Brainscape's Knowledge GenomeTM

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


See full index

Year 3 Medicine > Urology > Flashcards

Urology Flashcards

1
Q

How can obstructive nephropathy or significant infection secondary to kidney stones be treated?

A
  1. Stent Insertion - placed within the ureter via cystoscopy which allows the ureter to be kept patent and temporarily relieve the obstruction.
  2. Nephrostomy - tube placed directly into the renal pelvis and collecting system, relieving the obstruction proximally
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is AKI?

A

Acute kidney injury (AKI) is a syndrome of decreased renal function, measured by serum creatinine or urine output, occurring over hours-days.

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

How is AKI defined?

A

Rise in Serum Creatinine

  • >26µmol/L within 48h.
  • or >1.5 × baseline within 7 days

Reduced Urine Output

  • Urine output <0.5mL/kg/h for >6 consecutive hours.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the different stages of AKI?

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

What are the most common causes of AKI?

A
  • Sepsis.
  • Major surgery.
  • Cardiogenic shock.
  • Other hypovolaemia.
  • Drugs.
  • Hepatorenal syndrome.
  • Obstruction.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How can AKI causes be divided up?

A
  • Pre-renal: ↓ perfusion to the kidney
  • Renal: intrinsic renal disease
  • Post-renal: obstruction to urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are some of the RFs for AKI?

A
  • Diabetes
  • CKD
  • IHD/CCF
  • Elderly >75
  • Sepsis
  • Medications – ACEi, ARBs, NSAIDs, Antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do we assess a patient with AKI?

A
  • Assessment ABCDE
  • C: Circulation, volume status - BP, HR, JVP, skin turgor, cap refill <2s, urine output (cathetarise)
  • Hyperkalaemia: K+ on venous blood specimen + ECG
  • Drugs assessment
  • Examination: Full systemic exam. Palpable bladder/ kidneys, abdominal pelvic masses, renal bruits, rashes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What should you check in an AKI history?

A
  • Risk factors
  • Comorbidities
  • Previous renal disease
  • Recent fluid intake and losses
  • New drugs including chemotherapy
  • Systemic features: rash, joint pain, fr
  • Other systems: productive cough, haemoptysis, GU or GI symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What tests diagnose AKI?

A
  • Bedside: Urine dip, microscopy and culture. HR and BP
  • Bloods: UE, FBC, LFT, clotting, CK (rhabsomyolysis), creatinine, ESR, CRP. ABG. Blood cultures
  • If blood and protein on urine dipstick – perform c-ANCA (PR3) + p-ANCA (MPO) for vasculitis, anti-GBM, ANA, C3, C4 to look for lupus nephritis, serum immunoglobulins and electrophoresis to look for myeloma
  • Ipost-streptococcal GN – do Anti-Streptolysin O Titres
  • Thrombocytopenia - HUS/TTP/Disseminated Intravascular Coagulopathy, request haemolysis screen - blood film, LDH, bilirubin, reticulocytes, haptoglobin, and call Renal SpR urgently.
  • Cryoglobulins - if unexplained rash, peripheral neuropathy, hypocomplementaemia, known hepatitis C, history of lymphoproliferative disorder, or +ve RhF.
  • Imaging: renal USS, CTKUB (no contrast)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the indications for renal replacement therapy?

A
  • Fluid overload unresponsive to medical treatment.
  • Acidosis: Severe/prolonged
  • Hyperkalaemia: Recurrent/persistent despite medical treatment.
  • Uraemia: eg pericarditis, encephalopathy (more common in ckd).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What General measures are used for for AKI management?

A

STOP

  • Sepsis: Sepsis 6 screen + Abx (avoid nephrotoxins)
  • Toxins: Stop nephrotoxic drugs: NSAIDs, ACEi, ARBs, metformin (>150mmol/L), gentamycin
  • Optimise/ Assess Volume Status:
    • Look for: ↓urine volume, non visible JVP, poor tissue turgor, ↓BP/ JVP.
    • Fluid overload ↑BP/ JVP, lung crepitations, peripheral oedema, gallop rhythm
    • Aim for euvolaemia: consider IV fluid resuscitation: 500mL crystalloid (Hartman) 15 mins
  • Prevent Harm
    • Monitoring: ICU/ HDU: check BP, JVP, urine output, CVP
    • Daily: U+Es, fluid balance chart, daily weight
    • Nutrition: aim for a normal calorie intake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do you treat the underlying causes of AKI?

A
  • Pre-renal: correct volume depletion and/or ↑renal perfusion via circulatory/cardiac support, treat sepsis.
  • Renal: refer for likely biopsy and specialist treatment of intrinsic renal disease.
  • Post-renal: catheter, CTKUB no contrast (look for hydronephrosis) nephrostomy, or urological intervention.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some of the complications of AKI?

A
  • Hyperkalaemia
  • Acidaemia
  • Pulmomary Oedema
  • Uraemia - encephalopathy, pericarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is renal replacement therapy performed?

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

How do you manage the complications hyperkalaemia as a complication of AKI?

A

Hyperkalaemia

  • IV Calcium gluconate STAT 10%, 10mg over 5-10 minutes
  • IV fast acting Insulin (actrapid) 10 units + Dextrose/ glucose 50ml 50%
  • Salbutamol: 5-10 mg via nebulizer
  • IV Sodium bicarbonate (if acidotic)
  • Eliminating potassium from body:
    • Calcium resonium 15-45g orally - with sorbitol or lactulose
    • Furosemide 20-80mg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do you manage Pulmonary Oedema as a complication of AKI?

A

Pulmonary Oedema

  • O2 high flow 15L
  • Venous vasodilator - diamorphine
  • Furosemide 80-250mg
  • If not response: urgent haemodialysis, filtration
  • CPAP
  • IV nitrates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What defines Nephrotic Syndrome?

A
  • Proteinuria >3g/24h
  • Hypoalbuminaemia (usually <30g/L, can be <10g/L)
  • Oedema
  • Hypercholesterolaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are some of the causes of Nephrotic Syndrome?

A
  • Primary renal disease:
    • Minimal change disease
    • Membranous nephropathy
    • Focal segmental glomerulosclerosis (fsgs),
    • Membranoproliferative gn
  • Secondary causes:
    • Diabetes mellitus
    • SLE
    • Myeloma
    • Amyloid
    • Pre-eclampsia
    • Amyloidosis
    • Paraneoplastic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the pathophysiology of Nephrotic Syndrome?

A

Podocyte pathology:

  • Minimal change disease
  • Membranous nephropathy: abnormal function in , immune- mediated damage
  • FSGS: Podocyte injury/death in
  • Membranoproliferative GN: or pathology in the gbm/endothelial cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the presentation of Nephrotic Syndrome?

A
  • Generalized, pitting oedema, which can be rapid and severe
  • Look in dependent areas (ankles if mobile, sacral pad/elbows if bed-bound) and areas of low tissue resistance, eg periorbitally.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What should history taking in Nephrotic Syndrome ask about?

A
  • Systemic symptoms, eg joint, skin
  • Malignancy
  • Chronic infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are some of the complications of nephrotic syndrome?

A
  • Higher risk of infection
  • Venous Thromboembolism
  • Progression of CKD
  • Hypertension
  • Hyperlipidaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is Nephrotic Syndrome managed?

A
  1. Reduce Oedema:
    • Furosemide IV
    • Restrict their fluid intake to 1L per day
    • Reduce Salt
  2. Reduce Proteinuria : Acei/ ARB
  3. Reduce Complications: anticoagulate/ statin
  4. Treat the underlying cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are some of the complications of Nephrotic Syndrome?

A
  • Susceptibility to infections: cellulitis, strep
  • Thromboembolism: DVT/ PE as blood is hypercoagulable (↑ clotting factors/ platelet abnormalities)
  • Hyperlipidaemia: ↑Cholesterol/LDL/ triglycerides, ↓HDL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is Nephritic Syndrome?

A
  • Pathology in the glomerulus
  • Present with proteinuria, haematuria, or both
  • Hypertension
  • Diagnosed on renal biopsy
  • Can cause CKD or AKI (except minimal change disease).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does Glomerularnephritis present?

A
  • AKI (sometimes GFR can drop drastically)
  • On urine dipstick: blood +/- and/or protein+/-
  • Mild to moderate oedema
  • Proteinura <3.5g/24 hours
  • Hypertension
  • Sometimes visible haematuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How is Glomerulonephritis investigated?

A
  • Urine dipstick (haematuria +/- proteinuria)
  • Renal Biopsy
  • Bloods: FBC, U&E, LFT, CRP; immunoglobulins, electrophoresis, complement (c3, c4); autoantibodies ana, anca, anti-dsdna, anti-gbm; blood culture, asot, hepatitis serology.
  • Urine: mc&s, Bence Jones protein, rbc casts
  • Imaging: CXR (pulmonary haemorrhage), renal USS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are some of the common primary and secondary causes of Nephritis syndrome?

A
  • Primary: IgA nephropathy, Mesangiocapillary GN
  • Secondary: Post streptococcal, vasculitis, SLE, anti GBM, cryoglobuminaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How is Glomerulonephritis managed?

A

Supportive therapy:

  • If suspect GN – discuss with Renal team
  • MDT approach depending on underlying diagnosis
  • ACEi/ARB for proteinuria
  • Control BP
  • Salt and water restriction if volume overloaded
  • Diuretics for fluid overload
  • If hypoalbuminaemic <20g/dl then higher risk for VTE – consider therapeutic LMWH
  • Statins for hypercholesterolaemia

Immunosuppressive Therapy

  • Specific to cause of GN – decided by Renal team (+/- Respiratory / Rheumatology teams if lung or systemic involvement )
  • Oral Corticosteroids, IV pulsed methylprednisolone, Cyclophosphamide, Tacrolimus, Ciclosporin, Rituximab, MMF, Azathioprine

Invasive therapy

  • Renal replacement therapy/haemodialysis for those in severe AKI or ESRF
  • Plasma exchange for AAV, anti-GBM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is Chronic Kidney Disease?

A
  • CKD is defined as the presence of kidney damage, manifested by abnormal albumin excretion
  • Or decreased kidney function (GFR<60ml/min), quantified by measured or estimated GFR that persists for more than > 3months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What GFR is kidney failure

A

15ml/min/1.73m2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are some of the causes of CKD?

A
  • Diabetes
  • Hypertension
  • Glomerulonephritis
  • Renovascular Disease
  • Polycystic Kidney disease
  • Obstructive nephropathy – urological problems
  • Chronic/recurrent Pyelonephritis
  • Others
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are some of the complications of CKD?

A
  • Anaemia of Chronic Kidney Disease
  • CKD – Mineral & Bone Disease
  • Secondary & Tertiary Hyperparathyroidism
  • Hypertension
  • Cardiovascular Disease – No 1 cause of Mortality
  • Malnutrition/sarcopenia
  • Dyslipidaemia
  • Electrolyte disturbances
  • Fluid overload
  • Metabolic acidosis
  • Uraemic pericarditis
  • Uraemic encephalopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What should the history of CKD focus on?

A
  • Possible cause:
    • UTI/ LUTI sx, PMH of ↑BP, DM, IHD, systemic disorder, renal colic.
    • Drug history: medications started.
    • FMH: renal disease and subarachnoid haemorrhage.
    • Systems review: look out for more than is immediately obvious, consider rare causes, ask about eyes, skin, joints, ask about symptoms suggestive of systemic disorder (‘When did you last feel well?’) and malignancy.
  • Current state: Patients may have symptomatic CKD if GFR <30.
  • Symptoms: fluid overload (sob, peripheral oedema), anorexia, nausea, vomiting, restless legs, fatigue, weakness, pruritus, bone pain, amenorrhoe
36
Q

What are some of the symptoms of CKD?

A
  • Symptoms:
    • Fluid overload (SOB, peripheral oedema)
    • Anorexia, nausea, vomiting, restless legs, fatigue, weakness, pruritus, bone pain, amenorrhoe
37
Q

What are some of the tests that done for CKD?

A
  • Bloods: Hb, ESR, glucose, ↓Ca2+, ↑alk phos/ PO43/ PTH
  • Urine: dipstick, MC+S, albumin: creatinine
  • Imaging: USS
  • Histology: renal biopsy
38
Q

How do you manage CKD?

A
  • Treat underlying disease
    • ADPKD: Tolvaptan
    • Diabetic control
    • Infections promptly
    • Immunosuppression for GN if appropriate
    • Cardiovascular Control: Statin, Diet: Advise weight loss / exercise, hypertension
    • Reduce progression of CKD
    • Proteinuria – ACEi/ARB
    • Monitor blood tests

Manage Complications

  • BP Control BP Prevent or treat complications of CKD
  • Dietary advice regarding low phosphate/low potassium diet
  • Phosphate binders

Anaemia of Chronic Disease

  • IV Iron/Folate/Vit B12 replacement
  • EPO (Erythropoesis stimulating agent)
  • Replace Vitamin D deficiency
  • Consider Calcimimetics for tertiary hyperparathyroidism
  • Dietician input Plan for the future
  • Start discussions of what options they have if they reach ESRF
  • Home care team input
  • Renal Replacement Therapy
  • Home therapies – APD, CAPD, Home HD o Unit-based therapies – Nocturnal HD, conventional HD
  • Active conservative management o Transplant
  • Refer for fistula
  • Venous mapping
  • Refer for PD tube insertion
  • Work-up for transplant
  • Further tests
  • Refer to Transplant work-up clinic
39
Q

What is PCKD?

How is it diagnosed?

How is it treated?

What is a complication of PCKD?

A
  • 2 types (both autosomal dominant)
    • T1 - PKD1 mutation Chromosome 16 - 85%
    • T2 - PKD2 mutation Chromosome 4
  • Diagnosis: FH, USS
  • Treatment:
    • Control BP
    • CKD mgmt
    • Tolvaptan: ADHR2 ntagonist - slow progression
  • Complications: berry aneurysms due to cyst formation in brain -> increased risk of subarachnoid haemorrhage
40
Q

What is Diabetic Nephropathy?

How is it screened for?

How is it treated?

A
  • Big cause of CKD (in T1 + T2 DM)
  • Associated with other diabetic microvascular complications e.g.
    • Retinopathy
    • Peripheral Neuropathy
  • Screening: most pt will undergo screening
    • Raised urine albumin: creatinine ratio
    • Evidence of long standing poorly controlled DM
    • Evidence of other microvascular disease
  • Treatment:
    • ​Acei/ ARB
    • Anti hypertensives for BP control
    • CVS risk modification
    • Continue screens - eye and foot
41
Q

What is hypertensive nephropathy?

A
  • Big cause of CKD!
  • Chronic raised BP -> nephrosclerosis
  • Diff to tell if HT causes the renal impairment or renal impairment causes HT
  • Ix:
    • 24 hr urinary metanephrines - phaechromacytomy
    • Aldosterone: renin ratio - primary aldosteronism
    • Cortisol + dexamethasone suppression test - Cushings
    • TSH - Hyperthyroidism
    • MRA (Magnetic resonance angiography) - Renal artery stenosis
  • Treatment: anti hypertensives
42
Q

What is CKD Mineral Bone Disease?

How does it arise?

How is it diagnosed and treated?

A
  • Complication of CKD
  • Diagnosis: Bloods:
    • Decreased: Ca, Vit D
    • Increased: PO43-, PTH, ALP, fibroblast GF 23
  • Complications: Can cause abnormalities of bone turnover, metabolism, volume
    • Low turnover: adynamic bone disease, osteomalacia
    • High turnover: osteoitis fibrosis
  • Treatment: Vit D, calcimimetics for tertiry hyperparathyroidism
    • Reduce occurence + severity of renal bone disease
    • CVS morbidity and mortality causedby elevated PTH + high phosphate levels
43
Q

What are the main types of RRT?

A
  • Peritoneal Dialysis
  • Haemodialysis
  • Haemofiltration
  • Kidney transplant
44
Q

When is RRT started?

A
  • Inability to control volume status, including pulmonary oedema
  • Inability to control blood pressure
  • Serositis
  • Acid-base or electrolyte abnormalities
  • Pruritus
  • Nausea/vomiting/deterioration in nutritional status
  • Cognitive impairment.
45
Q

What eGFR is expected on commencing RRT?

A

~5–10

46
Q

What is haemodialysis?

A
  • Dialysis maching pumps blood from pt through disposable tubing (dialyser)/ fake kidney -> then back to pt
  • Blood is passed over a semi-permeable membrane against dialysis fluid flowing in the opposite direction
  • Access via arteriovenous fistula
47
Q

What are some of the advantages of haemodialysis?

A
  • Efficient
  • Unit based
48
Q

What are some of the disadvantages of haemodialysis?

A
  • Dialysis must be secure
  • Infection
  • Haemodynamic instability
  • Reactions to dialyser
  • Muscles cramps
  • Anaemia
  • AVF steal syndrome
49
Q

What types of transplantation can you have?

A
  1. Live donor - related/ non related - better
  2. Deceased donor - sudden death
50
Q

What are the dis-/advantages of transplantation?

A
  • Advantages: normal lifestyle and better mortality/morbidity
  • Disadvantages
    • Criteria to meet suitability
    • Life long meds
    • ? rejection
    • Risk of malignancies over time
    • Risk of infection (on immunosuppression)
    • Long waiting times
51
Q

What methods of access are used for haemodialysis?

A
  • Central lines
  • AV fistula
  • Tunelled lines
52
Q

What is peritoneal dialysis?

A
  • Pt own peritoneal membrane acs as dialysis membrane
  • A catheter is inserted into the peritoneal cavity and fluid infused
  • Osmotic gradient created by high [glucose] in diasylate fluid
  • Solutes move from pt blood -> down conc. gradient > into diasylate fluid
53
Q

What is Steal Syndrome secondary to an AV fistula (RRT)?

A
  • Reduced perfusion to the hand secondary to too much blood now travelling through the AV fistula and reduced bloodflow through the distal arteries.
  • Hypoperfusion of hands will cause pain and tingling and numbness of hands
54
Q

What are the advantages and disadvantages of peritoneal dialysis?

A
  • Advantages: QoL, individualised regimes
  • Disadvantages: technical aspects, unsuitable if previous surgery/ stoma, infection, complications p drainage malposition hernia
55
Q

Who does post streptococcal GN affect? When does it occur?

A
  • Kids: 3-12
  • 1-2 weeks post tonsillitis/ pharyngitis
  • 3-4 weeks after impetigo/ cellulitis
56
Q

What investigation findings would you expect to see for post strep GN?

A
  • +ve anti-streptococcal ABs
  • Low C3
  • Biopsy: immune complex deposition on IgM, IgG, C3
57
Q

What is IgA nephropathy and who does it affect?

A
  • Most common cause of nephritis
  • Haematuria post infection: URTI, GI, exercise
  • Who? 20s to 30s
58
Q

What would ix show for IgA nephropathy?

A
  • Increase in serum IgA
  • Haematuria
  • Normal C3 + C4
  • Biopsy: immune complex depositions on mesangial glomeruli cells
  • Treatment: supportive Ace / ARB
59
Q

What is anaemia of chronic disease?

Why does it arise?

How is it managed?

A
  • Complication of CKD
  • Factors
    • Reduced EPO from kidney
    • Absolute iron deficiency (poor absorption + malnutrition)
    • Functional iron deficiency (inflammation, infection)
    • Blood loss
    • Short RBC survival
    • Bone marrow suppression
    • Vit b12/ folate deficiency
  • Management of anaemia of CKD
    • Measure haematinics - vitb12, folate, ferritin, iron, transferring, sats, CHr
      • Replace any of these deficiencies first - IV iron better than PO iron
    • Start erythropoeitin stimulating agents (ESA) - discuss w renal team
    • Aim for Hg 100-120
60
Q

What sx are associated with Alports?

A
  • Haematuria
  • Sensorineural hearing loss
  • Biopsy: splitting of GBM and alternating thickening + thinning of GBM
61
Q

What is ANCA associated vasculitis and who does it affect?

A
  • Vasculitis
  • Pulmonary and pharnygeal involvement - haemoptysis, nasal ulcers, polyps
  • If eosinophilic pt will have: asthma, alergies, purpura, peripheral neuropathy
62
Q

What would investigations show for ANCA?

A
  • c-ANCA raised
  • p-ANCA raised
  • Raised eosinophilia
  • Biopsy: focal segmental necrotizing GN
63
Q

What is anti GBM disease and who gets it?

A
  • ABs against T4 collagen react with pulmonary BM causing haemmorhage and haemoptysis
  • 30s and 0ver 60s
64
Q

What would Ix for anti GBM show?

A
  • Biopsy: Linear deposition of IgG along basement membrane
  • Anti GBM Abs
  • Pulmonary infiltrate of CXR
65
Q

What is alport syndrome?

A
  • X linked mutation in the gene coding for T4 collagen
  • Associated with hearing loss and eye troubles
  • Persistent microscopic haematuria + intermittent visible haematuria
  • Sensorineural hearing loss
  • Biopsy: splitting of GBM + alternating thickening + thinning of GBM
  • Treatment: RRT, transplant (could lead to Goodpastures)
66
Q

What are the contraindications of renal transplantation?

A
  • Active infection or malignancy
  • Severe heart disease not suitable for correction
  • Severe lung disease
  • Reversible renal disease
  • Uncontrolled substance abuse, psychiatric illness
  • On-going treatment non-adherence
  • Short life expectancy
67
Q

What induction therapy is given for renal transplantation?

A
  • Immunosuppressive drugs are used to create tolerance of the graft
  • These include methylprednisolone in combination with any of the following: basiliximab and thymoglobulin;
68
Q

What maintenance therapy is used for renal transplantation?

A
  • Lifelong immunosuppression
  • Drugs commonly used are grouped as:
    • Steroids: prednisolone (or prednisone)
    • Calcineurin inhibitors (CNI): tacrolimus, cyclosporine, voclosporin
    • Antimetabolite medications: mycophenolate, azathioprine
    • Rapamycin inhibitors: sirolimus and everolimus
    • T-cell regulation: Belatacept and belimumab
69
Q

How do you monitor long term the care of transplant patients?

A
  • For the firsts months, follow up happens several times a month, after 6 months it happens less often
  • Monitor GFR, CNI levels, proteinuria, Ca, phosphate and PTH, lipids and glucose
  • Screen for infections (common and opportunistic)
  • Vaccination (except live or live attenuated viral vaccines)
  • Monitor and control CVS disease, bone and mineral metabolism disease
  • Screen for malignancies as patients are three times more likely to have any cancer
  • Annual skin checks for skin cancers
  • Contraception is obligatory in the first year, counsel about pregnancy one year after
  • Mortality is related to: cardiovascular disease, infections and malignancies
70
Q

What are some of the important infections to consider for with transplant patients?

A
  • CMV
  • Hepatitis B
  • Herpes simplex virus
  • Varicella zoster
  • EBV
  • BK
  • Aspergilllus
  • Pneumocystis jirovecii
  • Listeria
  • Mycobacterium tuberculosis
  • Toxoplasma gondii
  • Within the first year, some patients can develop new-onset diabetes after transplant (NODAT)
71
Q

Where do kidney stones commonly form?

A
  1. Pelviureteric junction
  2. Pelvic brim
  3. Vesicoureteric junction.
72
Q

What types of kidney stones do you get?

A
  • Calcium oxalate (75%).
  • Magnesium ammonium phosphate (struvite/triple phosphate; 15%).
  • Also: urate (5%), hydroxyapatite (5%), brushite, cystine (1%), mixed.
73
Q

How do kidney stones present generally?

A
  • Can be assymptomatic
  • Pain: ‘loin to groin’ (or genitals/inner thigh), with
  • Nausea/vomiting.
  • Cannot lie still
  • Haematuria
  • Proteinuria
  • Sterile pyuria
  • Anuria
74
Q

Depending on where the stone is obstructed, what type of symptoms do you get?

A
  • Obstruction of kidney: felt in the loin, between rib 12 and lateral edge of lumbar muscles (like intercostal nerve irritation pain; not colicky, worsened by specific movements/pressure on a trigger spot).
  • Obstruction of mid-ureter: mimic appendicitis/diverticulitis.
  • Obstruction of lower ureter: sx of bladder irritability. Pain in scrotum, penile tip, or labia majora.
  • Obstruction in bladder or urethra: pelvic pain, dysuria, strangury (desire but inability to void) ± interrupted flow.
75
Q

How do the stones appear depending on their composition?

A
  • Calcium (oxolate, phosphate) - radio-opaque (spikey, smooth)
  • Magnesium ammonium phosphate (struvite) - stag horn calculi, radio-opaque
  • Urate - radio lucent
76
Q

Why do kidney stones appear?

A
  • Over-saturation of urine
  • High levels of purine in the blood (diet, haematological disorders)
77
Q

What are some of the more specific reasons kidney stones appear?

A
  • Diet: chocolate, tea, rhubarb, strawberries, nuts, and spinach (↑oxalate)
  • Season: variations in calcium and oxalate levels mediated by vitamin d synthesis
  • Work: Water consumption (can they hydrate regularly)
  • Medications: diuretics, antacids, acetazolamide, corticosteroids, theophylline, aspirin, allopurinol, vitamin c and d, indinavir.
78
Q

What are some of the predisposing factors to kidney stones?

A
  • Recurrent UTIs (magnesium ammonium phosphate )
  • Metabolic abnormalities:
    • ​Hypercalciuria/hypercalcaemia, hyperparathyroidism, neoplasia, sarcoidosis, hyperthyroidism, Addison’s, Cushing’s, lithium, vitamin d excess
    • Hyperuricosuria/↑plasma urate: on its own, or with gout
    • Cystinuria
    • Renal tubular acidosis
  • Urinary tract abnormalities: PUJ obstruction, hydronephrosis, horseshoe kidney, vesicoureteric reflux, ureteral stricture
  • Foreign bodies: cathetar, stents
  • FMH: ↑3-fold
79
Q

What investigations are needed for diagnosis of kidney stones?

A
  • Urine dipstick: Usually +ve for blood (90%) (non visible haematuria)+ mc&s
  • Bloods: fbc, u&e, Ca2+, po43−, glucose, bicarbonate, urate
  • Urine pH; 24h urine for: calcium, oxalate, urate, citrate, sodium, creatinine; stone biochemistry (sieve urine & send stone)
  • Imaging:
    • GOLD STANDARD: CT KUB (high sensitivity and specificity)
    • AXR - sometimes used for initial assessment, - will only show radio opaque stones (80% but not all)
    • USS (hydronephrosis)
80
Q

What would the initial management be for kidney stones?

A
  • IV fluid resuscitation
  • Analgesia: PR diclofenac 100mg
  • If infection: Abx (eg piperacillin/tazobactam 4.5g/8h iv, or gentamicin)
  • Anti emetic: ondansetron
  • ↑Fluid intake

Renal stones will pass spontaneously if in the lower ureter or <5mm in diameter

Unless pregnant: remove stones via Ureteroscopy

81
Q

When should you admit a patient for kidney stones?

A
  • Post-obstructive AKI
  • Uncontrollable pain from simple analgesics
  • Infected stone(s)
  • Large stones (>5mm)
82
Q

What management is required for stones >5mm or pain not resolving?

A

Medical expulsive therapy:

  1. α‎-blockers (tamsulosin 0.4mg/d) - Most pass within 48h
  2. ESWL (extracorporeal shockwave lithotripsy) - US waves shatter stone. Small stones: <2cm, performed via radiological guidance (either X-ray or USS). SE: renal injury, may also cause ↑bp and dm
  3. PCNL (Percutaneous nephrolithotomy): Keyhole surgery to remove stones, when large, multiple, or complex. For: large renal stones (including staghorn calculi).
  4. URS (Flexible uretero-renoscopy) - passing a scope retrograde up into the ureter, allowing stones to be fragmented through laser lithotripsy and fragments removed
83
Q

How are kidney stones prevented generally and specifically?

A

Generally

  • Drink plenty
  • Normal dietary Ca2+ intake

Specifically:

  • Calcium stones: thiazide diuretic to ↓Ca2+ excretion.
  • Oxalate: ↓oxalate intake; pyridoxine
  • Struvite (phosphate mineral): treat infection
  • Urate: allopurinol (100–300mg/24h po)
  • Cystine: vigorous hydration and urinary alkalinization
84
Q

What are the nice guidelines for urological referral (haematuria)?

A
  • Aged ≥45yrs with either:
    • Unexplained visible haematuria without urinary tract infection
    • Visible haematuria that persists or recurs after successful treatment of urinary tract infection
  • Aged 60yrs with have unexplained non‑visible haematuria and either dysuria or a raised white cell count on a blood test.
85
Q

How is obstructive nephropathy or significant infection secondary to renal stones managed?

A
  • Retrograde stent insertion is the placement of a stent within the ureter, approaching from distal to proximal via cystoscopy
  • Nephrostomy is a tube placed directly into the renal pelvis and collecting system, relieving the obstruction proximally

Year 3 Medicine (11 decks)

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