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Med school > Renal > Flashcards

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
Q

state the pH equation

A
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26
Q

20% of CO = what in mL per minute?

A

1000 mL / min

Haematocrit = 45% = renal plasma of 550 mL / min

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27
Q

The renal arteries branch from the aorta below what arteries?

A

Below the coeliac arteries and superior mesenteric

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28
Q

What do the renal arteries supply?

A
  • suprarenal galnd
  • ureter
  • capsule
  • renal pelvis
  • peeri-renal area
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29
Q

state the capillary pressure and oncotic pressure in the glomerulus plus the pressure in the bowmans capsule

A

capillary pressure 61 mmHg

oncotic pressure in caps 31 mmHg

bowmans capsule 20 mmHg

= net filtration pressure of 9 mmHg

30
Q

what are the mechanisms behind autoregulation in the kidneys

A
  • Myogenic reflex (short term)
  • Tubuloglomerular feeback
  • Neuronal control
31
Q

what does the myogenic feedback cause?

A
  • ↑ stretch = ↑ GFR - causes reflex constriction of AFF arteriole to reduce flow into glomerulus
  • or ↓ stretch = ↓ GFR = AFF dilation and EFF constriction to ↑ GFR
32
Q

what happens in tubularglomerular feedback?

A
  • ↑ 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
Q

Describe the various aspects of neuronal control of renal blood flow

A
  • 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
Q

What does ANP do and where?

A
  • 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
Q

What pathways cause a reduction in GFR?

A
  • Autoregulation via:
    • myogenic reflex
    • tubuloglomerular feedback
  • Neuronal NE release - constricts AFF
  • Ang II - contricts AFF
36
Q

what is the difference between osmolality and osmolarity?

A

osmoLALITY = lead = Kg’s

osmolaRITY = runny = litres

37
Q

what is the daily solute excess excreted by the kidneys?

A

1200 mOsm/day

38
Q

Where is ADH produced, in response to what, and what does it do?

A
  • 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
Q

define acute renal failure

A

the acute loss of function in the renal parenchyma which can be reversed.

40
Q

what signs and symptoms will you find in AKD?

A
  • ↑ serum creatinine and urea
  • oliguria (<500mL/day)
  • confusion
  • drowsiness
  • anorexia
  • nausea-vom
41
Q

what are the causes of pre-renal AKD?

A
  • hypovolaemia - dehydration, burns, vom-diarrhoea
  • ↓ CO
  • ↓ renal autoregulation/perfusion (thrombus, stenosis, venous or arterial)
42
Q

If pre-renal AKD is not reversed, it can cause intrinsic AKD due to ischaemic damage.

What else may cause this?

A
  • nephrotoxic drugs
  • glomerular disease
  • arterial or veous blockage
  • sepsis
  • DIC
  • rhabdomyolysis

all of which result in acute tubular necrosis

43
Q

What are the three phases of intrinsic AKD?

A
  • Initiation phase
  • Maintainance phase
  • recovery phase
44
Q

what occurs in the initiation phase of intrinsic AKD?

A
  • 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
Q

what occurs in the maintainance phase of intrinsic AKD?

A
  • 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
Q

what occurs in the recovery phase of intrinsic AKD?

A
  • tubular epithelial repair
  • GFR returns
  • complicated by a marked diuretic phase due to excretion of retained Na and H2O
47
Q

what are the causes of post-renal AKD?

A
  • 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
Q

what do type A intercalated cells control?

A
  • A - active in ACIDOSIS
  • A - apical H+ secretion
49
Q

what do type B intercalated cells do?

A
  • B - basic
  • B - bicarb - secrete
  • B - basolateral H+ reabsorption
50
Q

where does aldosterone act?

what does it do?

A
  • 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
Q

How is EPO produced in the kidneys?

A
  • ↓ 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
Q

In CKD what happens to EPO production?

A
  • 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
Q

What is the GFR equation?

A

GFR = Kf x (P cap - P bow) - Onc cap

  • Kf reliant on surface area and permiability
  • a reduction of either = ↓ GRF
54
Q

what is the Cockcroft-Gault equation for estimating GFR?

A

GFR = 140 - age x lean body weight (kg) / serum creatinine x 815

  • for women multiply weight by .85
55
Q

what is the renal plasma clearance equation which can be used to estimate GFR when looking at creatinine or inulin?

A

GFR = unine conc (mg/ml) x urine flow (ml/min) / plasma conc (mg/ml)

  • end unit is mL/min
56
Q

Describe how calcium is handled in the kidneys

A
  • 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
Q

What happens in CKD in relation to vit D, phosphate and calcium?

A
  • 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
Q

Define CKD

A
  • 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
Q

What are the risk factors for CKD, modifiable and non-modifiable

A

Modifiable

  • diabetes, HT, smoking, fatty fat fatty

Non-modifiable

  • age (>50 yrs), FHx CKD, indigenous, established CVD
60
Q

what are the common causes of CKD?

A
  • diabetes 36%
  • glomerulonephritis 19%
  • HT vascular disease 12%
  • PKD 5%
61
Q

what are some symptoms of CKD?

A
  • 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
Q

what are the complications of CKD?

A
  • anaemia - due to ↓ EPO
  • Acidosis - metabolic - treat w bicarb
  • Hyperkalaemia
  • Renal ostoedystrophy and vascular calcification
  • infection risk
  • malnutrition - hyperalbuminuria
  • restless legs
  • sleep apnoea
63
Q

when do you refer to a nephrologist?

A
  • 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
Q

what are the stages of CKD?

A
  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
Q

what is the pathophysiology of diabetic nephropathy?

A
  • ↑ 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
Q

How does secondary hyperparathyroidism occur?

A

CKD = ↓ GFR

= ↓ phosphate extrection

= calcium binding with phosphate = ↓ serum Ca

= ↑ PTH release

+ ↓ Vit D conversion = ↓ neg feedback to PT gland

= ↑ PTH release unregulated

67
Q

what is the target BP of people with CKD?

A

< 130/80 mmHg

68
Q

what happens in the kidneys with hypertension?

A

↑ BP =

↑ medial thickening of renal arteries =

↓ GFR =

RAAS activation =

↑ blood volume =

↑ BP = glomerulosclerosis = nephron loss

69
Q

Bladder innervation - at what levels of the spinal cord do the following occur.

  • Sympathetic
  • parasympathetic
  • somatic
A
  • 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
Q

What higher centres are involved in micturation?

A
  • 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
Q

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
A
  • 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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