23
Q

State in % the potassium reabsorption through the nephron

A

PCT 65%

LoH 20-25%

CD + intercalated cells can reabsorb + principal cells can secrete

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24
Q

State in % the chloride reabsorption through the nephron

A

PCT 50% by diffusion

LoH 35%

DCT 5%

CD principal cells can reabsorb

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25
state the pH equation
26
20% of CO = what in mL per minute?
1000 mL / min Haematocrit = 45% = renal plasma of 550 mL / min
27
The renal arteries branch from the aorta below what arteries?
Below the coeliac arteries and superior mesenteric
28
What do the renal arteries supply?
* suprarenal galnd * ureter * capsule * renal pelvis * peeri-renal area
29
state the capillary pressure and oncotic pressure in the glomerulus plus the pressure in the bowmans capsule
capillary pressure 61 mmHg oncotic pressure in caps 31 mmHg bowmans capsule 20 mmHg = net filtration pressure of 9 mmHg
30
what are the mechanisms behind autoregulation in the kidneys
* Myogenic reflex (short term) * Tubuloglomerular feeback * Neuronal control
31
what does the myogenic feedback cause?
* ↑ stretch = ↑ GFR - causes reflex constriction of AFF arteriole to reduce flow into glomerulus * or ↓ stretch = ↓ GFR = AFF dilation and EFF constriction to ↑ GFR
32
what happens in tubularglomerular feedback?
* ↑ GFR = ↑ tubular flow = ↓ NaCl reab is LoH = ↑ tubular levels of NaCL * Detected by macula densa * JGA release adenosine which binds to A1 receptors * = AFF constriction = ↓ GFR * + adenosine = ↑ PCT Na reabsorption
33
Describe the various aspects of neuronal control of renal blood flow
* Normal conditions = little sympathetic stim * Modertate sympathetic stim = both AFF and EFF stimulated * Stong sympathetic stim = AFF constricts to ↓ GFR Nerves arrise from coeliac plexus and act via alpha adrenergic receptors
34
What does ANP do and where?
* released by cardiac myocytes - ANP atrial, BNP ventricle * Causes VC of EFF and dilates AFF * relaxes mesangial cells * inhibits aldosterone and renin * ↑ flow in vasa recta which ↓ medullary osmolarity causing ↓ H2O reab in the LoH * Blocks the Na channel in the apical cell of the CD
35
What pathways cause a reduction in GFR?
* Autoregulation via: * myogenic reflex * tubuloglomerular feedback * Neuronal NE release - constricts AFF * Ang II - contricts AFF
36
what is the difference between osmolality and osmolarity?
osmoLALITY = lead = Kg's osmolaRITY = runny = litres
37
what is the daily solute excess excreted by the kidneys?
1200 mOsm/day
38
Where is ADH produced, in response to what, and what does it do?
* produced in the **supraoptic and paraventricular** nucleus of the **hypothalamus** * stored in granules in the **posterior pituitary** * released when plasma osmolality **\>285 mOsm/Kg** * binds to basolateral V2 receptors in the CD, causing: * activation adenylyl cyclase * ↑ cAMP * activation protein kinase A * ↑ insertion of AQ2 in apical membrane to reab H2O * Increased gene transcription in nucleus to produce more AQ2's * causes 20x H2O reab in CD than normal
39
define acute renal failure
the acute loss of function in the renal parenchyma which can be reversed.
40
what signs and symptoms will you find in AKD?
* ↑ serum creatinine and urea * oliguria (\<500mL/day) * confusion * drowsiness * anorexia * nausea-vom
41
what are the causes of pre-renal AKD?
* hypovolaemia - dehydration, burns, vom-diarrhoea * ↓ CO * ↓ renal autoregulation/perfusion (thrombus, stenosis, venous or arterial)
42
If pre-renal AKD is not reversed, it can cause intrinsic AKD due to ischaemic damage. What else may cause this?
* nephrotoxic drugs * glomerular disease * arterial or veous blockage * sepsis * DIC * rhabdomyolysis all of which result in acute tubular necrosis
43
What are the three phases of intrinsic AKD?
* Initiation phase * Maintainance phase * recovery phase
44
what occurs in the initiation phase of intrinsic AKD?
* ischaemia * necrosis, epithelial sloughing - casts - can block the filtrate * back leakage of filtrate via the damaged epithelia * Ischaemia is worse in the PCT and LoH due to ATP dependant transport
45
what occurs in the maintainance phase of intrinsic AKD?
* over 1-2 weeks injury occurs * GFR remains low \<5mL/min * urine out v low even if reversed by fluid replacement due to * dysregulated release of vasoconstrictors * congested medullary blood vessels * reperfusion injury due to ROS
46
what occurs in the recovery phase of intrinsic AKD?
* tubular epithelial repair * GFR returns * complicated by a marked diuretic phase due to excretion of retained Na and H2O
47
what are the causes of post-renal AKD?
* ureter blockage - still have one remaining kidney unless bilateral or you only have one kidney * bladder neck blockage - prostatic disease * urethral blockage - calculi, clots, urethritis combined with spasm
48
what do type A intercalated cells control?
* A - active in ACIDOSIS * A - apical H+ secretion
49
what do type B intercalated cells do?
* B - basic * B - bicarb - secrete * B - basolateral H+ reabsorption
50
where does aldosterone act? what does it do?
* steroid hormone so no membrance receptor * intracellular receptor * increased production of ENaC - epithelial Na channel in apical membrance of CD * Increased insertion of Na/K/ATPase in BL membrane
51
How is EPO produced in the kidneys?
* ↓ O2 causes HIF1 (hypoxia inducable factor) to not be broken down * This combines with it Beta unit to induce EPO gene expression * EPO produced * Causes the inctreased production of RBCs and BFU and CFU level
52
In CKD what happens to EPO production?
* Interstitial fibrosis causes PT cells to reduce the production of HIF1 * This reduces the binding of the alpha and beta units = ↓ production of EPO * causes a normocytic normochromic anaemia
53
What is the GFR equation?
GFR = Kf x (P cap - P bow) - Onc cap * Kf reliant on surface area and permiability * a reduction of either = ↓ GRF
54
what is the Cockcroft-Gault equation for estimating GFR?
GFR = 140 - age x lean body weight (kg) / serum creatinine x 815 * for women multiply weight by .85
55
what is the renal plasma clearance equation which can be used to estimate GFR when looking at creatinine or inulin?
GFR = unine conc (mg/ml) x urine flow (ml/min) / plasma conc (mg/ml) * end unit is mL/min
56
Describe how calcium is handled in the kidneys
* extracellular Ca bound to proteins - not filtered in the kidneys * free Ca can be filtered * Ca reab is passive and paracellular - driven by Na gradient * PCT 70% * 20% in LoH * DCT driven by PTH - uses protein binding which is driven by Vit D
57
What happens in CKD in relation to vit D, phosphate and calcium?
* Kidneys normally activate Vit D which ↑ reab of Ca and phosphate from food * Vit D also provides neg feedback for PTH release * Renal failure = * loss neophrons = ↓ Vit D * ↓ Ca reb * ↓ phosphate excretion * = ↑ serum phosphate - binds to Ca * = ↑ PTH release * = ↑ Ca released from bones = ↑ risk fractures
58
Define CKD
* the presence of kidney damage (urininary albumin \>30mg/day), or haematuria, structural abnormalities or biopsy abnormalities or * decreased kidney function (eGFR \< 60mL/min) for *three months or more* irrespective of cause.
59
What are the risk factors for CKD, modifiable and non-modifiable
Modifiable * diabetes, HT, smoking, fatty fat fatty Non-modifiable * age (\>50 yrs), FHx CKD, indigenous, established CVD
60
what are the common causes of CKD?
* diabetes 36% * glomerulonephritis 19% * HT vascular disease 12% * PKD 5%
61
what are some symptoms of CKD?
* Anaemia * platelet abnoramlities - bleeding * skin - pruritis, pigmentation * renal oseodystrophy * CNS - confusion, coma, fits * CV - HT, atheroscleosis, PVD, uraemic pericarditis * GIT - anorexia, N & V, diarrhoea * Renal - polyuria, oedema * Endocrine - Amenorrhea, erectil dys, infertility
62
what are the complications of CKD?
* anaemia - due to ↓ EPO * Acidosis - metabolic - treat w bicarb * Hyperkalaemia * Renal ostoedystrophy and vascular calcification * infection risk * malnutrition - hyperalbuminuria * restless legs * sleep apnoea
63
when do you refer to a nephrologist?
* GFR \<30mL/min or \<45 if diabetic * GFR \< 60 + anaemia * persistent albuminuria ACR \>30mg/mmol * Sudden substantial ↓ GFR or sustained ↓ GFR * CKD with unmanageable HT
64
what are the stages of CKD?
1. GFR \>90 + haematuria and/or patho abnormalities 2. GFR 60-89 + haematuria and/or patho 3. a = GFR 45-59 3.b = 30-44 4. GFR 15 - 29 5. GFR \<15 all also dep on UCR (micro or macro albuminuria)
65
what is the pathophysiology of diabetic nephropathy?
* ↑ BGL = AFF dialtion = ↑ GFR - hyperfiltration * ↑ PCT Na reab = ↓ DCT flow = RAAS * ↑ BGL = mesangial injury via AGE/ROS = mesangial hypertrohophy and ↑ ECM * basement membrane thickens and gets leaky * ↑ glomerular pemiability = proetinuia = ↑ protein uptake in PCT = fibrosis * All = ↓ GFR
66
How does secondary hyperparathyroidism occur?
CKD = ↓ GFR = ↓ phosphate extrection = calcium binding with phosphate = ↓ serum Ca = ↑ PTH release + ↓ Vit D conversion = ↓ neg feedback to PT gland = ↑ PTH release unregulated
67
what is the target BP of people with CKD?
\< 130/80 mmHg
68
what happens in the kidneys with hypertension?
↑ BP = ↑ medial thickening of renal arteries = ↓ GFR = RAAS activation = ↑ blood volume = ↑ BP = glomerulosclerosis = nephron loss
69
Bladder innervation - at what levels of the spinal cord do the following occur. * Sympathetic * parasympathetic * somatic
* sympathetic - T10-L2 via the hypogastic nerve * relax bladder * excite urethra * parasympathetic - S2-S4. Post ganglionic fibres in detrusor and pelvix plexus * excites bladder * relax urethra * somatic - S2 - S4 via pudendal nerve * excites extrinsic sphrincter
70
What higher centres are involved in micturation?
* in adults pre-frontal cortex can inhibit the pontine micturation centre to prevent voiding. * can inhibit sacral preganglionic fibres preventing micturation * pontine MC shifts from storage to voiding phase, removing parasympathetic and somatic inhibition
71
Pathology in the nervous system, what symtoms may the following cause? * lesion above the brainstem * lesion below brainstem but above miturition centre * lesion below T12
* lesion above the brainstem * detrusor overactive - sphincters intact = freq and urgency * lesion below brainstem but above miturition centre * detrusor overactive - sphincters uncoordinated = poor emptying, overflow incontinence * lesion below T12 * flaccid bladder - overactive sphinters = urine retention

Med school (13 decks)

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