MRCP Part 2 > Renal > Flashcards

Renal Flashcards

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1
Q

What are the causes of rapidly progressing nephritic syndrome?

A
  • Goodpasture’s (anti-GBM)
  • cANCA PR3 positive vasculitis (e.g. granulomatosis with polyangiitis)
  • ANCA MPO positive vasculitis

These conditions lead to rapid deterioration of kidney function.

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2
Q

What are the causes of mixed nephritic/nephrotic syndromes?

A
  • Diffuse proliferative glomerulonephritis (e.g. Post-strep glomerulonephritis, SLE)
  • Membranoproliferative glomerulonephritis (type 1 = cryoglobulinaemia/hep C; type 2 = partial lipodystrophy)

These syndromes exhibit features of both nephritic and nephrotic presentations.

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3
Q

What are the causes of nephrotic syndrome?

A
  • Minimal change disease
  • Membranous glomerulonephritis
  • Focal segmental glomerulosclerosis

Nephrotic syndrome is characterized by significant proteinuria and edema.

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4
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal change disease

Most cases are idiopathic.

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5
Q

What are the drug causes of minimal change disease?

A
  • NSAIDs
  • Rifampicin

These drugs can induce minimal change disease, leading to nephrotic syndrome.

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6
Q

What are the malignant causes of minimal change disease?

A
  • Hodgkin’s lymphoma
  • Thymoma

These malignancies can be associated with minimal change disease.

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7
Q

What is the infective cause of minimal change disease?

A

EBV

Epstein-Barr virus can trigger minimal change disease.

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8
Q

What is the pathophysiology of minimal change disease?

A

T-cell and cytokine-mediated damage to glomerular basement membrane → polyanion loss → reduces electrostatic charge → increased glomerular permeability to serum albumin

This leads to significant proteinuria.

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9
Q

What is the clinical presentation of minimal change disease?

A
  • Nephrotic syndrome
  • Normotension
  • Highly selective proteinuria

Only intermediate-sized proteins such as albumin and transferrin leak through the glomerulus.

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10
Q

What are the renal biopsy findings in minimal change disease?

A
  • Normal glomeruli on light microscopy
  • Fusion of podocytes and effacement of foot processes on electron microscopy

These findings are characteristic of minimal change disease.

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11
Q

What is the management of minimal change disease?

A
  • Oral steroids
  • If steroid resistant → cyclophosphamide

Steroids are the first-line treatment.

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12
Q

What is the prognosis of minimal change disease?

A
  • Relapse is common
  • 1/3 have 1x relapse
  • 1/3 have infrequent relapses
  • 1/3 have frequent relapses which stop before adulthood

The prognosis varies among patients.

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13
Q

What is the viral cause of focal segmental glomerulosclerosis?

A

HIV

HIV infection can lead to focal segmental glomerulosclerosis.

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14
Q

What is the most common cause of nephritic syndrome?

A

IgA nephropathy

This condition is characterized by mesangial deposition of IgA immune complexes.

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15
Q

What is the clinical presentation of IgA nephropathy?

A
  • URTI → macroscopic haematuria 1-2 days later
  • Often male

This condition typically follows a respiratory infection.

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16
Q

What are the conditions associated with IgA nephropathy?

A
  • Alcoholic cirrhosis
  • Coeliac disease
  • HSP

These conditions can be linked to the development of IgA nephropathy.

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17
Q

What is the pathophysiology of IgA nephropathy?

A

Mesangial deposition of IgA immune complexes

This leads to inflammation and damage in the glomeruli.

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18
Q

What are the renal biopsy findings in IgA nephropathy?

A
  • Mesangial hypercellularity
  • Positive immunofluorescence for IgA and C3

These findings are indicative of IgA nephropathy.

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19
Q

What is the management of IgA nephropathy?

A
  • Isolated haematuria in normal eGFR = no tx needed
  • Persistent proteinuria = ACE inhibitor
  • Falling eGFR/failure to respond to ACE i = steroids

Treatment is based on the severity of the condition.

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20
Q

What is the prognosis of IgA nephropathy?

A

25% of patients develop ESRF

End-stage renal failure is a significant risk in this condition.

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21
Q

What is a marker of good prognosis in IgA nephropathy?

A

Frank haematuria

This finding is associated with a better outcome.

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22
Q

What are the markers of poor prognosis in IgA nephropathy?

A
  • Male
  • Proteinuria
  • Hypertension
  • Smoking
  • Hyperlipidaemia
  • ACE genotype DD

These factors increase the risk of progression to renal failure.

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23
Q

What is the clinical presentation of post-streptococcal glomerulonephritis?

A
  • Occurs 7-14 days post-streptococcal infection
  • Visible haematuria + proteinuria
  • HTN
  • Oliguria

This condition follows a streptococcal infection.

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24
Q

What is the pathophysiology of post-streptococcal glomerulonephritis?

A

Immune complex deposition (IgG, IgM and C3) in glomeruli

This leads to inflammation and damage in the kidneys.

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25
What are the **blood test results in post-streptococcal glomerulonephritis**?
* Raised anti-streptolysin O titre * Low C3 ## Footnote These results are characteristic of the condition.
26
What are the **renal biopsy findings in post-streptococcal glomerulonephritis**?
* Diffuse, proliferative glomerulonephritis * Endothelial proliferation with neutrophils * Subepithelial humps caused by lumpy immune complex deposits * Starry sky/granular appearance ## Footnote These findings are indicative of post-streptococcal glomerulonephritis.
27
What are the **causes of focal segmental glomerulosclerosis**?
* Idiopathic * HIV * Heroin * Alport’s syndrome * Sickle cell ## Footnote These factors can lead to focal segmental glomerulosclerosis.
28
What are the **renal biopsy findings in focal segmental glomerulosclerosis**?
* Focal and segmental sclerosis and hyalinosis on light microscopy * Effacement of foot processes on electron microscopy ## Footnote These findings are characteristic of focal segmental glomerulosclerosis.
29
What is the **management of focal segmental glomerulosclerosis**?
* Steroids +/- immunosuppressants ## Footnote Treatment may vary based on the patient's response.
30
What is the **prognosis of focal segmental glomerulosclerosis**?
Untreated FSGS has <10% chance of spontaneous remission ## Footnote This indicates a poor prognosis without treatment.
31
What are the **renal biopsy findings in Goodpasture’s syndrome**?
* IgG deposits along basement membrane ## Footnote This is a hallmark finding in Goodpasture’s syndrome.
32
What are the **blood test findings in Goodpasture’s syndrome**?
Raised transfer factor ## Footnote This is secondary to pulmonary hemorrhages.
33
What are the **clinical features of Goodpasture’s syndrome**?
* Pulmonary hemorrhage * Rapidly progressive glomerulonephritis ## Footnote These symptoms are critical for diagnosis.
34
What is the **pathophysiology of Goodpasture’s syndrome**?
Anti-GBM antibodies against type IV collagen ## Footnote This leads to damage in the lungs and kidneys.
35
What is the **tissue type associated with Goodpasture’s syndrome**?
HLA DR2 ## Footnote This genetic marker is linked to the condition.
36
What is the **management of Goodpasture’s syndrome**?
* PLEX * Steroids * Cyclophosphamide ## Footnote These treatments aim to reduce antibody levels and inflammation.
37
What are the **factors that increase the chance of pulmonary hemorrhage in Goodpasture’s syndrome**?
* Smoking * Lower respiratory tract infection * Pulmonary edema * Inhalation of hydrocarbons * Young males ## Footnote These factors heighten the risk of severe complications.
38
What are the **renal biopsy findings in membranous glomerulonephritis**?
Electron microscopy: the basement membrane is thickened with subepithelial electron dense deposits, creating a 'spike and dome' appearance ## Footnote This is a characteristic finding in membranous glomerulonephritis.
39
What are the **causes of membranous glomerulonephritis**?
* Idiopathic (due to anti-phospholipase A2 antibodies) * Infections (hepatitis B/C, HIV, malaria, syphilis) * Malignancy (in 5-20%: prostate, lung, lymphoma, leukaemia) * Drugs (gold, penicillamine, NSAIDs) * Autoimmune diseases (SLE, thyroiditis, rheumatoid) ## Footnote These factors can lead to the development of membranous glomerulonephritis.
40
What is the **antibody associated with membranous glomerulonephritis**?
Anti-PLA2R ## Footnote This antibody is crucial for diagnosis.
41
What nephrotic syndrome is associated with malignancy?
Membranous glomerulonephritis (a.k.a. membranous nephropathy) ## Footnote This condition is often linked to various malignancies.
42
What is the **management of membranous glomerulonephritis**?
* ACE-i or ARB * Immunosuppression (e.g. steroids plus cyclophosphamide) ## Footnote Treatment is based on the severity and response to initial therapy.
43
What is the **prognosis of membranous glomerulonephritis**?
* One-third: spontaneous remission * One-third: remain proteinuric * One-third: develop ESRF ## Footnote The prognosis varies significantly among patients.
44
What are the **good prognostic factors in membranous glomerulonephritis**?
* Female * Young age at presentation * Asymptomatic proteinuria ## Footnote These factors are associated with a better outcome.
45
What is the **pathophysiology of amyloidosis**?
Extracellular deposition of amyloid (insoluble fibrillar protein) ## Footnote This leads to organ dysfunction and damage.
46
What are the **diagnostic investigations for amyloidosis**?
* Serum amyloid precursor (SAP) scan * Skin/rectal mucosa/abdominal fat biopsy * Congo red staining → apple-green birefringence ## Footnote These tests help confirm the diagnosis of amyloidosis.
47
What are the **renal biopsy results in amyloidosis**?
Stains positively for congo-red and appears apple-green under polarized light ## Footnote This is a hallmark finding in renal amyloidosis.
48
What are the **causes of AL amyloidosis**?
* Myeloma * Waldenström’s * MGUS ## Footnote These conditions lead to the production of immunoglobulin light chain fragments that cause amyloidosis.
49
What are the **clinical features of AL amyloidosis**?
* Nephrotic syndrome * Macroglossia * Periorbital ecchymoses ## Footnote These symptoms are characteristic of AL amyloidosis.
50
What are the **causes of AA amyloidosis**?
* TB * Bronchiectasis * Rheumatoid arthritis ## Footnote These conditions lead to the production of serum amyloid A protein.
51
What is the **clinical feature of AA amyloidosis**?
Renal involvement is the most common feature ## Footnote This is a key aspect of AA amyloidosis.
52
What is the **cause of B2-microglobulin amyloidosis**?
Associated with patients on haemodialysis ## Footnote Long-term dialysis leads to the accumulation of B2-microglobulin.
53
What is the **pathophysiology of B2-microglobulin amyloidosis**?
In long-term dialysis, B2 microglobulin accumulates in blood → forms amyloid fibrils that deposit in joints/bones/peri-articular tissues ## Footnote This leads to various clinical manifestations.
54
What is the **clinical presentation of B2-microglobulin amyloidosis**?
* Carpal tunnel syndrome * Joint pain/stiffness ## Footnote These symptoms are common in patients with B2-microglobulin amyloidosis.
55
What are the **causes of type 1 membranoproliferative glomerulonephritis**?
* Cryoglobulinaemia * Hepatitis C ## Footnote These conditions are linked to type 1 membranoproliferative glomerulonephritis.
56
What are the **renal biopsy findings in type 1 membranoproliferative glomerulonephritis**?
Subendothelial and mesangial immune deposits of electron-dense material resulting in ‘tram-track’ appearance ## Footnote This is a characteristic finding in type 1 membranoproliferative glomerulonephritis.
57
What is the **cause of type 2 membranoproliferative glomerulonephritis**?
* Partial lipodystrophy * Factor H deficiency ## Footnote These conditions are associated with type 2 membranoproliferative glomerulonephritis.
58
What are the **blood test results in type 2 membranoproliferative glomerulonephritis**?
* Low C3 * C3b nephritic factor antibody ## Footnote These findings are indicative of type 2 membranoproliferative glomerulonephritis.
59
What are the **renal biopsy findings in type 2 membranoproliferative glomerulonephritis**?
Intramembranous immune complex deposits with ‘dense deposits’ ## Footnote This is a hallmark finding in type 2 membranoproliferative glomerulonephritis.
60
What are the **causes of type 3 membranoproliferative glomerulonephritis**?
* Hepatitis B * Hepatitis C ## Footnote These infections are linked to type 3 membranoproliferative glomerulonephritis.
61
What is the **management of membranoproliferative glomerulonephritis**?
Steroids ## Footnote Treatment typically involves corticosteroids.
62
What are the **complications of nephrotic syndrome**?
* Increased VTE risk (due to loss of antithrombin III and plasminogen) * Hyperlipidaemia * CKD * Increased infection due to urinary immunoglobulin loss ## Footnote These complications arise due to the underlying pathophysiology of nephrotic syndrome.
63
What is the **electrolyte disturbance associated with nephrotic syndrome and reason**?
Hypocalcaemia → vit D and binding protein lost in urine ## Footnote This leads to decreased calcium absorption.
64
What is the **investigation for lupus nephritis**?
Renal biopsy → clinical features do not reliably predict histological class ## Footnote This is essential for accurate diagnosis.
65
What are the **renal biopsy findings in lupus nephritis**?
* Class I: mesangial immune deposits * Class II: mesangial hypercellularity + expansion * Class III: <50% glomeruli affected, endocapillary/extracapillary proliferation * Class IV: ‘wire-loop’ appearance - endothelial/mesangial proliferation, immune complex deposition * Class V: diffuse capillary wall thickening, subepithelial deposits * Class VI: >90% globally sclerosed glomeruli ## Footnote These findings help classify the severity of lupus nephritis.
66
What is the **management of lupus nephritis**?
* Treat HTN * Class III/IV → glucocorticoids PLUS either mycophenolate or cyclophosphamide * Subsequent therapy → continue mycophenolate * Class VI → immunosuppression not helpful as irreversible damage ## Footnote Treatment varies based on the class of lupus nephritis.
67
What are the **complications of PLEX**?
* Hypocalcaemia * Metabolic alkalosis * Coagulation factor depletion (increased bleeding risk) * Immunoglobulin depletion ## Footnote These complications can arise during or after plasmapheresis.
68
What are the **absolute contraindications to renal biopsy**?
* Polycystic kidneys * Urinary tract obstruction * Hydronephrosis ## Footnote These conditions pose significant risks for renal biopsy.
69
What is the **most common organism associated with peritonitis relating to PD**?
Staphylococcus epidermidis ## Footnote This organism is frequently implicated in peritoneal dialysis-related infections.
70
What is the **management of peritonitis relating to PD**?
* Intraperitoneal vancomycin OR teicoplanin PLUS intraperitoneal ceftazidime * OR Intraperitoneal vancomycin PLUS oral ciprofloxacin ## Footnote These regimens are used to treat peritonitis effectively.
71
What is the **time taken for an AV fistula to develop**?
6-8 weeks ## Footnote This is the typical maturation time for an arteriovenous fistula.
72
What are the **complications of AV fistula**?
* Infection * Thrombosis * Stenosis * Steal syndrome (retrograde blood flow due to proximal stenosis or occlusion) ## Footnote These complications can affect the function of the fistula.
73
What are the **complications associated with haemodialysis**?
* Site infection * Endocarditis * Stenosis at site * Hypotension * Cardiac arrhythmia * Air embolus * Disequilibrium syndrome ## Footnote These complications can arise during or after haemodialysis.
74
What are the **complications associated with peritoneal dialysis**?
* Peritonitis * Sclerosing peritonitis * Catheter infection/blockage * Constipation * Fluid retention * Hyperglycaemia * Hernias ## Footnote These complications can impact the effectiveness of peritoneal dialysis.
75
What are the **complications associated with renal transplant**?
* DVT/PE * Opportunistic infection * Lymphoma and skin cancer (SCC) * Bone marrow suppression * Recurrence of original disease * Graft rejection ## Footnote These complications can affect transplant outcomes.
76
What is the **average life expectancy of a patient with renal failure who does not receive RRT**?
6 months ## Footnote This highlights the severity of untreated renal failure.
77
What are the **risk factors for developing prostate cancer**?
* Increasing age * Obesity * Afro-Caribbean ethnicity * Family history (BRCA) ## Footnote These factors increase the risk of prostate cancer.
78
What are the **isotope bone scan results in multiple osteoblastic metastasis**?
Multiple, irregular, randomly distributed foci of high-grade activity involving spine/ribs/sternum/pelvic and femoral bones ## Footnote This finding is indicative of osteoblastic metastasis.
79
What is the **management of localized prostate cancer (T1/T2)**?
* Conservative * Radical prostatectomy * Radiotherapy ## Footnote Treatment options depend on the stage and patient preference.
80
What is the **management of localized advanced prostate cancer (T3/T4)**?
* Hormone therapy * Radical prostatectomy * Radiotherapy ## Footnote These treatments aim to control disease progression.
81
What is the **management of metastatic prostate cancer disease**?
* Hormone therapy * Bilateral orchidectomy (to rapidly reduce testosterone levels) * Chemotherapy with docetaxel ## Footnote These treatments are used to manage advanced disease.
82
What are the **hormone therapies available for prostate cancer**?
* Anti-androgen therapies * Synthetic GnRH agonist (e.g. s/c goserelin) * Synthetic GnRH antagonist (e.g. s/c degarelix) * Non-steroidal anti-androgen (e.g. bicalutamide) * Steroidal anti-androgen (e.g. cyproterone acetate) * Androgen synthesis inhibitor (e.g. abiraterone) ## Footnote These therapies are used to manage hormone-sensitive prostate cancer.
83
What medication is given alongside GnRH agonists on initiation to minimize the risk of tumor flare?
Bicalutamide ## Footnote This is used to prevent tumor flare during hormone therapy.
84
What is the **most common form of renal cancer**?
Renal cell cancer ## Footnote This type of cancer arises from the renal tubular epithelium.
85
From which structure does **renal cell cancer** arise?
Proximal renal tubular epithelium ## Footnote This is the origin of renal cell carcinoma.
86
What is the **most common histological subtype of renal cell cancer**?
Clear cell ## Footnote This subtype is the most prevalent among renal cell cancers.
87
What are the **conditions/syndromes associated with renal cell cancer**?
* Tuberous sclerosis * Von Hippel-Lindau syndrome ## Footnote These genetic conditions increase the risk of developing renal cell cancer.
88
What is the **clinical presentation of renal cell cancer**?
* Haematuria * Loin pain * Abdominal mass * Left-sided varicocele ## Footnote These symptoms are characteristic of renal cell carcinoma.
89
What are the **CT findings in renal cell cancer**?
Heterogeneously enhancing mass ## Footnote This finding is typical in imaging studies of renal cell cancer.
90
What is the **histological subtype** of renal cell cancer?
Clear cell ## Footnote Clear cell is the most common subtype of renal cell carcinoma.
91
Name the **conditions/syndromes** associated with renal cell cancer.
* Tuberous sclerosis * Von Hippel-Lindau syndrome ## Footnote These syndromes increase the risk of developing renal cell carcinoma.
92
What are the **clinical presentations** of renal cell cancer?
* Haematuria * Loin pain * Abdominal mass * Left sided varicocele ## Footnote These symptoms are common indicators of renal cell carcinoma.
93
What is a common **CT finding** in renal cell cancer?
Heterogeneously enhancing mass ## Footnote This finding is indicative of renal cell carcinoma on imaging.
94
Which **hormones** are sometimes produced by renal cell cancer?
* Erythropoietin → resulting in polycythaemia * PTH → resulting in hypercalcaemia * Renin * ACTH ## Footnote These hormones can lead to paraneoplastic syndromes.
95
What is the **paraneoplastic syndrome** associated with renal cell cancer?
Stauffer syndrome → cholestasis/ hepatosplenomegaly ## Footnote This syndrome is thought to be due to increased IL-6 levels.
96
What are the **stages** of renal cell cancer?
* T1 = tumour 7cm and confined to kidney * T3 = tumour extends into major veins/ perinephric tissues but not into ipsilateral adrenal gland and not beyond Gerota’s fascia * T4 = tumour invades beyond Gerota’s fascia ## Footnote Staging is crucial for determining treatment options.
97
What is the **management** of renal cell cancer?
* Confined disease = partial/ total nephrectomy * Sorafenib / sunitinib = receptor tyrosine kinase inhibitors * Alpha-interferon and interleukin-2 (to reduce tumour size) ## Footnote Treatment varies based on the stage of the disease.
98
What is the **most common form** of testicular cancer?
Germ cell tumours e.g. seminoma or non-seminoma ## Footnote Germ cell tumours account for the majority of testicular cancers.
99
Name examples of **non-germ cell tumours**.
* Leydig cell tumours * Sarcomas ## Footnote These tumours are less common compared to germ cell tumours.
100
What is the **peak incidence** of teratomas?
25 years ## Footnote Teratomas are most commonly diagnosed in young adults.
101
What is the **peak incidence** of seminomas?
35 years ## Footnote Seminomas typically occur in younger males.
102
What are the **risk factors** for testicular cancer?
* Infertility * Klinefelter’s syndrome * Cryptorchidism * Mumps orchitis * Family history ## Footnote These factors increase the likelihood of developing testicular cancer.
103
What is a common **clinical presentation** of testicular cancer?
* Painless lump * Hydrocele * Gynaecomastia (due to increased oestrogen: androgen ratio) ## Footnote These symptoms are often the first signs of testicular cancer.
104
What is the **tumour marker** associated with seminomas?
* hCG (elevated in 20%) → most specific * LDH (elevated in 40% of all germ cell tumours) ## Footnote hCG is a key marker for diagnosing seminomas.
105
What is the **tumour marker** associated with non-seminomas?
* AFP and/or beta-hCG elevated in 80-85% * LDH (elevated in 40% of all germ cell tumours) ## Footnote These markers help differentiate between germ cell tumour types.
106
What is the **investigation** for testicular cancer?
US testes ## Footnote Ultrasound is the first-line imaging modality for testicular masses.
107
What is the **management** of testicular cancer?
* Orchidectomy * Chemo/ radiotherapy depending on staging/ tumour type ## Footnote Treatment is tailored based on the type and stage of cancer.
108
What is the **prognosis** of testicular cancer?
* 5 year survival for seminomas ~95% in stage I * 5 year survival for teratomas ~85% in stage I ## Footnote Early-stage testicular cancer has a high survival rate.
109
What is the **ACR** (mg/mmol) conversion to urinary protein excretion (g/24 hour)?
ACR 70mg/mmol = 1g/24 hours ## Footnote This conversion is important for assessing proteinuria.
110
How to collect an **ACR sample**?
Early morning urine sample ## Footnote This method provides a more accurate assessment of protein levels.
111
What to do if first urine ACR is between 3-70mg/mmol vs if it is >70mg/mmol?
* If 3-70 → repeat urine ACR * If >70 → no repeat urine ACR required ## Footnote This protocol helps in the management of proteinuria.
112
What are the **referral criteria** to nephrology for CKD?
* Urine ACR >70mg/ mmol * Urine ACR >30 PLUS persistent haematuria in absence of UTI * Urine ACR 3-29 PLUS persistent haematuria PLUS other risk factors e.g. declining eGFR/ cardiovascular disease ## Footnote These criteria help identify patients needing specialist care.
113
What is the **management** of proteinuric CKD?
* ACE inhibitors * SGLT-2 inhibitors ## Footnote These medications are used to slow the progression of kidney disease.
114
What is the **CKD 1 classification**?
Greater than 90 ml/min, with some sign of kidney damage on other tests ## Footnote If all the kidney tests are normal, there is no CKD.
115
What is the **CKD 2 classification**?
60-90 ml/min with some sign of kidney damage ## Footnote If kidney tests are normal, there is no CKD.
116
What is the **CKD 3A classification**?
45-59 ml/min, a moderate reduction in kidney function ## Footnote This classification indicates a decline in kidney function.
117
What is the **CKD 3B classification**?
30-44 ml/min, a moderate reduction in kidney function ## Footnote This stage reflects worsening kidney function.
118
What is the **CKD 4 classification**?
15-29 ml/min, a severe reduction in kidney function ## Footnote Patients may require dialysis or transplant.
119
What is the **CKD 5 classification**?
Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed ## Footnote This stage indicates end-stage renal disease.
120
What is the **CKD A1 classification**?
Urine ACR <3 ## Footnote This classification indicates normal protein levels.
121
What is the **CKD A2 classification**?
Urine ACR 3-30 ## Footnote This classification indicates mild proteinuria.
122
What is the **CKD A3 classification**?
Urine ACR >30 ## Footnote This classification indicates significant proteinuria.
123
What type of **anaemia** is seen in CKD?
Normochromic normocytic anaemia ## Footnote This type of anaemia is common in chronic kidney disease.
124
What are the **causes of anaemia** in renal failure?
* Reduced erythropoietin levels * Reduced absorption of iron due to: - Increased hepcidin levels - Metabolic acidosis * Reduced erythropoiesis due to toxic effects of uraemia on bone marrow * Reduced red cell survival * Blood loss due to capillary fragility, poor platelet function and stress ulceration ## Footnote These factors contribute to the development of anaemia in CKD.
125
What is the **target Hb** in CKD?
Hb 100-120 ## Footnote Maintaining hemoglobin levels within this range is important for patient health.
126
What is the **management of anaemia** in CKD?
* 1st line if not on dialysis = oral iron * 2nd line if not on dialysis and iron levels not adequate after oral iron = IV iron * Once ferritin >100 / transferrin sat >20% = ESA’s e.g. EPO or darbepoetin ## Footnote This management strategy aims to correct anaemia in CKD patients.
127
What is the **main benefit of EPO**?
Improved exercise tolerance ## Footnote EPO therapy helps enhance the quality of life in CKD patients.
128
What are the **causes of renal vascular disease**?
* Renal artery stenosis secondary to atherosclerosis (most common, 90% of cases) * Fibromuscular dysplasia ## Footnote These conditions can lead to hypertension and renal impairment.
129
What are the **investigation findings** in renal vascular disease?
* High aldosterone * High renin * Hypokalaemia ## Footnote These findings are indicative of renal artery stenosis.
130
What are the **clinical features** of fibromuscular dysplasia?
* HTN * CKD or acute renal failure * Flash pulmonary oedema ## Footnote These symptoms are associated with renal vascular disease.
131
What are the **US findings** in fibromuscular dysplasia?
Asymmetrical kidneys (affected side is smaller) ## Footnote This finding is characteristic of fibromuscular dysplasia.
132
What is the **MR angiography finding** in fibromuscular dysplasia?
String of beads appearance of renal arteries ## Footnote This appearance is diagnostic for fibromuscular dysplasia.
133
What condition is associated with a **sharp rise in creatinine** following ACE-inhibitor initiation?
Renal artery stenosis ## Footnote ACE inhibitors can exacerbate renal function in patients with renal artery stenosis.
134
What test differentiates between **pre-renal uraemia** and acute tubular necrosis?
Urine sodium ## Footnote This test helps determine the cause of acute kidney injury.
135
For **pre-renal uraemia**, what is the urine sodium level?
Urine sodium <20 ## Footnote Low urine sodium indicates pre-renal causes of AKI.
136
For **acute tubular necrosis (ATN)**, what is the urine sodium level?
Urine sodium >40 ## Footnote High urine sodium indicates ATN.
137
What is the **urine microscopy finding** in ATN?
Brown granular casts ## Footnote This finding is characteristic of acute tubular necrosis.
138
What are the **drug causes** of acute interstitial nephritis?
* Penicillin * Rifampicin * NSAIDs * Allopurinol * Furosemide ## Footnote These medications can trigger acute interstitial nephritis.
139
What are the **systemic diseases** associated with acute interstitial nephritis?
* SLE * Sarcoidosis * Sjogren’s syndrome ## Footnote These conditions can lead to kidney inflammation.
140
What are the **infective causes** of acute interstitial nephritis?
* Hanta virus * Staphylococci ## Footnote These infections can cause acute interstitial nephritis.
141
What are the **renal biopsy findings** in acute interstitial nephritis?
Marked interstitial oedema and interstitial infiltrate in connective tissue between renal tubules ## Footnote These findings confirm the diagnosis of acute interstitial nephritis.
142
What is the **clinical presentation** of acute interstitial nephritis?
* Fever * Rash * Arthralgia * Eosinophilia * HTN ## Footnote These symptoms are indicative of acute interstitial nephritis.
143
What are the **investigation results** for acute interstitial nephritis?
* Sterile pyuria * White cell casts ## Footnote These findings help diagnose acute interstitial nephritis.
144
What are the **clinical features** of tubulointerstitial nephritis with uveitis?
* Fever * Weight loss * Painful red eyes ## Footnote These symptoms are associated with this condition.
145
Which chromosome is **HLA** coded for on?
Chromosome 6 ## Footnote HLA stands for human leukocyte antigen.
146
What is **HLA**?
Human leucocyte antigen system = the major histocompatibility complex in humans ## Footnote HLA plays a crucial role in the immune system.
147
Name the **class 1 HLA antigens**.
* A * B * C ## Footnote These antigens are involved in presenting endogenous antigens.
148
Name the **class 2 HLA antigens**.
* DP * DQ * DR ## Footnote These antigens present exogenous antigens to T cells.
149
What are the **3 most important HLA antigens** when matching for a renal transplant?
* DR * B * A ## Footnote Matching these antigens is crucial for transplant success.
150
What is the **graft survival percentage** after 1 year and 10 years in cadaveric transplants?
* 1 year = 90% * 10 years = 60% ## Footnote These statistics reflect the longevity of cadaveric kidney transplants.
151
What is the **graft survival percentage** after 1 year and 10 years in living-donor transplants?
* 1 year = 95% * 10 years = 70% ## Footnote Living-donor transplants generally have better outcomes.
152
What are the **post-op complications** of renal transplant?
* ATN of graft * Vascular thrombosis * Urine leakage * UTI ## Footnote These complications can arise after kidney transplantation.
153
What is the **pathophysiology of hyperacute transplant rejection**?
* Pre-existing ABO or HLA antigen antibodies * Type II hypersensitivity reaction * Widespread thrombosis of graft vessels → ischaemia and necrosis of transplanted organ * Occurs within minutes to hours ## Footnote This type of rejection is immediate and severe.
154
What type of **hypersensitivity reaction** is hyperacute transplant rejection?
Type II hypersensitivity reaction ## Footnote This reaction is mediated by antibodies.
155
What is the **management of hyperacute transplant rejection**?
Graft must be removed, no treatment is possible ## Footnote Once hyperacute rejection occurs, the graft cannot be salvaged.
156
What is the **pathophysiology of acute graft failure**?
* Usually due to mismatched HLA * Cell mediated (cytotoxic T cells) * Occurs <6 months post-transplant ## Footnote This type of rejection is often reversible.
157
What is the **viral cause of acute graft failure**?
CMV ## Footnote Cytomegalovirus can lead to graft dysfunction.
158
What are the **biochemical findings** in acute graft failure?
* Rising creatinine * Pyuria * Proteinuria ## Footnote These findings indicate graft dysfunction.
159
What is the **management of acute graft failure**?
May be reversible with steroids/ immunosuppression ## Footnote Early intervention can improve outcomes.
160
What is the **pathophysiology of chronic graft failure**?
Both antibody and cell-mediated fibrosis of transplanted kidney (chronic allograft nephropathy) ## Footnote This process leads to gradual loss of graft function.
161
What are the **causes of chronic graft failure** in renal transplant?
* Reoccurrence of original renal disease (MCGN → IgA → FSGS) * Occurs >6 months post-renal transplant ## Footnote Chronic graft failure can result from underlying kidney disease.
162
What is the **malignancy associated with immunosuppression**?
SCC/ BCC ## Footnote Skin cancers are more common in immunosuppressed patients.
163
What is the **pathophysiology of diabetes insipidus**?
ADH deficiency or insensitivity to ADH ## Footnote This condition leads to excessive urination and thirst.
164
What are the **causes of cranial DI**?
* Idiopathic * Post-head injury * Pituitary surgery * Craniopharyngiomas * Wolfram’s syndrome (DIDMOAD) ## Footnote These conditions affect ADH production or release.
165
What are the **causes of nephrogenic DI**?
Genetic (affects ADH receptor more commonly, or less commonly mutation in gene that encodes aquaporin 2 channel) ## Footnote Nephrogenic DI results from the kidneys' inability to respond to ADH.
166
What are the **biochemical findings** in nephrogenic DI?
* High calcium * Low potassium ## Footnote These findings can help diagnose nephrogenic diabetes insipidus.
167
What are the **drug causes of nephrogenic DI**?
* Lithium * Demeclocycline ## Footnote These medications can induce nephrogenic diabetes insipidus.
168
What are the **hereditary conditions associated with nephrogenic DI**?
* Haemochromatosis * Sickle-cell ## Footnote These genetic disorders can lead to nephrogenic diabetes insipidus.
169
What is the **clinical presentation** of DI?
* Polyuria * Polydipsia ## Footnote These symptoms are characteristic of diabetes insipidus.
170
What is the **investigation for DI**?
1st test = water deprivation test → high plasma osmolality, low urine osmolality ## Footnote This test helps differentiate between types of diabetes insipidus.
171
What is the **investigation to differentiate between cranial and nephrogenic DI**?
Desmopressin test ## Footnote This test assesses the kidneys' response to synthetic ADH.
172
What are the **investigation results in cranial DI**?
Urine osmolality high (kidneys respond to synthetic ADH) ## Footnote This finding indicates cranial diabetes insipidus.
173
What are the **investigation results in nephrogenic DI**?
Urine osmolality remains low (kidneys resistant to synthetic ADH) ## Footnote This finding confirms nephrogenic diabetes insipidus.
174
What is the **management of nephrogenic DI**?
* Thiazides * Low salt/ protein diet ## Footnote These interventions can help manage nephrogenic diabetes insipidus.
175
What is the **management of nephrogenic DI secondary to lithium**?
* Thiazide diuretic + amiloride ## Footnote This combination can help mitigate the effects of lithium on kidney function.
176
What is the **management of cranial DI**?
Desmopressin ## Footnote This synthetic ADH is used to treat cranial diabetes insipidus.
177
What is the **triad of features in haemolytic uraemic syndrome**?
* AKI * Haemolytic anaemia (microangiopathic haemolytic anaemia - MAHA) * Low platelets ## Footnote This triad is characteristic of haemolytic uraemic syndrome.
178
What are the **causes of secondary HUS**?
* Shiga toxin-producing E. Coli (STEC) * Pneumococcal infection * HIV * SLE ## Footnote These infections and conditions can lead to secondary haemolytic uraemic syndrome.
179
What is the **pathophysiology of primary HUS**?
Complement dysregulation ## Footnote This dysregulation leads to the clinical features of HUS.
180
What is the **most useful initial diagnostic test in HUS**?
Blood film ## Footnote A blood film can reveal characteristic findings of haemolytic anaemia.
181
What are the **biochemical findings in HUS**?
* Coombs negative haemolysis * Schistocytes on blood film * Anaemia * Low platelets * AKI ## Footnote These findings are indicative of haemolytic uraemic syndrome.
182
What are the **stool culture findings in HUS**?
* Shiga toxins * STEC (shiga toxin producing E. coli) ## Footnote Stool cultures can confirm the presence of the causative organism.
183
What is the **management of typical HUS**?
* Fluids * Red cell transfusions * May require dialysis * PLEX in severe cases that are NOT a/w diarrhoea ## Footnote Supportive care is crucial in managing typical HUS.
184
What is the **management of atypical HUS**?
Eculizumab ## Footnote This monoclonal antibody is used for atypical haemolytic uraemic syndrome.
185
What are the **causes of rhabdomyolysis**?
* Seizure * Collapse/ coma * Ecstasy * Crush injury * Statins ## Footnote These factors can lead to muscle breakdown and subsequent kidney injury.
186
What is the **syndrome that can cause rhabdomyolysis**?
McArdle’s syndrome (metabolic myopathy disorder, glycogen storage disease type 5) ## Footnote This condition leads to muscle pain and breakdown during exercise.
187
What are the **biochemical findings in rhabdomyolysis**?
* AKI, disproportionately raised creatinine * Raised CK (5x upper limit of normal) * Low calcium (myoglobin binds calcium) * Hyperkalaemia * Raised phosphate (released from myocytes) * Metabolic acidosis ## Footnote These findings are indicative of rhabdomyolysis.
188
What are the **urine findings in rhabdomyolysis**?
Myoglobinuria (dark /reddish-brown colour urine) ## Footnote This finding is characteristic of rhabdomyolysis.
189
What is the **management of rhabdomyolysis**?
* IVF * Urinary alkalinization is sometimes used (IV sodium bicarb) ## Footnote These interventions help prevent kidney damage.
190
What are the **types of renal stones**?
* Calcium oxalate (40%) * Calcium phosphate * Urate * Cystine * Xanthine * Struvite ## Footnote These types of stones vary in composition and treatment.
191
What is the **urine pH of calcium phosphate renal stones**?
Normal - alkaline (>5.5) ## Footnote This pH level is associated with calcium phosphate stone formation.
192
What is the **urine pH of calcium oxalate renal stones**?
Variable ## Footnote Calcium oxalate stones can form in a range of urine pH levels.
193
What is the **urine pH of uric acid renal stones**?
Acidic (5.5) ## Footnote Uric acid stones typically form in acidic urine.
194
What is the **urine pH of struvite renal stones**?
Alkaline (>7.2) ## Footnote Struvite stones form in alkaline urine, often due to infection.
195
What is the **urine pH of cystine renal stones**?
Normal (6.5) ## Footnote Cystine stones can form in urine with a neutral pH.
196
What is the **radiographic appearance of calcium oxalate stones**?
Opaque i.e. white ## Footnote Calcium oxalate stones are visible on X-rays.
197
What is the **radiographic appearance of calcium phosphate stones**?
Opaque i.e. white ## Footnote These stones are also visible on X-rays.
198
What is the **radiographic appearance of urate stones**?
Radio-lucent (transparent to radiation therefore invisible) ## Footnote Uric acid stones may not be visible on standard X-rays.
199
What is the **radiographic appearance of cysteine stones**?
Semi-opaque ## Footnote Cystine stones may appear partially visible on imaging.
200
What is the urine pH of **struvite renal stones**?
Alkaline (>7.2) ## Footnote Struvite stones are associated with urinary infections and alkaline urine.
201
What is the urine pH of **cystine renal stones**?
Normal (6.5) ## Footnote Cystine stones are less common and occur due to a genetic disorder.
202
What is the radiographic appearance of **calcium oxalate stones**?
Opaque i.e. white ## Footnote These stones are visible on X-rays due to their density.
203
What is the radiographic appearance of **calcium phosphate stones**?
Opaque i.e. white ## Footnote Similar to calcium oxalate stones, they are also visible on X-rays.
204
What is the radiographic appearance of **urate stones**?
Radio-lucent (transparent to radiation therefore invisible) ## Footnote These stones cannot be seen on standard X-rays.
205
What is the radiographic appearance of **cystine stones**?
Semi-opaque ‘ground-glass’ appearance ## Footnote This appearance can be challenging to interpret on imaging.
206
What is the radiographic appearance of **xanthine stones**?
Radio-lucent ## Footnote Like urate stones, xanthine stones are not visible on X-rays.
207
Define **staghorn calculus**.
Stone that involves renal pelvis and extends into at least 2 calyces ## Footnote These stones are often associated with struvite stones.
208
What is the composition of **staghorn calculus**?
Struvite (ammonium magnesium phosphate, triple phosphate) ## Footnote These stones form in alkaline urine, often due to infection.
209
List the **pre-disposing risk factors** for staghorn calculus.
* Ureaplasma urealyticum and proteus infections * Alkaline urine ## Footnote These factors contribute to the formation of struvite stones.
210
What is the management for renal stones less than **5mm**?
Watchful waiting if < 5mm and asymptomatic ## Footnote Small stones often pass on their own without intervention.
211
What is the management for renal stones between **5-10mm**?
Shockwave lithotripsy ## Footnote This non-invasive procedure uses sound waves to break stones.
212
What is the management for renal stones between **10-20 mm**?
* Shockwave lithotripsy * Ureteroscopy ## Footnote Both methods can be used depending on the situation.
213
What is the management for renal stones greater than **20 mm**?
Percutaneous nephrolithotomy ## Footnote This is a surgical procedure for large stones.
214
What is the management for ureteric stones less than **10mm**?
Shockwave lithotripsy +/- alpha blockers ## Footnote Alpha blockers can help facilitate stone passage.
215
List the **prevention strategies** for calcium renal stones.
* High fluid intake * Add lemon juice to drinking water * Avoid carbonated drinks * Limit salt intake * Potassium citrate may be beneficial * Thiazides diuretics ## Footnote These strategies help reduce stone formation.
216
List the **prevention strategies** for oxalate renal stones.
* Cholestyramine reduces urinary oxalate secretion * Pyridoxine reduces urinary oxalate secretion ## Footnote These medications can help manage oxalate levels.
217
List the **prevention strategies** for uric acid renal stones.
* Allopurinol * Urinary alkalinization e.g. oral bicarbonate ## Footnote These treatments help lower uric acid levels.
218
What infection predisposes to **struvite kidney stones**?
Proteus mirabilis ## Footnote This bacterium is associated with alkaline urine and struvite stone formation.
219
What is the first-line management for **cysteine stones**?
Potassium citrate + hydration ## Footnote This approach helps to alkalinize urine and dissolve stones.
220
What is the second-line management for **cysteine stones**?
D-penicillamine ## Footnote This medication can help reduce cystine levels in urine.
221
What is the inheritance pattern of **Alport’s syndrome**?
X-linked dominant ## Footnote This genetic condition primarily affects males.
222
What is the pathophysiology of **Alport’s syndrome**?
Defect in gene which codes for type IV collagen → abnormal glomerular-basement membrane ## Footnote This leads to kidney dysfunction and other symptoms.
223
List the **clinical features** of **Alport’s syndrome**.
* Microscopic haematuria * Progressive renal failure * Bilateral sensorineural deafness * Retinitis pigmentosa * Lenticonus ## Footnote These features are characteristic of the syndrome.
224
What are the renal biopsy findings in **Alport’s syndrome**?
Longitudinal splitting of lamina densa of the glomerular basement membrane, resulting in a ‘basket-weave’ appearance ## Footnote This finding is specific to Alport's syndrome.
225
What is the cause of failing renal transplant in **Alport’s syndrome**?
Anti-GBM antibodies (targeted against type IV collagen) ## Footnote This can lead to a Goodpasture’s syndrome-like picture.
226
What is the genetic mutation in **ADPKD type 1**?
Polycystin-1 (PKD1) on chromosome 16 ## Footnote This is the most common mutation associated with ADPKD.
227
What is the genetic mutation in **ADPKD type 2**?
Polycystin-2 on chromosome 4 ## Footnote This mutation is less common than PKD1.
228
What is the screening investigation for patients with family history of **ADPKD**?
Abdominal ultrasound ## Footnote This imaging technique helps identify cysts in the kidneys.
229
What are the diagnostic criteria for **ADPKD**?
* 2 cysts, unilateral or bilateral in aged <30 * 2 cysts in both kidneys in aged 30-59 * 4 cysts in both kidneys in aged >60 ## Footnote These criteria help in the diagnosis of ADPKD.
230
What is the management for **ADPKD**?
Tolvaptan (vasopressin receptor 2 antagonist) ## Footnote This medication can slow the progression of kidney disease.
231
List the **cardiac manifestations** of **ADPKD**.
* Mitral valve prolapse * Aortic root dilation * Aortic dissection ## Footnote These cardiovascular issues are associated with ADPKD.
232
What is the neurological manifestation of **ADPKD**?
Berry aneurysms → can rupture and cause SAH ## Footnote These aneurysms are a significant risk in patients with ADPKD.
233
What is the genetic mutation in **ARPKD**?
Defect in gene that encodes fibrocystin on chromosome 6 ## Footnote This mutation leads to the development of ARPKD.
234
What are the renal biopsy findings in **ARPKD**?
Multiple cylindrical lesions at right angles to the cortical surface ## Footnote These findings are characteristic of ARPKD.
235
When is **ARPKD** often discovered?
* Prenatal US * Early infancy with abdominal masses/ renal failure ## Footnote Early detection is crucial for management.
236
What is the pathophysiology of **Fanconi syndrome**?
Generalised reabsorptive disorder of renal tubular transport in the proximal convoluted tubule ## Footnote This leads to various biochemical abnormalities.
237
List the **biochemical findings** in **Fanconi syndrome**.
* Type 2 (proximal) renal tubular acidosis * Polyuria * Aminoaciduria * Glycosuria * Phosphaturia * Osteomalacia ## Footnote These findings reflect the tubular dysfunction.
238
What is the pathophysiology of **vesicoureteric reflux**?
Ureters displaced laterally, entering bladder more perpendicularly → shortened intramural course of ureter → abnormal backflow of urine from bladder into the ureter/ kidney ## Footnote This condition can lead to recurrent urinary infections.
239
What is the clinical presentation of **vesicoureteric reflux** in the antenatal period?
Hydronephrosis on US ## Footnote This finding is often detected during prenatal ultrasounds.
240
What is the clinical presentation of **vesicoureteric reflux** in childhood?
Recurrent childhood infections ## Footnote Children may present with frequent urinary tract infections.
241
What is the investigation for **vesicoureteric reflux**?
* Micturating cystourethrogram * DMSA scan to look for renal scarring ## Footnote These tests help assess the reflux and any associated damage.
242
What is the most common cause of **chronic pyelonephritis**?
Reflux nephropathy ## Footnote This condition leads to recurrent kidney infections and damage.
243
List the **food causes** of red/orange urine.
* Beetroot * Rhubarb ## Footnote These foods can cause harmless discoloration of urine.
244
List the **drug causes** of red/orange urine.
* Rifampicin * Doxorubicin ## Footnote These medications can lead to urine discoloration as a side effect.
245
List the **causes of transient/spurious non-visible haematuria**.
* UTI * Menstruation * Vigorous exercise * Sex ## Footnote These factors can cause temporary changes in urine appearance.
246
List the **causes of persistent non-visible haematuria**.
* Cancer * Stones * BPH * Prostatitis * Urethritis e.g. chlamydia * IgA nephropathy * Thin basement membrane disease ## Footnote Persistent haematuria requires further investigation.
247
What is the inheritance pattern of **thin basement membrane disease**?
AD with variable penetrance ## Footnote This genetic condition can manifest differently among individuals.
248
What is the pathophysiology of **thin basement membrane disease**?
Diffuse thinning of GBM ## Footnote This leads to increased susceptibility to haematuria.
249
What is the clinical presentation of **thin basement membrane disease**?
Persistent microscopic haematuria ## Footnote Patients often present with blood in urine without other symptoms.
250
What are the urgent referral criteria for **haematuria**?
Aged >= 45 years AND: * Unexplained visible haematuria without urinary tract infection, or * Visible haematuria that persists or recurs after successful treatment of urinary tract infection ## Footnote These criteria help identify potential malignancies.
251
What are the non-urgent referral criteria for **haematuria**?
Aged >= 60 years with recurrent or persistent unexplained urinary tract infection ## Footnote This group requires monitoring for underlying issues.
252
How do you calculate the **anion gap**?
(Na + K) - (Cl + HCO3) ## Footnote This calculation helps assess metabolic acidosis.
253
What is the **normal range** of anion gap?
10-18 ## Footnote Values outside this range can indicate metabolic disturbances.
254
List the **causes of metabolic acidosis with normal anion gap**.
* GI bicarb loss (diarrhoea, ureterosigmoidostomy, fistula) * Renal tubular acidosis * Drugs e.g. acetazolamide * Ammonium chloride injection * Addison’s disease ## Footnote These conditions lead to hyperchloraemic metabolic acidosis.
255
List the **causes of metabolic acidosis with raised anion gap**.
MUD PILES * Methanol * Uraemia * DKA * Paracetamol use (chronic) * Isoniazid * Lactate * Ethanol * Salicylates ## Footnote This mnemonic helps remember the causes.
256
List the **causes of lactic acidosis type A**.
* Sepsis * Shock * Hypoxia * Burns ## Footnote These conditions lead to tissue hypoxia and lactic acid accumulation.
257
What is the cause of **lactic acidosis type B**?
Metformin ## Footnote This medication can lead to lactic acidosis, especially in renal impairment.
258
List the **organisms associated with epididymo-orchitis**.
* Chlamydia trachomatis * Neisseria gonorrhoeae * E. coli ## Footnote These pathogens are common causes of this condition.
259
What is the clinical presentation of **epididymo-orchitis**?
Unilateral testicular pain and swelling ## Footnote Patients typically present with localized discomfort.
260
What is the management for **epididymo-orchitis** if STI is the most likely cause?
IM ceftriaxone + 2/52 doxycycline ## Footnote This regimen targets the most common STIs.
261
What is the management for **epididymo-orchitis** if enteric organism is the most likely cause?
Oral quinolone e.g. ofloxacin ## Footnote This treatment is effective against enteric pathogens.
262
What is the **annual screening** for nephropathy in diabetes?
Urine ACR ## Footnote This test helps detect early signs of kidney damage.
263
What are the **diagnostic criteria** for diabetic nephropathy?
* Persistent albuminuria >30mg/g / >3mg/mmol * Reduced eGFR * Diabetic ## Footnote These criteria are essential for diagnosis.
264
What is the management for **diabetic nephropathy**?
* Tight glycaemic control * ACE-i or ARB if ACR >3.0 regardless of BP ## Footnote These strategies help slow the progression of kidney disease.
265
What are the **BP targets** in diabetic nephropathy?
<130/80 if ACR >3.0 or <140/90 if ACR <3.0 ## Footnote These targets help manage blood pressure in diabetic patients.
266
List the **clinical features** of organic causes of erectile dysfunction.
* Gradual onset of symptoms * Lack of tumescence * Normal libido ## Footnote These features suggest a physiological cause.
267
List the **clinical features** of psychogenic causes of erectile dysfunction.
* Sudden onset of symptoms * Decreased libido * Good quality spontaneous or self-stimulated erections * Major life events * Problems/ changes in relationship * Mental health * HX of premature ejaculation ## Footnote These features indicate a psychological component.
268
List the **risk factors** for erectile dysfunction.
* CVD risk factors * Alcohol * SSRI’s * Beta-blockers ## Footnote These factors can contribute to erectile dysfunction.
269
What are the **investigations** for erectile dysfunction?
* Lipid/ fasting glucose levels * Morning free testosterone → if low, repeat with FSH/ LH/ prolactin ## Footnote These tests help identify underlying causes.
270
What is the management for **erectile dysfunction**?
* PDE-5 inhibitors e.g. sildenafil * Vacuum erection devices if unable to take PDE-5 inhibitors * Stop cycling if cycle for >3 hours per week ## Footnote These strategies help improve erectile function.
271
What is the pathophysiology of **renal papillary necrosis**?
Coagulative necrosis of renal papillae ## Footnote This condition can lead to significant renal damage.
272
List the **renal causes** of renal papillary necrosis.
* Acute pyelonephritis * Diabetic nephropathy * Obstructive nephropathy ## Footnote These conditions can lead to necrosis of the renal papillae.
273
What is a **haematological cause** of renal papillary necrosis?
Sickle cell anaemia ## Footnote This condition can lead to vascular occlusion and necrosis.
274
List the **drug causes** of renal papillary necrosis.
* NSAIDs ## Footnote These medications can cause renal damage through various mechanisms.
275
What are the **clinical features** of renal papillary necrosis?
* Visible haematuria * Loin pain * Proteinuria ## Footnote These symptoms indicate renal injury.
276
What is the diagnostic investigation and findings in **renal papillary necrosis**?
IVU (IV urography) → papillary necrosis with renal scarring - ‘cup and spill’ ## Footnote This imaging technique reveals characteristic changes.
MRCP Part 2
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