Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Renal > Renal Clinical 6-10 > Flashcards

Renal Clinical 6-10 Flashcards

1
Q

Where is the transplanted kidney placed?

A

Iliac fossa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is the transplanted kidney joined to the circulation?

A

Anastomosed to the iliac vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why would the native kidneys be removed?

A

Size (polycystic kidneys)

Infection (chronic pyelonephritis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are transplant surgical complications?

A

Vascular complications: bleeding, arterial thrombosis, venous thrombosis, lymphocele
Ureteric: urine leak
Infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are immunosuppressive agents for transplantation?

A

Corticosteroids
Calcineurin inhibitors e.g. Tacrolimus, Cyclosporine
Anti-proliferatives e.g. Azathioprine
mTOR inhibitors e.g. Sirolimus
Costimulatory signal blockers e.g. Belatacept
Depeleting agents e.g. Basiliximab, Anti-thymocyte globulin, Rituximab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the side effects of corticosteroids?

A

Hypertension, hyperglycaemia, infections, bone loss, GI bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the side effects of Tacrolimus (calcineurin inhibitor)?

A

Hyperglycaemia, AKI, tremor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the side effects of Cyclosporin (calcineurin inhibitor)?

A

Hirsutism, hypertension, AKI, gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the immunosuppression protocols for transplantation?

A

Induction: Basiliximab
Maintenance: Tacrolimus + Mycophenolate + steroids
Steroid free if possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the type of kidney donors?

A

Deceased donors - donation after brain death or cardiac death
Living donors - related or unrelated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the brain death criteria for transplant?

A 
Coma - unresponsive to stimuli
Apnoea off ventilator
Absence of cephalic reflexes - pupillary, oculocephalic, oculovestibular, corneal, gag, purely spinal reflexes may be present
Body temp above 34
Absence of drug intoxication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the complications after renal transplant?

A

Rejection: cell mediated, humoral
Cardiovascular: underlying renal disease, CRF, hypertension, hyperlipidaemia, new onset diabetes mellitus
Infective: bacterial, viral, fungal
Malignancy: skin, lymphoma, solid cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the types of acute rejection?

A

T cell mediated rejection (TCMR)

Acute antibody mediated rejection (ABMR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the features of T cell mediated rejection (TCMR)?

A

Lymphocytic infiltrate
Tubulitis
Endarteritis
Endothelialitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the features of antibody mediated rejection?

A

Microvascular inflammation: neurophil infiltration
Donor specific antibodies
Positive C4d: peritubular capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the most important transplant-related infection?

A

Cytomegalovirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Approximately what percentage of transplant patients are affected by cytomegalovirus despite prophylaxis therapy?

A

8%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do patients get cytomegalovirus after transplantation?

A

Transmission from donor tissue

Reactivation of latent virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are other infections that are possible after tranplantion (apart from cytomegalovirus)?

A

Tissue invasive disease: pneumonitis, hepatitis, retinitis, gastroenteritis, colitis, nephritis
Polyomaviriae: BK virus and JC virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are clinical manifestations of the BK virus after renal transplantation?

A

Ureteral stenosis
Interstitial nephritis
ESRF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Apart from renal transplantation, when else might BK virus manifest?

A

Bone marrow transplantation
AIDs
Immunocompromised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the risk factors for BK virus?

A

Intensity of immunosuppression
Patients determinants: age, male, white, DM
Organ determinants: graft injury, ureteral stents
Viral determinants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the management of BK virus?

A

Reduce immunosuppression

Antiviral therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Which type of cancers are most common after renal transplantation?

A

Renal - 15%

Non-melanoma skin, non-Hodgkins Lymphoma - 20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the definition of acute renal failure?

A

Rapid loss of glomerular filtration and tubular function over hours to days
Retention of urea/creatinine - failure of homeostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the relationship between GFR and creatinine?

A

As creatinine levels increase, GFR lowers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is current definition of AKI?

A

Increase in serum creatinine by >26.5umol/l within 48hrs
or to >1.5x baseline which is known or presumed to have occurred within the prior 7 days or
Urine volume <0.5ml/kg/hr for 6hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How many stages of AKI are there as defined by KDIGO?

A

3 stages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How many times the baseline is AKI 1?

A

1.5-1.9 x baseline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How many times the baseline is AKI 2?

A

2.0-2.9 x baseline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How many times the baseline is AKI 3?

A

3.0 x baseline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the immediate dangerous consequences of AKI?

A 
AEIOU
A = acidosis
E = electrolyte imbalance
I = intoxication TOXINS
O = overload
U = uraemic complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is a pre-renal cause of AKI?

A

Blood flow to kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is a renal (intrinsic) cause of AKI?

A

Damage to renal parenchyma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is a post-renal cause of AKI?

A

Obstruction to urine exit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are some pre-renal causes of AKI?

A 
Sepsis
Hypovolaemia
Hepatorenal syndrome
Cardiac failure
Hypotension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are some intrinsic causes of AKI?

A 
Acute tubular injury/necrosis - ischaemic
Tubulointerstitial injury
Acute GN
Myeloma
Vasculitits
Toxin related - drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are some post-renal causes of AKI?

A

Kidney stones
Prostatic hypertrophy
Tumours
Retroperitoneal fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How does hypovolaemia/hypotension/cardiac failure cause AKI?

A

Reduce effective circulation volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the most common cause of AKI?

A

Pre-renal = poor perfusion leading to established tubular damage (hypotension/hypovolaemia)

41
Q

Why is the kidney susceptible to hypoperfusion?

A

Intrarenal demands of blood supply, oxygenation, metabolic demand
Cortex is richly perfused

42
Q

What may happen if GFR recovers quicker than tubule reabsorptive capacity?

A

Excessive diuresis (post-obstructive diuresis)

43
Q

What is common contributor to hospital acquired AKI (iatrogenic)?

A

Radiocontrast nephropathy (RCN)

44
Q

What are risk factors for RCN?

A 
Diabetes
Renovascular disease
Impaired renal function
Paraprotein
High volume of radiocontrast
All of the above
45
Q

What is multiple myeloma?

A

A disease of plasma cells where there is monoclonal proliferation and the production of an excess of immunoglobulins and light chains

46
Q

What are the clinical features of multiple myeloma?

A

Anaemia, back pain, weight loss, fractures, infections, cord compression, markedly elevated ESR, hypercalcaemia

47
Q

How is multiple myeloma diagnosed?

A

Bone marrow aspirate
Serum paraprotein and immunoparersis
Urinary Bence-Jones protein (BJP)
Skeletal survey

48
Q

How does renal failure occur in multiple myeloma?

A 
Cast nethropathy
Light chain nethropathy
Amyloidosis
Hypercalcaemia
Hyperuricaemia
49
Q

What is cast nethropathy?

A

Formation of plugs in the renal tubules from free immunoglobulin light chains leading to renal failure

50
Q

So, the main causes of AKI?

A

Pre-renal: Cardiac failure, haemorrhage, sepsis, vomiting and diarrhoea
Post-renal: Tumours, prostate disease, stones
Intrinsic: GN, vasculitis, radiocontrast, myeloma, drugs
Multifactoral

51
Q

What are the investigations for AKI?

A 
Renal function
Urine dipstick/urine PCR/urine BJP
FBC: U+E, bicarbonate, LFTs, bone, clotting
USS
Blood gas
?ANCA, Ig
?Renal biopsy
52
Q

To pre-empt AKI, what are AKI risk events?

A 
Surgery
Sepsis
Toxins
Hypovolaemia
Hypotension
53
Q

To pre-empt AKI, what are AKI risk factors?

A 
Age >75
Previous AKI
Heart failure
Liver disease
CKD
Diabetes mellitus
Vascular disease
Cognitive impairment
54
Q

What is the STOP mnemonic for identifying patients are risk of AKI?

A 
STOP
S = sepsis - treat
T = toxins - avoid
O = optimise BP and volume status
P = prevent harm - daily U+Es, fluid balance, medication review
55
Q

What is the general management for the causes of AKI?

A

Pre-renal: do they need fluid/BP support?
Intrinsic: can you remove precipitant?
Post-renal: do they need a catheter?

56
Q

How do you optimise BP in someone with AKI?

A

Give fluid/vasopressores

Stop ACEi/anti-hypertensives

57
Q

What are nephrotoxic drugs to stop in someone with AKI?

A

NSAIDs

Aminoglycosides

58
Q

What can excessive loss of gastric fluid cause?

A

Metabolic alkalosis

59
Q

What are the 5 R’s for IV prescribing?

A 
Resuscitation
Routine maintenance
Replacement
Redistribution
Reassessment
60
Q

What is normal total intake of fluids per day?

A

2500ml

61
Q

What is normal total output of fluids per day?

A

2100-2600ml

62
Q

What are the ECG changes seen in hyperkalaemia?

A

Peaked T waves
P wave widens and flattens
PR segment lengthens
P waves eventually disappear

63
Q

What is the treatment for hyperkalaemia?

A

Stabilize myocardium = calcium gluconate
Shift (K+ intracellularly) = salbutamol, insulin-dextrose
Remove = diuresis, dialysis, anion exchange resins
Antidote if available = morphine/digoxin

64
Q

How do haemidialysis and haemofiltration differ?

A 
Haemodialysis = solute removal by diffusion
Haemofiltration = solute removal by convection
65
Q

What are the advantages of haemodialysis?

A

Rapid solute removal
Rapid volume removal
Rapid correction of electrolyte disturbances
Efficient treatment for hyper catabolic patient

66
Q

What are the disadvantages of haemodialysis?

A

Haemodynamic instability
If dialysis associated with hypertension, may prolong AKI
Fluid removal only during short treatment time

67
Q

What are the advantages of CRRT?

A

Slow volume removal associated with greater haemodynamic stability
Absence of fluctuation in volume and solute control over time
Greater control over volume status

68
Q

What are the disadvantages of CRRT?

A

Need for continuous anticoagulation
May delay weaning/mobilisation
May not have adequate clearance in hypercatabolic patient

69
Q

What is the syndrome of advanced CKD called?

A

Uraemia

70
Q

What are the earliest and cardinal symptoms of uraemia?

A

Malaise and fatigue

71
Q

When is renal replacement therapy usually indicted (GFR)?

A

eGFR <10ml/min

72
Q

What are the types of RRT?

A

Renal transplant
Haemodialysis
Peritoneal dialysis
Conservative kidney management

73
Q

What is the principle of dialysis?

A

The solute composition of solution A is altered by exposing solution A to a solution B through a semipermeable membrane

74
Q

What are the pre-requisites for dialysis?

A

Semipermeable membrane = artificial kidney in haemodialysis or peritoneal membrane
Adequate blood exposure to membrane = extracorporeal blood in haemodialysis, mesenteric circulation in PD
Dialysis access = vascular or peritoneal
Anticoagulation

75
Q

What is permanent vascular access in haemodialysis?

A

Arteriovenous fistula

AV prosthetic graft

76
Q

What is temporary vascular access in haemodialysis?

A

Tunnelled venous catheter

Temporary venous catheter

77
Q

What are the restrictions for dialysis patients?

A

Fluid restriction

Dietary restriction - potassium/sodium/phosphate

78
Q

What are the types of PD?

A

Continuous ambulatory peritoneal dialysis (CAPD)
Automated peritoneal dialysis (APD)
Hybrid

79
Q

How does PD work?

A

A balanced dialysis solution is instilled into the peritoneal cavity via a tunnelled, cuffed catheter, using the peritoneal mesothelium as a dialysis membrane
The fluid is drained and fresh dialysate instilled

80
Q

What is the most common osmotic agent for ultrafiltration of fluid in PD?

A

Glucose

81
Q

What are complications of PD?

A

Exit site infection
PD peritonitis
Ultrafiltration failure
Encapsulating peritoneal sclerosis

82
Q

What are the indications for dialysis in ESRD?

A 
Advanced uraemia (GFR <10ml/min)
Severe acidosis (bicarbonate <10mmol/l)
Treatment resistant hyperkalaemia
Treatment resistant fluid overload
Clinical judgement
83
Q

What is the fluid restriction is a haemodialysis patient normally?

A

Restricted to 500-800ml/24hrs

84
Q

What are dialysis related drugs?

A

Anaemia: erythropoietin injections/IV iron supplements
Renal bone disease: activated vitamin D, phosphate binders with meals
Heparin
Water soluble vitamins
?antihypertensives

85
Q

What are the complications of haemodialysis?

A

CV: intra-dialytic hypotension and cramps, arrhythmias
Coagulation: clotting of vascular access, heparin related problems
Other: allergic reaction, accidents (rare)
Infection
Mechanical: tube malfunction
Ultrafiltration problems

86
Q

What are upper urinary tract symptoms?

A

Pain
Frank haematuria
Symptoms of complications

87
Q

What are upper urinary tract signs?

A

Palpable mass
Microscopic haematuria
Signs of complications

88
Q

What are complications of upper urinary tract problems?

A

Infection and sepsis

Renal failure

89
Q

What are the investigations for upper urinary tract symptoms?

A

USS

CT (non-contrast)

90
Q

50yo man with left sided loin pain. Pain is colicky and causes nausea and vomiting. No PMH, no medications. Temp 40’, HR 100bpm, BP 90/60mmHg, O2 sats 89% on air. He is extremely tender over left loin and flank areas. What investigations would you organise and what is most important step in management?

A

USS + CT (non-contrast)

Check for UTI

91
Q

What is pyonephrosis?

A

Infection of kidneys collecting system = pus collects in renal pelvis

92
Q

What is the management of upper urinary tract obstruction?

A 
Resuscitaton: ABCs, IV access, bloods, ABG, urine and blood cultures, fluid balance monitoring
IV fluids, broad-spectrum antiobiotics
Analgesia
Investigations
Emergency treatment for obstruction
Treat underlying cause/obstruction
93
Q

What is a nephrostomy?

A 
Percutaneous puncture (US/XR guidance)
Drains pus out of kidney so obstruction is relieved
94
Q

How does a ureteric stent work?

A

Ureter dilates around tube, urine goes on outside of tube

95
Q

How does high pressure chronic retention usually present?

A

Painless
Incontinent
Raised creatinine
Bilateral hydronephrosis

96
Q

How does low pressure chronic retention usually present?

A

Painless
Dry
Normal creatinine
Normal kidneys

97
Q

Which is more dangerous: high or low pressure chronic retention?

A

High pressure

98
Q

Why is post obstructer diuresis so dangerous?

A

Can lead to life threatening sodium and water depletion

Renal (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions