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General Medicine Block > Renal Medicine > Flashcards

Renal Medicine Flashcards

1
Q

advantages of haemodialysis?

A

can be done at home
4 days free of treatment
long term survivers, proven to be effective
better provision, resources having been increased for it

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2
Q

disadvantages of haemodialysis?

A

nausea, cramps and low BP during and after due to rapid fluid shifts
significant dietary restrictions
transport to dialysis unit
difficulty with vascular access

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3
Q

advantages of peritoneal dialysis?

A

low tech, at home, taught quickly
less fluid shifts as continuous therapy
mobility

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4
Q

disadvantages of peritoneal dialysis?

A

infection, sclerosing peritonitis- bowel becomes fibrosed and obstructed=LT risk
limited survival

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5
Q

life-threatening consequences of AKI?

A

volume overload-pulmonary oedema
hyperkalaemia
metabolic acidosis
uraemia?

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6
Q

prevention strategies in AKI?

A

maintaining adequate BP
ensuring adequate volume status
avoid potentially nephrotoxic drugs e.g. gentamicin

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7
Q

commonest cause of intrinsic renal disease?

A

acute tubular necrosis (ATN)

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8
Q

name of criteria used to classify AKI based on degree and outcome?

A

RIFLE criteria

This defines 3 degrees of increasing severity of AKI, and 2 possible outcomes.

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9
Q

what is the RIFLE criteria?

A

the risk, injury and failure, and loss and end-stage renal disease=classification system of AKI.
Risk of renal dysfunction: 50% increase creatinine, or >25% decrease GFR AND/OR urine output less than 0.5ml/kg/hr for at least 6 hrs.
Injury to kidney: 2 fold increase creatinine or >50% decrease GFR AND/OR urine 75% decrease GFR, or creatinine more than 350 AND/OR urine 4wks but

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10
Q

what is the KDIGO staging of severity of AKI?

A

kidney disease improving global outcomes staging, based on creatinine or urine output.
3 stages of increasing severity

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11
Q

how is renal blood flow and GFR normally kept constant through autoregulation?

A

myogenic resonse
tubuloglomerular feedback- based on NaCl delivery to DCT and detection by macula densa cells, which subsequently control release of adenosine and ATP, and PGs and NO, which cause vasoconstriction or vasodilation of afferent arteriole respectively.
efferent arteriole vasoconstriction-AngII

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12
Q

in what circumstances is GFR maintenance part. AngII-dependent?

A

in cases of renal artery stenosis or volume depletion

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13
Q

site of ACE production?

A

lungs-surfaces of pulmonary and coronary endothelial cells

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14
Q

if ibuprofen is being used by a pt in the setting of volume depletion e.g. severe diarrhoea, why might AKI occur with acute GFR decline?

A

ibuprofen= NSAID-COX inhibitor, so inhibiting PG synthesis which acts to vasodilate, and NA and AngII high in vol depletion, so unopposed action of local vasoconstrictors on both afferent and efferent arterioles, so inadequate renal perfusion.

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15
Q

Give 4 overall causes of pre-renal AKI, and causes for each of these.

A

hypovolaemia-haemorrhage, GI losses-diarrhoea and vomiting, urinary losses-glycosuria, post-obst diuresis, diuretics and fluid redistribution e.g GI obstruction, pancreatitis.
hypotension- cardiogenic shock e.g. post MI, distributive shock e.g. sepsis, anaphylaxis, with vasodilation.
renal hypoperfusion- reduced perfu plus impaired autoregulation, AAA, renal artery stenosis/occlusion, hepatorenal syndrome.
oedema states- CHF, hepatic cirrhosis, nephrotic syndrome partic. minimal change nephropathy. Fluid o.load can damage kidneys, and fluid in interstitium reduces perfusion to kidneys?

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16
Q

commonest cause of intrinsic renal AKI in intensive care?

A

sepsis

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17
Q

3rd commonest cause of hospital-acquired AKI?

A

radiocontrast nephropathy

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18
Q

important clinical consequence of relieving AKI caused by obstruction?

A

substantial diuresis, requires careful monitoring and appropriate fluid replacement to avoid vol depletion.

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19
Q

how is obstructive nephropathy rapidly diagnosed?

A

USS-detects dilatation of renal pelvis and calyces

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20
Q

principal causes of post renal AKI?

A

intrinsic: intraluminal=stones, blood clots, papillary necrosis
intramural=urethral stricture, bladder tumour, prostatic hypertrophy or malignancy, radiation fibrosis
extrinsic: pelvic malignancy, retroperitoneal fibrosis

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21
Q

causes of intrinsic renal AKI?

A

glomerular disease-inflammatory e.g. SLE, thrombotic e.g. DIC, thrombotic microangiopathy
tubular injury-ischameia, toxins-drugs, radiocontrast, pigments, heavy metals, metabolic-hypercalcaemia, crystals e.g. urate, oxalate
interstitial nephritis-drug induced e.g. NSAIDs, Abx, infiltrative e.g. lymhoma, granulomatous e.g. TB, sarcoidosis, infection e.g. post-infective, pyelonephritis.
vascular-vasculitis- usually ANCA assoc., cryoglobulinaemia-blood has large numbers of cryoglobulin proteins insoluble at reduced temps., assoc. with conditions such as multiple myeloma and Hep C infection. Cholesterol emboli, renal artery or vein thrombosis.
HRS
HUS

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22
Q

a disproportional increase in urea:creatinine ratio is indicative of which type of AKI?

A

pre-renal

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23
Q

characteristics of pulmonary oedema on CXR?

A 
widespread opacification, poorly defined edges, CP angle blunting
kerley B lines
fluid in fissures
upper lobe diversion
bats wing hilar shadowing?
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24
Q

in pre-renal AKI, there is typically avid retention of Na+ and H20, why is this and what does this mean for the fractional excretion of Na+?

A

pre-renal- decreased blood flow to the kidney, often due to hypovolaemia so high levels of ADH, Ang-II and aldosterone (RAAS activation?).
FE less than 1%

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25
key investigations in AKI?
haematology: FBC, blood film, clotting profile-eosinophilia, thrombocytopenia, DIC, anaemia in CKD immunology BC: Us and Es, creatinine, blood gas analysis, serum HCO3-, CK, myoglobinuria, CRP, serum Igs, protein electrophoresis, Bence Jones proteins proteinuria virology-Hep B and C and HIV, as import. for infection control in dialysis area radiology: renal USS- size, symmetry and evidence of obstruction
26
Management principles in AKI?**
identify and correct pre and post renal factors optimise CO and renal b.flow review meds: cease nephrotoxic agents, adjust doses where approp, monitor levels accurately mon fluid intake and output and daily body weight identify and treat acute complications e.g. hyperkalaemia, acidosis, hyperphosphataemia, pulmonary oedema optimise nutri suppport, but minimise nitrogenous waste prod., and K+ restriction identify and aggressively treat infection, minimise indwelling lines, remove bladder catheter if anuric identify and treat bleeding tendency, prophylacis with PPI or H2 antagonist, transfuse if req, avoid aspirin initiate dialysis before uraemic comp.s emerge
27
define significant progression of CKD
>5ml/min decline in eGFR within 1 yr, or >10ml within 5 yrs
28
why is it important to identify those with early CKD?
CKD has strong assoc. with risk of death, CVD and hospitilisation and to prevent/delay progression to end stage renal disease (ESRD), assoc. with considerable morbidity, mortality, and high healthcare costs.
29
stage 5 CKD (end stage renal failure) is defined as what eGFR and what is the typical testing frequency of this?
less than 15ml/min pts eGFR on average when placed onto RRT is 6ml/min 6 weekly testing
30
how is CKD routinely assessed for in hypertensive and diabetic pts?
hypertensive pts should have urinary ACR checks and urinalysis for haematuria all diabetics should have 1st pass urine tests for ACR
31
according to NICE, people with what RFs should be offered testing for CKD?
diabetes hypertension CVD-IHD, chronic HF, PVD or CVD structural renal tract disease, renal calculi or prostatic hypertrophy multisystem diseases with potential kidney involvement e.g. SLE FH of stage 5 CKD or hereditary kidney disease e.g. polycystic kidneys opportunistic detection of proteinuria or haematuria
32
factors to bear in mind when checking eGFR?
``` age ethnicity weight diet exercise gender muscle mass ```
33
when might eGFR be less reliable?
``` AKI pregnancy muscle wasting disorders oedematous states amputees malnutrition ```
34
how should eGFR be corrected with afro-caribbean or african pts?
multiply by 1.21
35
if 1st test eGFR is less than 60ml/min, what should be done?
retest within 2 wks to exclude causes of acute deterioration of GFR
36
The most important management consideration in pts with CKD?
BP control: essential to slow down rate of renal impairment AND reduce risk of CVS events.
37
definition of stage 1 CKD?
eGFR is 90 or more must be other evidence of kidney damage e.g. structural abnormality eGFR tested typically yrly
38
definition of stage 3 CKD?
eGFR 30-59 stage 3a= 45-59 stage 3b= 30-44 tested 6 mnthly
39
definition of stage 2 CKD?
eGFR 60-89 must be other evidence of kidney damage eGFR tested 12 mnthly
40
definition of stage 4 CKD?
eGFR between 15 and 29 | tested 3 mnthly
41
most common secondary cause of nephrotic syndrome?
diabetes mellitus
42
diagnostic criteria for nephrotic syndrome?
proteinuria-more than 3-3.5g/24hr, or spot urine PCR of more than 300-350 mg/mmol serum albumin less than 25g/L peripheral oedema clinically hyperlipidaemia, total cholesterol more than 10mmol/L
43
complications of nephrotic syndrome?
VTE- DVT, PE, renal vein, arterial, as increased clotting factors as loss of proteins which inactivate clotting factors e.g. antithrombin III, and platelet abnormalities. INFECTION-cellulitis, bacterial peritonitis, bacterial infections e.g. streptococcus and SBP, as reduced serum igG, complement activity and T cell function- loss of Igs in urine and immunosuppressive tments, viral infections in IC hyperlipidaemia- increased hepatic lipoprotein synthesis in response to low oncotic pressure malnutrition AKI
44
% risk of RRT if CKD stage 4 in 5 years?
20%
45
what do most pts with CKD die from?
CVD
46
other than high BP, what else is know to worsen IgA nephropathy?
smoking
47
adverse prognostic factors in IgA nephropathy?
HTN already developed CKD significant proteinuria
48
4 features that define AKI?
rise in serum creatinine of 26 micromol/L or more within 48hrs 50% or greater rise in serum creatinine from a baseline known or presumed to have occurred in last 7 days fall in UO to less than 0.5ml/kg/hr for more than 6 hrs in adults or 8 hrs in children and young people 25% or greater fall in eGFR in children and young people within last 7 days
49
stage 1 AKI according to KDIGO criteria?
serum creatinine increase by 26micromol/L or more within 48 hrs or 1.5-1.9 times baseline UO less than 0.5ml/kg/hr for 6-12 hrs
50
stage 2 AKI according to KDIGO criteria?
serum creatinine 2-2.9 times baseline | UO less than 0.5ml/kg/hr for 12 hrs or more
51
stage 3 AKI according to KDIGO criteria?
serum creatinine 3 times baseline OR increase to 354 micromol/L or more OR decrease in eGFR to below 35ml/min in children and young people OR initiation of RRT UO less than 0.3ml/kg/hr for 24hrs or more OR no UO for 12hrs or more
52
proportion of people in hospital who suffer AKI?
1/6, or 16.7%
53
most common causes of severe sepsis?
pneumonia UTI bowel perforation severe skin infections
54
6 signs of sepsis recognised in a pneumonic by UK Sepsis Trust?
``` SEPSIS slurred speech extreme muscle pain passing no urine severe breathlessness I feel I might die skin mottled or discoloured ```
55
why is urine output not included in NEWS?
not routine in hospitals | cannot be measured in every patient
56
Urine dipstick testing for what should be carried out as soon as AKI suspected or detected?
``` Blood Protein Leucocytes Nitrites Glucose ```
57
Uraemic symptoms in CKD?
``` Malaise Appetite loss Insomnia Nocturia and polyuria as impaired concentrating ability Itching N and V, diarrhoea Paraesthesia Restless legs Bone pain Tetany and paraesthesia Oedema Amenorrhoea Erectile dysfunction ``` More severe-neurological common e.g. Seizures, mental slowing, clouding of consciousness, myoclonic twitching
58
1st step in managing AKI?
identifying and treating underlying cause
59
how is lipid modification for CVD addressed in CKD?
NICE recommends atorvastatin 20mg should be offered to all CKD patients for primary or secondary prevention of CVD dose should be increased if greater than 40% reduction in non-HDL cholesterol is not achieved and eGFR is 30ml/min or more agree use of higher doses with renal specialist if eGFR less than 30 (stage 4 CKD)
60
when is erythropoiesis stimulating agent (ESA- injectable form of erythropoietin) given to CKD patients?
to people with anaemia of CKD likely to benefit in terms of QOL and physcial function ,and not in presence of absolute Fe deficiency without also managing the Fe deficiency.
61
key aspects of AKI management?
cause diagnosis-urinalysis, USS correction of cause-IV fluids as per FLARE tool minimise nephrotoxic drugs e.g. aminoglycosides, NSAIDs, ACEIs, AngII blockers, diuretics unless fluid o.loaded, and metformin as risk of lactic acidosis monitoring- fluid balance, consider catherterisation, Us and Ex to reassess response to tment renal team referral
62
ECG changes of hyperkalaemia?
tall, tented T waves P wave small/loss widening of QRS complex loss of ST segment
63
hyperkalaemia management?
monitor ECG 10ml calcium gluconate 10% IV over 2min, repeated as necessary if severe ECG changes- avoid injecting into small peripheral cannulae as extravasation can cause skin necrosis. insulin and glucose e.g. 50ml of 50% glucose with 10U of rapidly acting insulin given into a large vein over approx 30 mins. Monitor for hypoglycaemia. nebulised salbutamol (2.5mg) calcium resonium-polystyrene sulfonate resin. if vomiting, may have to give as enema, so will require colonic irrigation after 9hr to remove K+ from colon. continued monitoring, repeat ECG if medical management fails, then indication for RRT-dialysis.
64
MAIN difference between haemofiltration and haemodialysis?
haemodialysis is DIFFUSION driven | haemofiltration is convection/pressure driven
65
contrast pt histories in IgA nephropathy and post-streptococcal glomerulonephritis?
PSG- had a cough a few weeks ago, now peeing blood | IgA nephropathy- has a cough currently and is peeing out blood.
66
normal protein urinary excretion?
150mg/24hr
67
characteristics of nephritic syndrome?
``` PHAROAH proteinuria- but tends to be less than that in nephrotic haematuria azotemia- blood contains excess nitrogen containing compounds e.g. urea and creatinine. red cell casts anti streptolysin 0 titres oliguria HTN ```
68
characteristics of haemofiltration?
form of RRT used in HDU patients as cheaper, safer and can be given 24/7. plasma water and its dissolved constituents e.g. K+, Na+, urea and phosphate removed by convective flow across a high-flux semipermeable membrane, and is replaced with a solution of desired biochemical composition. can be used in pts with haemodynamic instability high volumes must be exchanged to achieve adequate small molecule removal NOT diffusion mediated as haemodialysis is.
69
why is lactate used as a buffer in the replacement solution in haemofiltration?
rapid infusion of acetate causes vasodilatation, and bicarbonate may cause precipitation of calcium carbonate.
70
hypokalaemia ECG changes?
increase in U wave T wave flattening ST segment depression progressive lengthening of PR interval
71
danger of hyperkalaemia to the heart?
ventricular fibrillation
72
indications for acute dialysis in AKI?
persistent hyperkalaemia- K+ more than 7mmol/L severe metabolic acidosis-pH less than 7.2, or base excess less than 10. fluid overload- pulmonary oedema refractory to tment uraemic encephalopathy uraemic pericarditis- pericardial rub
73
2 reasons for hyperlipidaemia in nephrotic syndrome?
hypoalbuminaemia with proteinuria and albumin binds cholesterol albumin produced by liver, so with low albumin stimulating the liver to increase production, there is a co-stimulation to increase cholesterol production by the liver.
74
clinical features of nephrotic syndrome?
ask about acute or chronic infections, drugs, allergies, systemic symptoms e.g. considering vasculitis, malignancy. signs= oedema- typically pitting and dependent, occurs periorbitally as low tissue resistance here, and peripherally in limbs- genital oedema, ascites and anasarca devlop later= increase fluid in organs and cavities with severe oedema and tissue hardening, this also occurs in CCF, liver failure, protein losing enteropathy.
75
commonest cause of nephrotic syndrome in children?
minimal change glomerulonephritis
76
tests in suspected nephrotic syndrome?
FBC, Us and Es, LFTs, ESR, CRP, Igs, electrophoresis, C3 and C4, autoantibodies: ANCA, ANA, anti-dsDNA, anti-GBM, blood culture, urine- RBC casts, MC and S, Bence-Jones protein, 24 hr urine protein or spot urine sample early morning for PCR or ACR. CXR, renal USS and renal biopsy- do in all adults, but as most children have MCGN usually steroid course tried initially and biospy reserved for those who proteinuria not resolved after 1 mnth, or features suggestive or another cause e.g. age
77
features of minimal change glomerulonephritis?
``` T cell mediated selective proteinuria, podocyte loss assoc with Hodkin's lymphoma and drugs such as NSAIDs predisposition to FSGS as an adult podocyte fusion on electron microscopy appro 1% develop ESRF most respond to steroids-remission if frequent relapses or steroid SE/dependence, may use cyclophosphamice or ciclosporin. ```
78
how is membranous nephropathy diagnosed?
biopsy- diffuse thickened GBM | IgG and C3 subepithelial deposits
79
causes of FSGS?
idiopathic | secondary- vesicoureteric reflux, IgA nephropathy, Alport's, vasculitis, sickle-cell, herorin use, HIV.
80
why is the renal vein particularly prone to thrombosis in nephrotic syndrome?
Antithrombin III is lowest here presents with loin pain, palpable kidney, haematuria, sudden renal function deterioration, PE. diagnose with Doppler US, CT, MRI or renal angiography give tment dose of LMWH, or warfarin 3-6mnths- target INR 2-3 common in membranous nephropathy
81
appearance of FSGS on renal biopsy?
scarring of glomeruli also podocyte foot process fusion IgM and C3 deposits in affected areas with immunoflurescence
82
tment of FSGS?
30% respond to corticosteroids consider ciclosporin-calcineurin inhibitor, or cyclophosphamide, if steroid resistant. 30-50% progress to ESRF, and ESRF can occur within 2-20yrs recurs in 20-50% of transplanted kidneys, may respond to plasma exchange.
83
general measures in nephrotic syndrome tment?
treat underlying cause e.g. with steroids monitor Us and Es, BP, weight and fluid balance regularly aim for Na+ intake less than 3g/day and fluid intake less than 1.5L diuretics e.g. furosemide 80-250mg/24h PO ACEIs/A2A to reduce risk of CVD as proteinuria is an independent RF and is reduced with these tments treat infections, pneumococcal vaccin statin if hyperlipidaemia doesn't resolve with tment of underlying cause avoid prolonged bed rest, consider anticoag. prophylaxis treat HTN, target 125/75 if proteinuria more than 1g/24hr, address other RFs e.g. smoking, exercise, diet.
84
normal eGFR in men and women?
men: 90-140 ml/min women: 80-125 ml/min
85
what factors does the MDRD equation use to calculate eGFR?
age ethnicity gender creatinine modification of diet in renal disease study equation BUT doesn't take into account patient weight or muscle mass, so patients with greater muscle mass may be suggested to have kidney disease to higher than normal creatinine and subsequent eGFR, and elderly pts can be mistaken for having normal renal function due to lower muscle mass so creatinine and eGFR.
86
triad of haemolytic uraemic syndrome (HUS)?
AKI thrombocytopenia microangiopathic haemolytic anaemia
87
most common cause of primary nephrotic syndrome in adults?
membranous glomerulonephritis
88
causes of secondary membranous glomerulonephritis?
VITAMIN C vascular-N/A infection- Hep B, C, HIV, syphilis, malaria, schistosomiasis trauma/toxins-mercury, hydrocarbons, formaldehyde AI-SLE, RA, Sjogrens, thyroid metabolic-N/A iatrogenic-penicillamine, gold, NSAIDs and COX-2 inhibitors, lithium neoplastic- lung, GO, prostate, breast Cas congenital-N/A
89
why does hypocalcaemia occur in CKD?
``` increased phosphate as not excreted by the kidneys reduced calcitriol (active Vit D) as normally formed by the kidneys via renal 1 alpha hydroxylase activity ```

General Medicine Block (10 decks)

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