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CSIM > Renal > Flashcards

Renal Flashcards

1
Q

Renal anatomy

A

Kidneys lie retroperitoneal. L is slightly higher with its haul @ L1 due to the presence of the liver on the R. They are surrounded by layers of fat and fascia and encased in a thick fibrous capsule

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2
Q

Blood supply kidneys

A

Supplied by renal arteries branching directly from the abdominal aorta distal to the SMA. They divide into segmental then to interlobar to arcuate and finally to interlobular arteries.

The afferent arteriole is crucial in regulating the volume of blood delivered to the nephron. It forms an extensive capillary network where the

  • Vasa recta supplies the inner 1/3 of the cortex + medulla
  • Outer 2/3rd of the cortex is supplied by the peritubular network

These the form the efferent artiole via via the renal veins drains directly into the IVC

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3
Q

Filtration @ Bowmans Capsule

A

Hydrostatic pressure forces fluid out. The filtration barrier consists of fenestrated endothelium with 60-80nm sizes pores on top of this sits the -vely charged GBM so large molecules such as albumin are retained. Podocytes foot processes form an interdigitated 40nm filtration slit

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4
Q

Juxtaglomerular apparatus

A

Regulates flow and filtration to each nephron. Column cells in the macula densa sense the concentration of Na+ in the tubular fluid. They can trigger adenosine mediated vasoconstriction of the afferent arteriole to reduce eGFR and retain more sodium and hence increase BP. This is mediated by renin and aldosterone

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5
Q

Endocrine function of the Kidney

A

Epo, renin via juxtaglomerular apparatus, 1a hydroxylation of vit D

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6
Q

Proximal tubule

A

Glucose and 80% of Na reabsorbed via Na+/Glucose co transporter. Cl- is reabsorbed to maintain electric neutrality. Na+/H+ exchanger allows HCO3 formed from c02 and h20 by carbonic anhydrase to be reabsorbed

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7
Q

Thick descending loop of Henle

A

H20 reabsorbed giving hypertonic urine

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8
Q

Thick ascending loop

A

Na+/K+/2Cl- symporter

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9
Q

Distal convoluted tubule

A

Ca2+ reabsorption mediated by PTH, Thiazide dependent Na+/Cl- transporter

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10
Q

Collecting duct

A

ENaC aldosterone mediated Na+ exchanged for K+ and H+

ADHs stimulates aquaporin insertion and h20 retention

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11
Q

Autocrine functions

A

Autocrine = actions on self

Endothelins = vasoconstrictors
Prostaglandins= act to maintain renal blood flow in the face of angiotensin II and adrenergic stimulation
ANP = Secreted from the cardiac atria in response to stretch produce Na+ excretion, lower BP and reduce renin and aldosterone secretion
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12
Q

Renal Hx

A

PMHx = gout, HTN, DM
Childhood UTI = vesicouteric reflux
Hx of renal stones or cystitis
Dix = Abx, NSAIDs, methotrexate, gentamicin/vancomycin

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13
Q

Nephritic syndrome

A

Inflammation leads to reactive cell proliferation and breaks in the GBM. Crescent forming. PC = haematuria and red cell casts

Causes = anti GBM (goodpastures), Vasculitis, post strep glomerular nephritis. SLE and IgA can

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14
Q

Nephrotic syndrome

A

Injury to podocytes leading to changed architecture and scarring. PC = oedema, hypoalbuminea, proteinuria and hypercholesterolemia

Causes = minimal change disease, FSGS, diabetic nephropathy, amyloidosis

Iga and SLE can

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15
Q

O/E renal disease

A

Parlour, fatigue and SOB ?anemia due to low epo
Purpuric rash, epistaxis, wt loss, arthralgia ?vasculitis
Palpable bladder ?retention/cancer
Palpable kidney ?ADPKD, transplat @ iliac fossa
Oedematous = nephrotic syndrome
Renal bruit ? renal artery stenosis

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16
Q

eGFR

A

Clinically used to assess degree of renal impairment (Not useful in acute setting). Uses for drug dosing and ESRF

Calculations take into account age, weight, race and serum creatinine

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17
Q

Limitations of eGFR

A

Too pessimistic in mild renal failure, most elderly patients are in stage III CKD yet have no impairment on their lives

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18
Q

Creatinine clearance

A

Produced by skeletal muscle filtered freely at the glomerulus with only a small amount secreted in the proximal tubule. Creatinine levels vary with muscle mass, activity and gender

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19
Q

Equation for creatinine clearance

A

(140-age x wt x constant)
Serum creatinine

Constant = 1.04 females, 1.23 males

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20
Q

Myeloma screen

A

CRAB symptoms. Serum free light chains/electrophoresis

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21
Q

Glomeluronephritis screen

A

ANCA (PR3 and MPO), anti-GBM, complement, ANA, dsDNA

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22
Q

Urine dipstick

A

Colour - haemturia? nephritic syndrome or myoglobin
Glucose - very sensitive indicated DM
Proteinuria - common sometimes benign (postural, exercise and pyrexia)
If two +ve dipsticks for protein offer ACR

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23
Q

Causes of Haemturia

A

Intra-renal = TIN, papillary necrosis, GN, Cysts, RCC, trauma

Extra-renal = ureteric stones, bladder cancer, infections, BPH, parasites, urethral trauma

False +ve = myoglobin, rifampicin, porphyria

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24
Q

Glomerular disease

A

Red cell casts, haematuria and proteinuria

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25
Q

Inv Renal

A

USS - safe, non invasive so imaging of choice allows visualisation of stones, assess size and symmetry of kidneys, characterisation of renal masses as cystic or complex and solid, guided biopsy, renal artery patency with duplex

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26
Q

Glomerulus structure

A

Network of capillaries at the beginning of the nephron

i) Fenestrated endothelium have large pores 50-100nm allowing passage of small molecules but not protein or RBC
ii) GBM strong collagen matrix with heparan sulphate giving -ve charge to repel albumin.
iii) Podocytes attach to the GBM by foot processes, adjacent podocytes are joined by slit diaphragms creating a sieve

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27
Q

Glomerulus in disease

A

Effacement of for processes leads to disruption is architecture of the filtration slit this may manifest as proteinuria.

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28
Q

Tubular disease

A

White cell casts, minimal proteinuria

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29
Q

Classification of glomerular disease

A

a) Nephrotic = massive proteinuria, oedema and hypoabluminemia due to podocyte injury

b) Glomerulonephritis = nephritic syndrome
Acute = abrupt onset haematuria, red cell casts and transient renal impairment

RPGN - acute nephritis, focal crescent necrosis and ESRF

c) Mixed nephrotic/nephritic = SLE, IgA, HSP
d) Asymptomatic proteinuria/haematuria

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30
Q

Causes of proteinuria

A

Glomerular in origin >1g

  • Diabetic nephropathy, minimal change, FSGS, membraneous GN
  • SLE and amyloidosis

Tubular in origin < 1g
ATN/ITN
UTI, ureteric stones
Bengin = fever, exercise and postural

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31
Q

Nephrotic syndrome

A

Massive proteinuria >3.5g a day may PC as frothy
Hypoalbuminemia <35g/l
Gross oedema = periorbital, ascites, ankles
Dyslipidemia

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32
Q

Complications of nephrotic syndrome

A

Can cause progressive renal failure

Hyperlipidemia - low levels of albumin lead to hepatic compensation by producing lipopoteins. Apolipoproteins are lost in the urine leading to reduced lipid catabolism and action of lipoprotein lipase. If prolonged = acceleration of CVD and atherosclerosis

Thrombophila - antithrombin III lost giving hypercoaguable state = increased DVT/PE risk

Infection risk due to loss of immunoglobulins

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33
Q

Causes of nephrotic syndrome

A

1 - minimal change disease, FGGS, membranous nephropathy

2 - SLE, amyloidosis, diabetic nephropathy

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34
Q

Minimal change disease PC

A

Seen commonly in children approx 20% causes of adult nephrotic syndrome. PC = facial oedema, selective protein loss albumin > immunoglobulins

Glomeruli appear normal on light microscopy however on electron microscopy fusion and effacement of the foot processes can be seen.

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35
Q

Causes of minimal change

A

Idiopathic - majority!

Hodgkin lymphoma, drugs - NSAID’s, ABx, HBV and HCV

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36
Q

Mx minimal change

A

Good prognosis <10% progress to ESRF. Steriods

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37
Q

Focal segmental glomerulosclerosis (FSGS) PC

A

Sclerotic glomerular lesions which affects some glomeruli and certain segments in each tuft. Evidence of hylanosis

Increased incidence in afro-carribeans

PC = massive proteinuria (no selective), HTN and haematuria

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38
Q

Inv and Mx for FSGS

A

Immunohistochemistry shows IgM and complement deposition
Biopsy = diagnostic

Mx = steroids and cyclophosphamide. 50% progress to ESRF @ 10yrs

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39
Q

Membranous glomerulonephritis

A

30% of adult nephrotic syndrome. Male predominance AI condition where autoantibodies target the GBM. Sub endothelial deposits activate the complement system which leads to damage to podocytes and mesangial cells

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40
Q

Haematuria referral

A

2wk wait if visable haematuria > 45y/o in absence of UTI

inviable haematuria >60y/o

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41
Q

IgA nephropathy

A

Most common form of glomerulonephritis worldwide caused by deposition of IgA complexes in the mesangium

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42
Q

IgA nephropathy

A

Most common form of glomerulonephritis worldwide caused by deposition of IgA complexes in the mesangium. This leads to proliferation and synthesis of mesangial matrix. Activation of complement and macrophage infiltration lead to glomerular injury

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43
Q

PC IgA nephropathy

A

Typically in childhood or young males post URTI or GI infection within a week. Microscopic or macroscopic haematuria.
Rapid recovery

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44
Q

Inv and Mx IgA

A

Biopsy shows mesangial proliferation and complex deposition. IgA on immunohistochemistry
USS to rule out obstructive cause

Mx = ACEi, steroids if needed

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45
Q

Thin basement membrane disease

A

AD condition typically presents with persistent microscopic haematuria + red cell casts.

Inv = Biopsy shows thinning of membrane due to collagen defect

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46
Q

Alport syndrome

A

X-linked disorder of type IV collagen which is found in the ears, glomerulus and eyes. This non functioning collagen undergoes progressive sclerosis = renal failure

PC = progressive proteinuria and haematuria, sensorineural hearing loss. 20% optic defect including anterior lexicons, myopia and corneal erosions

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47
Q

Diuretics

A

Loop - Furosemide acts block Na+/K+/Cl- transporter in the loop of Henle = potent effect

Thiazide - Bendroflumathiazide acts to block Na+/Cl- cotransporter in DC. Cause more urinary retention, glucose intolerance and hypokalemia than Loop.

Potassium sparing diuretics reduced Na+ reabsorption in exchange for K+ retention = spironolactone

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48
Q

Causes of membranous glomerulonephritis

A

1 - idiopathic 80%
2 - AI (SLE, thyroid, sarcoidosis)
Infections - HBV, HCV,
Cancer - lung, breast, colon + lymphoma
Drugs - gold, NSAIDs, penicillamine!!

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49
Q

Inv and Mx of membraneous glomerulonephritis

A

Invx - biopsy shows classic spike and dome pattern , IgG and C3 on immunofluorescent

Mx 1/3 = ESRF

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50
Q

Mx Nephrotic syndrome

A

LMWH tinzaparin to reduce risk of VTE
Statins for dyslipidemia
ACEi for proteinuria and HTN
Oedema = rest, fluid and Na+ restrict

Find and treat the cause!!
Myelomas = serum free light chains, Vasculitis ANCA +ve, anti-GBM, SLE =dsDNA

Biopsy is often needed for diagnosis

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51
Q

Glomerulonephritis

A

i) Non proliferative = nephrotic syndrome
Minimal change, FSGS, Membranous

ii) Proliferative GN = usually nephritic syndrome + crescents
IgA, post streptococcal, Membroproliferative
RPGN - anti-GBM and Vasculitis

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52
Q

Diabetic nephropathy

A

Glomerular hyper filtration leads to GBM thickening and mesangial proliferation - proteinuria occurs as filtration pressure rises and podcytes deplete.

In late stages of disease glomerulosclerosis occurs with with Kimmelstiel-Wilson lesion and hyaline deposits in the glomerular arterioles

ACEi

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53
Q

Mx diabetic nephropathy

A

Aim for good glycemic control, BP <120/80 with ACEi, control dyslipidemia

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54
Q

Nephritic syndrome

A

Haematuria + red cell casts on microscopy, HTN, proteinuria <3.5g daily, oliguria and progressive renal failure in some cases

55
Q

Causes of nephritic syndrome

A

Post streptococcal, IgA, infective endocarditis

RPGN - HSP, Vasculitis, anti GBM, SLE

56
Q

Post-streptococcal GN

A

Occurs in childhood often 1-3wks after a streptococcal infection often - otitis media, cellulitis or sore throat

Produces streptolysin leading to RBC haemolysis. Type III hypersensitivity deposition of complex in sub endothelium.
Inv - low complement, IgG and C3 deposition on biopsy

57
Q

Membranoproliferative GN

A

Can present as mixed nephritic and nephrotic syndrome

Biopsy shows thickened capillary loops, diffuse thickened mesangium and IgG deposits. Tram track appearance

Linked to hep C

Mx = most pt develop ESRF

58
Q

Stage I AKI

A

Creatinine rise > 26.4,
Creatinine 1.5-1.9x baseline
Urine output below 0.5ml/kg <12hrs

59
Q

Stage II AKI

A

Creatinine 2.0-2.9x baseline

Urine output <0.5ml/kg > 12hrs

60
Q

Stage III AKI

A

Creatinine rise >354
Creatinine 3x baseline
Urine output <0.3ml/kg for 24hrs or anuria

61
Q

AKI

A

Very common 18% of A&E admissions linked to high mortality and long admissions. 50% of patients with sepsis will have an AKI

Crucial to distinguish AKI from CKD. Baseline creatinine, symptoms and duration.

62
Q

Functions of the kidney

A

Endocrine = renin, epo and vit D hydroxylation
Excretion of waste urea, nitrogen and drugs
Fluid balance reabsorption of K+, P04, Ca2+

63
Q

Pre Renal AKI

A

Hypoperfusion of the kidney leads to compromised renal function. This occurs when the usual mechanisms that autoregulate the GFR fail If this persists can lead to ischemia and ATN. This causes approx 80% of AKI

64
Q

Causes of hypoperfusion

A

Hypovolemia = Burns, D/V, haemorrhage
Low cardiac output = MI, acute HF, PE
Vasoconstrictors = NSAIDs, ACEi
Distributive = Sepsis, hepatorenal, anaphylaxis

65
Q

NSAIDs and ACEi

A

NSAIDs acts to inhibit prostaglandin production, they are essential to vasodilate the afferent arteriole. Hence NSAIDs lead to vasoconstriction of the afferent arteriole and reduced blood flow to the glomerulus

ACEi this act to block the effects of angiotensin II a potent vasoconstrictor of the efferent arteriole. They lead to reduced glomerular pressure hence low GFR

66
Q

Intrinsic AKI

A

90% due to ATN
Acute tubular interstitial nephritis
Vasculitis, RPGN, ITP,HUS

67
Q

Acute tubular necrosis

A

Necrosis of tubular cells due to

i) Prolonged ischemia
ii) Nephrotoxins - constrast, aminoglycosides, myoglobin

68
Q

Pathology of ATN

A

Tubular injury leads to necrosis and apoptosis of the tubular cells, the tubules are then obstructed by the accumulation of necrotic cells leading to increased pressure in the tubules and reduced GFR

69
Q

Tubular obstruction

A

Myeloma - paraproteins
Tumour lysis syndrome - urate
Rhabdomyolysis - myoglobin

Agglutination of proteins leads to tubular blockage and reduced GFR

70
Q

Acute allergic interstitial nephritis

A

Rare. 80% of cases due to drugs. Rapid influx of inflammatory cells into interstitium

PC = may be asymptomatic, can present with a rash, fever, arthralgia and oliguria

Inv - biopsy shows eosinophils with variable tubular necrosis. Eosinophilia and eosinophiliuria

Mx stop the drug and steroids

71
Q

Rhabdomyolysis

A

Causes - compartment syndrome, crush injuries, status epileptics, statins, long lie, excess exertion

Rapid rise in CK, K+, lactate and phosphate

72
Q

Causes of TIN

A

Drugs - NSAIDs, Abx - penicillin, cephalosporins, quinones, carbamazepine, allopurinol, PPI, valproate, loop and thiazide diuretics

Can be due in infection or idopathic

73
Q

RPGN

A

Mass proliferation of Bowmans capsule and rupture leading to crescent formation

  • anti GBM (If lung involvement = Goodpastures)
  • Immune complex deposition SLE, IgA, HSP, endocarditis
  • Vasculitis
74
Q

GPA

A

PC = sinusitis, nasal polyps, c-anca and PR3 +ve

75
Q

EGPA

A

PC = asthma, eosinophils on biopsy, p-anca and MPO +ve, commonly anca -ve

76
Q

MPA

A

PC = no granulomas on biopsy, p-anca and MPO

77
Q

Anti GBM

A

20% of RPGN. If associated with pulmonary haemorrhage = Goodpasture’s. Anti-GBM antibodies present in serum and detected by ELISA and are directed against type 4 collagen in the BM

78
Q

Cholesterol embolisation syndrome

A

Occlusion of micro vessel by cholesterol emboli from atherosclerotic lesions. Usually post op or angioplasty. Increased risk with anticoagulation

79
Q

Haemolytic ureamic syndrome (HUS)

A

Characterised by intravascular haemolysis with red cell fragmentation, thrombocytopenia and AKI

80
Q

Diarrhoea HUS (E.coli 0157)

A

PC = bloody diarrhoea and abdo pain due to E.coli strain that produces a shiga toxin that destroys RBC. Renal failure occurs due to blockage of tubules with schisctocytes

Mx = can be very severe 5% die, 20 may need dialysis, 30% residual renal impairment

81
Q

Post renal AKI

A

Due to blockage of the ureter, bladder or outflow tract. If unilateral pt must have some pre-existing renal impairment. USS is crucial to identify cause

82
Q

Causes of post renal AKI

A 
Stones or neoplasms blocking ureter
BPH 
Bladder cancer 
Urinary retention due to UTI/constipation
Strictures
83
Q

PC of AKI

A

Hyperkalemia - K+ is excreted by the kidney, can present as muscle weakness and palpitations leading to ECG abnormalities and arrhythmias
- ECG = tall tented T, flattened P, widened QRS
Mx = calcium gluconate, 100ml 20% dextrose and 10U insulin, Neb salbutamol

Metabolic acidosis due to reduced excretion of H+ ions

Fluid overload and pul oedema due to Na+ and hence h20 retention

Accumulation of urea = impaired haemostasis, N/V, drowsiness, fits, confusion, asterxsis, pericarditis

84
Q

Pre-renal Hx and O/E

A

Hx - diarrhoea, bleeding and vomiting, symptoms of infection i.e. fever, cough, SOB, dysuria, fall and long lie

O/E - septic shock = warm peripherally, normal CRT,
cardiogenic = cold peripherally, hypotensive, JVP
Signs of infection crackles on auscultation

85
Q

Intra-renal Hx and O/E

A 
NSAIDs, Abx = TIN, Contrast recently?
CRAB symptoms ?Myeloma
Diarrhoea, purpura, young child ?HUS
Wt loss, epistaxis, haemoptysis, fever etc ?Vasculitis
Confused, fall = rhabdomyolysis
86
Q

Post-renal Hx and O/E

A

Obstructive symptoms = gradual poor flow, dribbling, incomplete voiding, nocturia
Loin pain and frank haematuria, smoking ? TCC

Bladder palpable = urinary retention
PR ? BPH smooth enlarged vs prostate cancer hard nodular and craggy

87
Q

Indications for acute dialysis

A 
Hyperkalemia >7.0mm
Ureamic encephalopathy
Refractory pul oedema 
Severe metabolic acidosis
Poisoning - aspirin
88
Q

Inv AKI

A

Pre-Renal causes often on clinical signs and symptoms. Catherise to monitor urine output/ if in acute retention
USS to rule out post-renal causes
Urine dip for infection
ECG crucial to monitor for arrythmias
U+E, coat screen, ABG, CRP
Urine microscopy = red cell casts glomerular damage

89
Q

Intrinsic screen

A 
Serum free light chains = myeloma
anti-GBM = Goodpastures
dsDNA and low complement = SLE
Blood film = HUS
ANCA = vascilitis
90
Q

Mx AKI

A

Treat oedema, hyperkalemia and uraemia as they present
Stop all nephrotoxic drugs - NSAIDs, ACEi, certain ABx
Adjust medications that will accumulate in renal failure - opioids and metformin

Fluid replacement stat. Let urine output guide

91
Q

When to suspect 2ndary HTN

A

Young pt <40y/o
No sign of underlying cause i.e. - obesity, DM, FHx
Refractory HTN despite compliance

92
Q

Primary hyperaldosteronism

A

Screening with a aldosterone:renin. If high indicates causes. Adrenal vein sampling may be required to decide whether Conns vs bilateral hyperplasia

93
Q

Phaechromocytoma

A 
PC = headache, sweating, tachycardia, HTN
Inv = plasma metaephrine level

Linked to MEN2, von hippel landau and NF1

94
Q

Acromegaly

A

PC = large feet and hands, carpal tunnel, macroglossia, spaced teeth, OSA, DM. 95% due to pituitary adenoma may - tunnel vision and headaches

95
Q

Cushings syndrome

A

PC = striae, hirsutism, facial plethora, central obesity, osteoporosis, DM, proximal myopathy

Inx = urinary free cortisol or low dose dex
Plasma ACTH levels
High dose dexamethasone

96
Q

Atherosclerotic renovascular disease (ARVD)

A

Atherosclerosis 16% of patients > 60. Pt with co-exisiting PVD, CCF are at increased risk.

PC = often asymptomatic. HTN in 50%, Na+ retention may precipitate flash pul oedema. Renal bruit. Small kidney on USS

Mx ACEi may precipitate AKI GFR will fall by 30% and then stabilise. If >75% stenosis

97
Q

Renal artery stenosis

A

ARVD or fibromuscular dysplasia

The effected kidney has reduced perfusion leading to chronic RAS activation. Renin production and aldosterone release to retain Na+ and h20. Effected kidney produces more concentrated urine and has a lower GFR

Inv - USS and MR angiogram

98
Q

Mx renal artery stenosis

A

wt loss, control cardiac factors. ACEi

Revascularisation

99
Q

When to revascularise in renal artery stenosis

A

Stenosis >75%, declining renal function, single kidney, flash refractory pulmonary oedema, severe HTN,

100
Q

Fibromuscular dysplasia

A

Rare - presents in young women with HTN and renal bruits. Can present at the carotid or coronary arteries

MRI = string of beads appearance

101
Q

HTN in hyperparathryoidism

A

Increased intracellular Ca2+ SM contraction in arterioles increasing PR

102
Q

Pathogens causing UTI

A

E.coli, proteus, stap saprophyticus, enterococcus

103
Q

Risk factors for UTI

A

Female, stones, sexual activity, indwelling catheter, DM, urinary tract stasis, dementia

104
Q

PC UTI

A

fever, dysuria, polyuria , smelly urine and haematuria.

105
Q

Causes of HTN in CKD

A

Impaired Na+ excretion leads to sodium retention and expansion of the extracellular volume. Activation of RAS leads to direct vasoconstriction to aid Na+ retention.

106
Q

CKD definition

A

Kidney dysfunction >3months. Albumin:creatinine >3mg/mmol, falling GFR <60, rising creatinine

107
Q

Causes of progressive CKD

A

HTN, DM, Urinary obstruction i.e. stones, BPH, recurrent UTI, Glomerular diseases = SLE, amyloidosis, Vasculitis. Nephrotoxic drugs

108
Q

Prognosis of CKD

A

Depends on eGFR and ACR

Poor prognosis if ACR >30

109
Q

Stages of CKD

A 
I >90
II 60-80
III a - 45-59, b - 30-44
IV 15-29
V <15
110
Q

PC CKD

A

Progressive asymptomatic decline in eGFR. Comorbidity such as DM, HTN, AI conditions. As renal function declines will lead to anaemia, electrolyte disturbances, fluid retention, HTN, restless legs and neuropathy,

111
Q

Progression of CKD

A

In CKD many of the nephrons are scarred and have failed, hence their job of filtration falls on the remaininf nephrons. This hyperfiltrative state imposed on the remaining nephrons despite no increase in renal blood flow leads to hypertrophy and reduced arteriole resistance. The increased flow and pressure perpetuates the system.

112
Q

Inv CKD

A

U+E, ACR, urinalysis.
USS to rule out reversible causes, if acute ?renal artery stenosis
Urine dip and microscopy - red cell casts ?GN, eosinophilia?TIN
Fragmented red cells +/- low platelets ?HUS/TTP
ANCA ? vasculitis

113
Q

Mx CKD

A 
BP control <140/90 unless DM <130/80
ACEi 
Low salt diet, fluid restriction
Reduce wt, stop smoking, CVD risk?statin
Monitor K+/urea levels
Hyperphosphatemia due to inability to secrete and cant hydroxylated vit D = hypocalcemia and possible 2ndary hyperparathryoidism
Epo if anaemia
114
Q

Uraemia complications

A

Ureamic pericarditis
Uraemic encephalopathy
Bleeding

115
Q

Bone disease in CKD

A

Spectrum can encompass osteomalacia, hyperparathyroid and osteoporosis

Phosphate excretion falls. Secondary hyperparathyroidism develops as renal function declines production of 1ahydroxylase leads to less active vit D so reduced GI calcium absorption. Trigger PTH release to increase Ca2+ blood levels caused by phosphate retention and reduced GI absorption.

2ndary hyperparathyroidism in response to low Ca2+leads to increased osteoclastic actitvity, cyst formation and osteitis fibrosis cystica. Inv = high PTH, low Ca2+, high PO4 and high ALP

116
Q

Tertiary hyperparathyroidism

A

Chronic hypocalcaemia leads to autonomous production of PTH by the parathyroid gland. Acts independently = high Ca2+, high PTH

117
Q

Mx bone disease in CKD

A

Phosphate binders and novel vit D metabolites

118
Q

Haemodialysis

A

Relies on a machine to monitor pressure, LMWH for anticoagulation, air trap to prevent air embolisms. Blood is passed in a countercurrent system through a semi-permeable membrane against dialysis fluid which is low in Na+, K+, urea, H+ allowing toxic metabolites to diffuse down concentration gradient

119
Q

Pros and cons of haemodialysis

A

-ve = restriction on life 3x weekly 4hrly sessions, pt tired after, can = hypotension due to large volume of fluid removed

120
Q

AV fistula

A

Created by anastomosing the brachial artery and cephalic vein. Takes 6 weeks to prepare. Veins walls thicken under arterial flow allowing repeated use, arterial blood flow needed for dialysis

O/E - thrill and bruit due to turbulent flow, often engorgement of veins in arms

121
Q

AV fistula pros and cons

A

+ve = higher flow rates gives more effective dialysis, lower risk of infection and thrombus

-ve = steal syndrome leading to cold extremities and cramping pains. Aneurysm formation

122
Q

Central venous catheter

A

Plastic catheter with 2x lumen inserted into large vein usually IVC or femoral. Tunnelled under the skin

They have an increased risk of infections compared to fistulas can lead to stenosis and occlusion of the veins with repeated use due to scaring and fibrosis.

123
Q

Aim of dialysis

A

Maintain euvolemic, prevent acidosis and hyperkalemia

124
Q

Peritoneal dialysis

A

Uses the peritoneum as a semi-permeable membrane, permeant catheter is inserted allowing fluid to be administered daily

125
Q

Pros and cons of peritoneal dialysis

A 
\+ve = increased independence, can be done overnight
-ve = bacterial peritonitis = fever, cloudy dialysate fluid, abdo pain. Hernias, catheter site infections.

Serious = sclerosing peritonitis leading to adhesions and strictures causing repeated small bowel obstruction

126
Q

Transplant

A

Treatment of choice. New kidney lasts 10-15yrs. Improved QoL, cost effectiveness, mortality benefit, correction of metabolic problems

127
Q

CI to renal transplant

A

Cancer, severe heart disease, active infection, low performance status

128
Q

Types of renal transplant

A

Living donor via paired pool exchange
Deceased donor
i) DBD = better prognosis due to increased perfusion
ii) DCD

129
Q

Mx renal transplant

A

HLA matching crucial!!
Steroids, antimetabolites = MMF/azothioprine,
calcinerin inhibitors = tacrolimus

130
Q

Red cell casts and white cell casts

A

Red cell casts = glomerular pathology - vasculitis, anti-GBM, SLE, post strep GN, endocarditis, renal infarction

White cell casts = TIN, nephrotic syndrome and pyelonephritis

131
Q

Cresentric glomerulonephritis

A

Indicates severe acute renal damage. Starts with a gap in the glomerular capillary wall and GBM. Inflammatory mediators move into Bowmans space. T-cells and fibroblasts proliferate

%age of glomeruli with crescents linked to recovery and prognosis

132
Q

Tacrolimus/ciclosporin

A

Calcineurin inhibitors disrupt T cell signalling

133
Q

Azathioprine/MMF

A

Inhibit purine synthesis hence the active proliferation of lymphocytes

CSIM (12 decks)

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