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Phase 3 > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Describe the pathophysiology, presentation and management of renovascular disease

A

Progressive narrowing of the renal arteries with atheroma causes reduced perfusion. GFR falls but tissue oxygenation of the cortex and medulla is maintained

Progression of RA stenosis to 70% causes cortical hypoxia and microvascular damage and activation of inflammatory and oxidative pathways.

Parenchymal inflammation and fibrosis progress and become irreversible and at this point, restoration of blood flow has no benefit

Presents with hypertension, pulmonary oedema, bruits, hx of vascular disease

Manage with BP control (not ACEi/ARB), statins, good glycaemic control if diabetic, smoking cessation, exercise, low sodium diet

Angioplasty only used if rapidly deteriorating renal failure, uncontrolled HTN or flash pulmonary oedema

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2
Q

Define acute kidney injury and describe factors contributing to its development

A

‘decline of renal excretory function over hours or days, recognised by the rise in serum creatinine and drop in urine output’

Pre-Renal - Circulatory Failure/Shock - Reduced Perfusion of the Glomerulus

Renal - Cells of the Kidney

Post-Renal - Obstruction

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3
Q

Define glomerulonephritis

A

Glomerulonephritis (GN) is a renal disease characterised by inflammation and damage to the glomeruli that allows protein (+/- blood) to leak out into the urine

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4
Q

State methods of assessing kidney function and their uses and limitations

A
  • 24hr Urine Collection (g/24h)
    • Cumbersome, not routinely used in clinical practice
  • Protein:Creatinine Ratio (PCR) (mg/mmol)
  • Albumin:Creatinine Ratio (mg/mmol)
  • Estimation of GFR
    • Based on plasma creatinine concentration
    • Not suitable in AKI
    • Affected by muscle mass
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5
Q

Describe the pathophysiology, presentation and management of amyloidosis

A

Deposition of highly stable insoluble protein material in extracellular space in the kidney, heart, liver and gut

AA = Systemic Amyloidosis - Treat underlying source of inflammation/infection

AL = Immunoglobulin fragments from haematological conditions (e.g. myeloma) - Treat the underlying haematological condition

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6
Q

State common types of renal stones

A
  • Calcium (80%)
    • Calcium Oxalate Monohydrate or Dihydrate
    • Calcium Phosphate
  • Infection (10%)
    • Struvite
  • Uric Acid Stone (5%)
    • Not seen on X-Ray
  • Others (1%)
    • Cystine, Xanthine, Silica
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7
Q

State functions of the kidneys

A

Metabolic waste excretion

Endocrine functions

Drug metabolism/excretion

Control of solutes and fluid status

Blood pressure control

Acid/base balance

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8
Q

State indications for renal replacement therapy

A

Hyperkalaemia

Acidosis

Uraemia

Fluid Overload (hypertension, pulmonary oedema)

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9
Q

Describe the management of UTI

A

Treatment with antibiotics empirically while awaiting cultures and sensitivities

Oral therapy should be used unless severely ill, vomiting or in infants <3 months

Oral - Trimethoprim, Cephalosporin, Co-Amoxiclav, Nitrofurantoin

IV - 3rd Gen Cephalosporins (Ceftriaxone) or Aminoglycosides (Gentamicin)

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10
Q

Describe IgA nephropathy, its diagnosis and management

A

Most common type of GN in adults worldwide

Proliferative

Characterised by mesangial proliferation, increased IgA production and IgA deposition

Often presents 24-48hrs after a URTI

Can present with haematuria, hypertension and proteinuria (nephritic syndrome)

Biopsy needed for definitive diagnosis

Managed with anti-hypertensives, ACEi, steroids

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11
Q

Describe the pathophysiology of renal stone disease

A
  • Abnormal Urine
    • Too much calcium
    • Too much acid
    • Hypercalciuria
    • Hyperoxaluria
    • Stone inhibitors (citrate, magnesium)
  • Obstruction
    • Congenital or Acquired
  • Infection
    • Particularly urease-producing organisms
    • Raises urine pH
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12
Q

Describe the two main congenital abnormalities of the kidneys and urinary tract

A
  • Vesico-Ureteric Reflux
    • Retrograde passage of urine from the bladder into the upper urinary tract
    • May present with UTI and pyelonephritis
    • Can result in renal scarring
    • Low-grade VUR is more likely to spontaneously resolve
    • Manage with antibiotic prophylaxis or STING procedure or open ureteric re-implantation surgically
  • Bladder Outlet Obstruction
    • Posterior Urethral Valve
    • Antenatal hydronephrosis, UTI, poor urinary stream, renal dysfunction
    • Manage with valve resection, antibiotic prophylaxis, CKD care
  • Pelvi-Ureteric Junction Obstruction
    • Abdominal mass, pain, haematuria, UTI
    • Manage with pyeloplasty
  • Vesico-Ureteric Junction Obstruction
    • Anatomical or functional narrowing
    • Antenatal dilation, UTI, abdominal mass, pain, haematuria
    • May improve or resolve spontaneously
    • May need resection
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13
Q

Describe the medical management of chronic kidney disease

A
  • Treatment to slow renal disease progression
    • Aggressive BP control (ACEi/ARB)
    • Improved glycaemic control
    • Exercise
    • Sodium restriction
  • Treatment of renal complications
    • Manage anaemia (iron, B12, folate, EPO stimulator)
    • Acidosis (sodium bicarb supplements)
    • Oedema (fluid/sodium restriction, diuretic)
    • Bone mineral disorders (Vit D supplements, phosphate binders)
  • Other
    • Statins
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14
Q

Describe other inherited cystic disorders of the kidneys

A
  • Von Hippel Lindau
    • Autosomal dominant
    • Causes multiple benign and malignant neoplasms
    • Renal cysts and multifocal renal cell carcinomas
  • Tuberous Sclerosis
    • Autosomal dominant
    • Benign hamartomas of multiple systems (brain, eyes, heart, lung, liver, skin, kidney)
    • Up to 80% have renal involvement with multiple cysts, angiomyolipomas (high risk of bleeding) and renal cell carcinoma
    • Replacement of renal tissue leads to kidney failure
  • Medullary Cystic Kidney Disease
    • Autosomal dominant
    • Cysts at the cortico-medullary junction
    • Causes hyperuricaemia and gout
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15
Q

Describe the diagnosis of UTI/Pyelonephritis

A
  • Multistix
    • Useful for children >3 years
    • +ve LE & Nitrite = UTI in 90%
  • Microscopy/Flow Cytometry
    • If -ve for pus cells and bacteria = No UTI
  • Urine Culture
    • Single Organism >= 105 CFU/ml
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16
Q

Define nephrotic syndrome

A

3.5g Proteinuria per 24h (Urine PCR>300)

Serum Albumin <30

Oedema

(Hyperlipidaemia)

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17
Q

Describe minimal change glomerulonephritis

A

Non-proliferative

Most common GN in children

Presents with nephrotic syndrome

Often idiopathic, but can be secondary to malignancy

Electron microscopy shows fused podocyte foot processes

Manage with supportive care (e.g. to reduce oedema) and prednisolone

18
Q

Describe membranous glomerulonephritis, its diagnosis, management and prognosis

A

Presents with nephrotic syndrome

Non-proliferative

Caused by immune complex deposition, which results in complement activation against glomerular basement membrane proteins

Microscopic analysis shows thickened glomerular basement membrane

Immunofluorescence shows diffuse uptake of IgG

Treat underlying disease if secondary

Supportive non-immunological - ACi, statin, diuretics, salt restriction

Immunotherapy can be used if disease progresses (steroids, cyclosporin)

1/3rd spontaneously remit, 1/3rd have chronic membranous GN, the remaining 1/3rd progress to end-stage renal failure

19
Q

Define chronic kidney disease and a system to classify its severity

A

‘kidney damage or GFR <60ml/min per 1/73m2 for three months or more’

Classified based on eGFR

20
Q

Describe haemodialysis and its potential complications

A

Aims to remove solutes (potassium, urea) by diffusion and fluid by convection

Blood is passed over a semi-permeable membrane against dialysis fluid flowing in the opposite direction

DIffusion of solutes occurs down the concentration gradient

Access is usually through an arteriovenous fistula

Most commonly hospital-based

Standard regimen is 4 hours, 3 times a week

Problems include access complications, hypotension, cramps, fatigue, infection, dialysis disequilibrium

21
Q

State risk factors for UTI

A

Infancy (<1 yr)

Abnormal Urinary Tract (Congenital or Other)

Female Sex

Bladder Dysfunction/Incomplete Emptying

Foreign Body (Catheter, Stone)

Diabetes Mellitus

Renal Transplant

Immunosuppression

22
Q

State the range of organisms that cause UTI

A

Usually anaerobes and gram -ve bacteria from bowel/vagina

E.coli is the most common community organism

Staphylococcus saprophyticus and klebsiella pneumonia are other organisms involved

23
Q

Describe the pathophysiology, presentation and management of diabetic nephropathy

A

Hyperglycaemia leads to volume expansion, intra-glomerular hypertension, hyperfiltration, proteinuria, hypertension and renal failure

Diabetic disease induces structural changes, thickening of glomerular basement membrane, fusion of podocyte foot processes and loss of podocytes

Often presents after retinopathy with proteinuria as a hallmark

Mainstay of treatment is tight glycaemic control, good BP control (with ACEi/ARB) and SGLT-2 inhibitors

24
Q

Describe the pathophysiology, presentation and management of SLE

A

Auto-immune disease with immune complex mediated glomerular disease

Multiple autoAbs, directed against DNA, histones etc.

Form intravascular immune complexes or attach to GBM

Complement is activated leading to renal damage

Can present with elevated creatinine, proteinuria, nephritic syndrome

Treated with immunosuppression - steroids, rituximab, cyclophosphamide

25
Q

Describe peritoneal dialysis and its potential complications

A

Uses the peritoneal membrane as a semi-permeable membrane

Catheter inserted into the peritoneal cavity and fluid is infused

Glucose is used as an osmotic agent to achieve ultrafiltration

Continuous process, home based

Requires patient to drain and refill

Complications include peritonitis, infection, hernia, loss of membrane function, glucose load

26
Q

Describe rapidly progressing (cresentic) glomerulonephritis, its diagnosis and management

A

An aggressive form of GN

Progresses to end-stage renal failure over a few weeks if left untreated

Common Causes:

Goodpasture’s - Antibodies against glomerular basement membrane (anti-GBM), present with nephritic syndrome and haemoptysis, require high dose immunosuppression (IV Prednisolone and Cyclophosphamide)

Microscopic Polyangiitis - MPO Antibody, +ve pANCA

Granulomatosis with Polyangiitis - PR3 Antibody, +ve cANCA

27
Q

Describe the emergency management of acute kidney injury

A

Protect Airway and Breathing

Restore Renal Perfusion

Assess for Pulmonary Oedema

Treat Hyperkalaemia if >6.5 (Calcium Chloride, IV Insulin, Salbutamol or Renal Replacement)

Treat Sepsis

Remove Offending Drugs

Correct Acidosis

Indications for RRT - Persistent Hyperkalaemia, Acidosis, Uraemia (pericarditis, encephalopathy), Toxins

28
Q

Describe the clinical consequences of progressive chronic kidney disease

A

Albuminuria

Pruritis, Nausea, Anorexia, Weight Loss, Fatigue, Leg Swelling, Breathlessness, Nocturia, Joint/Bone Pain, Confusion

Peripheral/Pulmonary Oedema, Pericardial Rub, Rash, Hypertension, Tachypnoea, Cachexia, Pallor

29
Q

Describe post-infectious glomerulonephritis, its diagnosis and management

A

Proliferative

Can occur after almost any infection, particularly after strep. pyogenes

Anti-body production and sub-epithelial deposition of immune complexes

Presents with oliguria, haematuria, proteinuria, oedema and hypertension

May require dialysis or antibiotics

Usually resolves over weeks, and almost always a benign prognosis

30
Q

Describe the pathophysiology, presentation and management of renal cancer

A

Renal cell carcinoma is the most common, others include transitional cell carcinoma, sarcoma and metastases

80% are found incidentally

Systemic symptoms include night sweats, fever, fatigue, weight loss, haemoptysis

10% present with the classic triad (mass, pain, haematuria)

Initial diagnosis is made with USS, CT, MRI or renal biopsy

Manage with partial or radical nephrectomy, cryotherapy

31
Q

Describe the epidemiology of renal stone disease

A

10-15% Lifetime Risk

Peak Incidence of 30-50 Yrs

Males > Females

Caucasian>Asian>Black>Hispanic

More common in hot, dry climates

Risk of further stone is 50% at 10 years and 90% at 30 years

32
Q

Describe adult polycystic kidney disease, its presentation and management

A

Autosomal dominant

Most common inherited kidney disorder

Most are associated with PKD-1 gene mutation, some with PKD-2 gene mutation

These genes code for Polycystin 1 and 2, located in renal tubular epithelia and overexpressed in cyst cells, membrane proteins involved in intracellular calcium regulation

Cysts gradually enlarge, kidney volume increases and there is some compensation

eGFR falls, usually 10yrs before the kidney fails

Diagnosed with USS:

If FHx - Age 15-30, 2 Unilateral or Bilateral Cysts. Age 30-59, 2 Cysts in Each Kidney. >60, 4 Cysts in Each Kidney

If No FHx - 10 or More Cysts in Both Kidneys, Renal Enlargement, Liver Cysts

Complications: End stage renal failure, hypertension, hernias, liver/pancreas cysts

Management is supportive, BP control, treat complications and extra-renal associations

May require renal replacement therapy

Tolvaptan - Vasopressin V2 receptor antagonist, can delay onset of RRT by around 4-5yrs. S/E include hepatotoxicity and hypernatraemia

33
Q

Describe the diagnostic process in acute kidney injury

A

Rise in serum creatinine >26micromol/L

Rise in serum creatinine >1.5x baseline

Urine output <0.5ml/kg/h for >6 consecutive hours

  1. CKD or AKI?
  2. History and Exam (Sepsis, Haemoptysis, Rhabdo)
  3. Drugs
  4. Urinalysis
  5. Renal USS
    1. Exclude obstruction
    2. Info on kidney size
  6. GN Screen
    1. ANCE, ANA, Ig, Complement, aGBM, Urine Bence Jones Protein
  7. Other Blood Film
34
Q

Describe the presentation of renal stones

A

Incidental

Pain (colic, radiates from loin to groin, cannot settle, unable to stay still)

Haematuria

UTI

Sepsis

Investigate with CT, Bloods (U&Es, CRP, FBC), Urinalysis, Urate, Calcium

35
Q

Describe other inherited renal disease

A
  • Alport’s Syndrome
    • Usually X-Linked
    • Abnormality in Collagen IV (found in basement membranes, so associated with anti-GBM disease)
    • Presents with haematuria, proteinuria and progressive renal insufficiency
    • Results in renal failure
    • Often associated with sensorineural hearing loss
  • Fabry’s Disease
    • X-Linked
    • Lysosomal storage disorder due to deficiency of alpha-glucosidase
    • Causes proteinuria, end-stage renal failure, lipid deposits in urine
    • Manage with IV enzyme replacement therapy
36
Q

Describe the pathophysiology and clinical presentation of pyelonephritis

A

UTI refers to infection anywhere along the urinary tract, from kidney to urethra

Pyelonephritis specifically refers to infection of the kidney/renal pelvis

Presents with dysuria, frequency, urgency, suprapubic pain, haematuria, fever, chills/rigor, flank pain, costovertebral angle tenderness, nausea, vomiting

37
Q

State the aetiology of acute and chronic glomerulonephritis

A

Group A Strep

Systemic Inflammatory Diseases (SLE, RA)

Drugs (e.g. NSAIDs)

Diabetes

Hypertension

Amyloidosis

38
Q

Describe the short and long-term consequences of renal transplantation

A

Far better outcome than dialysis

Cadaveric waiting list of approx. 3 years

  • Pros
    • No dialysis
    • Better level of renal function
    • Can live much more independently
    • Better life expectancy
    • Better fertility
  • Cons
    • Immunosuppressive medication for duration of transplant
    • Increased CV risk
    • Increased infection
    • Post-transplant diabetes
    • Skin malignancies and others
    • Risk of acute/chronic rejection, surgical bleeds

Immunosuppression with monoclonal antibodies, calcineurin inhibitors antimetabolites, glucocorticoids

39
Q

Describe the pathophysiology, presentation and management of bladder cancer

A

Majority are transitional cell carcinomas

Can be squamous carcinomas and adenocarcinomas

Classically presents with painless frank haematuria

Diagnosed with flexible cystoscopy

Manage with mitomycin, chemotherapy, radical cystectomy, radiotherapy

If metastatic, treat with M-VAC chemotherapy (methotrexate, vinblastine, doxorubicin, cisplatin)

40
Q

Describe the pathophysiology, presentation and management of prostate cancer

A

Most are primary adenocarcinoma, usually arising in the peripheral zone of the prostate

May be asymptomatic or present with painful/slow micturition, UTIs, haematuria, retention, lymphoedema

Metastatic features may include bone pain and renal failure due to ureteric obstruction

Diagnosed by digital rectal examination, prostate-specific antigen and trans-urethral guided needle biopsy

Note that PSA is tissue, not tumour specific and tends to rise with age

Manage localised disease with surveillance, radiotherapy, radical prostatectomy, cryotherapy

For advanced cancer, androgen ablation therapy (medical or surgical castration), chemotherapy, radiotherapy

41
Q

Describe the pathophysiology, presentation and management of testicular cancer

A

Most are germ cell tumours (seminoma, teratoma) but can be stromal (leydig or sertoli) or lymphoma

Majority present as a painless lump, or may be found after incidental trauma

Investigate with scrotal USS, alpha-fetoprotein, Beta-hCG, LDH

Treat with radical orchidectomy, chemotherapy, nodal radiotherapy

42
Q

Describe the management of renal stone disease

A

Analgesia (NSAIDs, e.g. Diclofenac)

Small stones are likely to pass spontaneously

Larger stones or if non-remitting pain, may require medical expulsive therapy (alpha-blocker - tamsulosin)

Surgical options include Extracorporeal Shockwave Lithotripsy, Ureteroscopy with Basket Extraction or Percutaneous Nephrolithotomy

Phase 3 (14 decks)

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