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Yr 3 MedEd > Renal > Flashcards

Renal Flashcards

1
Q

Pre-renal constitutes what percentage of AKIs?

What are the most common causes of pre-renal AKI?

A

40-70%
- Most cases are fluid loss causing hypotension and hypovolaemia.
No blood flow to kidney, no urination = AKI

  • Hypovolaemia- Renal loss from diuretic overuse
  • Systemic vasodilation- sepsis
  • Decreased cardiac output- HF/ MI
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2
Q

Give an example of intrinsic renal damage for the following anatomical locations:

  • Tubular
  • Glomerular
  • Interstitial
  • Vascular
A
  • Acute tubular necrosis- ischaemia, drugs, toxins
  • Glomerulonephritis: post infection and other causes
  • Interstitial nephritis: drugs, infections, infiltration
  • Vessel obstruction: Thrombosis, vasculitis, haemolytic microangiopathy
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3
Q

What are the 3 characteristic features of Haemolytic Ureamic syndrome.

What is the most common cause of HUS?

A

Microangiopathy characterised by

  1. Progressive renal failure
  2. Microangiopathic haemolytic anaemia
  3. Low platelets.

E. Coli, particularly children <5. Most common cause of renal failure in children.

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4
Q

Give 4 pathophysiological stages of Haemolytic Uraemic Syndrome.

A
  1. Gastroenteritis (E. Coli 90%)- toxin production
  2. Endothelial damage
  3. Thrombosis, platelet consumption + fibrin strand deposition.
  4. Destruction of RBCs = schistocytes, low Hb.
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5
Q

Give 2 symptoms and 3 investigation findings of Haemolytic Uraemic Syndrome

A

Symptoms: Abdominal pain, bloody diarrhoea
Investigation: Low Hb, Low platelet, haematuria/ proteinuria.

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6
Q

What is the pentad of features for Thrombotic Thrombocytopenic purpura?

Give 4 other symptoms.

A
  • Thrombocytopenia
  • Haemolytic anaemia
  • Uraemia
  • Neurological signs
  • Fever

Other symptoms are seizures, hemiparesis, reduced consciousness, reduced vision.

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7
Q

What is the genetic mutation in Thrombotic Thrombocytopenic Purpura?

What is the pathophysiology caused by this gene mutation?

A
  • Deficiency of von Willebrand Factor cleaving protease- ADAMTS13 in endothelial cells
  • Leads to increased vWF multimers promoting platelet activation and aggregation in circulation.
  • Also promotes fibrin deposition.
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8
Q

Give two ways in which glomerular inflammation is caused and how they present.

A
  • Loss of barrier function: proteinuria, haematuria

- Loss of filtering capacity: Reduced excretion > accumulation of waste products

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9
Q

What is the triad of nephrotic syndrome?
What happens to serum lipid level?
What happens to Antithrombin 3?

Give two examples of an underlying cause for nephrotic syndrome.

Give 1 peripheral stigmata of low albumin.

A

-Proteinuria >3.5g/24hrs.
- Low Serum albumin <25 g/L
- Oedema
NB: liver compensates for hypoalbuminaemia by causing hyperlipidaemia (>10 mmol/L)
- Reduced anti-thrombin 3 production. Can cause hypercoagulable state.

Break down of selectivity for glomerular filtration- protein leak. Loss of podocytes. E.g.

  • Minimal change glomerulonephritis- children < 5 years
  • Membranous glomerulonephritis/ Diabetes - adults.

Leukonychia is peripheral stigmata of hypoalbuminaemia.

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10
Q

What is the triad of Nephritic syndrome? What happens to urine level?

What is pathophysiology of nephritic syndrome?

A
  • Hypertension
  • Haematuria ( + white cells in urine, plus sediment)
  • Oedema (+ Oliguria <400 L/day)
    + granular casts- inflammatory cells.

Immune complexes lodge in capillaries, launch immune response against capillary. White cell recruitment- inflammation, cell breakdown. Allows white and red blood cells to leave bowman’s capsule alongside protein.
More severe glomerular damage than nephrotic syndrome.

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11
Q

Give two common primary causes of nephrotic syndrome.

Give 3 common secondary causes of nephrotic syndrome.

A

Primary:

  • Membranous glomerulonephritis - immune complex mediated.
  • Minimal change disease- children, glomeruli look normal under microscopy. Most common cause of nephrotic syndrome in children.

Secondary:
- Diabetes, SLE, Amyloid.

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12
Q

Give 1 common primary cause of nephritic syndrome.

Give 3 common secondary causes of nephritic syndrome

A

Primary:
- IgA nephropathy.

Secondary:
- Post streptococcal infection, SLE, anti-GBM disease (affects alveolar basement membrane also- lung haemorrhage)

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13
Q

What is IgA nephropathy?
What is anti-GBM (Goodpasture’s)?
What is Henoch Schonlein purpura?
What is Pauci-immune?

A
  • IgA nephropathy: days after URTI, increase in IgA immune complex formation. Episodic haematuria.
  • Anti-GBM: Auto Ab to type IV collagen (GBM and lung). Haematuria and haemoptysis.
  • HSP: Systemic variant IgA, causes purpuric rash- systemic involvement
  • Pauci-immune: ANCA associated antibodies bound to neutrophils, activation in glomerulus.
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14
Q

Give 5 blood tests for glomerulonephritis.
Give 1 other bedside test.
Give 2 further investigations.

A
  • FBC, U&E, CRP, complement, autoantibodies.
  • Also test urine.
  • Renal US, +/- renal biopsy.
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15
Q

Give two medications used to preserve proteinuria and renal function in glomerulonephritis.

Give two other medications used in treatment of glomerulonephritis.

A
  • ACEi or ARB.
  • Steroids.
  • Immunosuppressants.
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16
Q

What are the 3 stages of acute tubular necrosis due to ischaemia?

A
  1. Initiation: acute low GFR, high Creatinine, high urea.
  2. Maintenance- sustained low GFR, raised creatinine and urea.
  3. Recovery- tubular function regenerates, increased urine volume and gradual decreased urea and creatinine.
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17
Q

How does myeloma cause acute tubular necrosis?

What are the 4 clinical features of acute tubular necrosis due to myeloma?

A
  • Malignant bone marrow plasma cells increases plasma cell clones- leads to monoclonal paraprotein production.
  • Hypercalcaemia and paraprotein deposition causes inflammation and renal failure.

CRAB

  • Calcium- high
  • Renal failure
  • Anaemia: BM infiltration by plasma cells, anaemia of chronic disease, decreased EPO secondary to renal failure.
  • Bone- osteolytic bone lesions- pain, fracture, risk of cord compression
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18
Q

List 5 exogenous nephrotoxic agents.

A
  • NSAIDs
  • ACE inhibitors and ARBs
  • aminoglycosides- e.g. gentamicin, streptomycin
  • Contrast agents
  • Immunosuppresants e.g. ciclosporin
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19
Q

List 4 endogenous nephrotoxic agents.

A
  • Myoglobin (rhabdomyolysis), haemoglobinuria, crystals, myeloma paraprotein.
20
Q

Explain the pathophysiology of rhabdomyolysis leading to acute tubular necrosis.

Give two symptoms of rhabdomyolysis and 2 investigative blood tests.

A
  • Skeletal muscle breakdown
  • Release of myoglobin, potassium and creatine kinase (CK).
  • Obstruction of renal tubules.
  • Muscle pain/ swelling, dark urine (myoglobinuria)
  • Potassium , creatine kinase test.
21
Q

Which test measures proteinuria?

A

Urine ACR/ PCR

  • Albumin/ creatinine ratio - 30-300 is normal
  • Protein/ creatinine ratio
22
Q

What are the 4 main complications of AKI and how are they managed?

A
  • Hyperkalaemia: calcium gluconate IV, dextrose, insulin, nebulised salbutamol.
  • Pulmonary oedema: sit up, high flow oxygen, venous vasodilator
  • Uraemia: dialysis if severe complication
  • Acidaemia: IV sodium bicarbonate via central line infusion.
23
Q

Give 6 causes of chronic kidney disease.

How long is required to be chronic?

A
  • Diabetes
  • Hypertension
  • Atherosclerosis
  • Chronic glomerulonephritis
  • Infective or obstructive uropathy
  • Adult polycystic kidney disease. commonest inherited cause of CKD

> 3 months

24
Q

What is the pathophysiology of diabetic nephropathy

A
  • Glycation of efferent arteriole
  • Outflow obstruction
  • Increased pressure within glomerulus
  • Hyperfiltration
  • glomerulosclerosis
  • Reduced blood filtration/ GFR.
25
Q

Give 4 symptoms of severe chronic Kidney disease

A
  • Anorexia
  • Nausea and vomiting
  • Fatigue
  • Pruritus
  • Peripheral and pulmonary oedema
  • Muscle cramps

Often asymptomatic

26
Q

Give two examples of the following CKD consequences:

  • Failure of homeostatic function
  • Failure of hormonal function
  • Cardiovascular disease
A
  1. Homeostatic function: acidosis (failure of proton excretion), hyperkalaemia
  2. Hormonal: anaemia (EPO reduced), osteomalacia (kidneys cannot convert via D3 to calcitriol -> secondary hyperparathyroidism)
  3. Cardio: vascular calcification, uraemic cardiomyopathy.
27
Q

What would be seen in following blood tests in CKD:

  • Hb
  • Glucose
  • eGFR,
  • Ca2+, PO4
  • ALP
  • PTH
A
  • Low Hb
  • High glucose if due to diabetes
  • low GFR
  • low Calcium, high phosphate
  • High ALP in renal oesteodystrophy
  • High PTH if severe CKD
28
Q

In CKD are kidneys small or large?

Give 2 CXR findings in severe CKD.

A
  • Small kidneys in CKD, but may be enlarged in infiltrative disorders
  • CXR may show pericardial effusion or pulmonary oedema.
29
Q

Give the three general stages in management of CKD

A
  • Limit progression/ complications
  • Symptom control
  • Preparation for renal replacement therapy
30
Q

What 3 medications are used to treat renal osteodystrophy?

A
  • Calcichew- Ca supplement
  • Calcium acetate- phosphate binders
  • Cinacalcet- calcimimetic, reduces PTH levels.
31
Q

What is the anatomical difference between Lower UTI and Upper UTI?

A
  • Lower: urethra (urethritis), bladder (cystitis) or prostate.
  • Upper: renal pelvis- pyelonephritis
32
Q

Give 5 general signs of a UTI

A
  • Fever
  • Abdomen/ loin tenderness
  • Foul-smelling urine
  • Distended bladder (occasionally)
  • Enlarged prostate (if prostatitis).
33
Q

Give 4 signs of cystitis

A
  • Frequency
  • Urgency
  • Dysuria
  • Haematuria
34
Q

Give 3 signs of prostatitis

A
  • Suprapubic pain
  • Flu-like symptoms
  • Low backache

Few urinary symptoms.

35
Q

Give 5 signs of acute pyelonephritis

A
  • High fever
  • Rigors
  • vomiting
  • loin pain and tenderness
  • oliguria
36
Q

Give two bedside investigations for UTI.

A
  • Urine dipstick for presence of nitrates

- MSU for urine MCS

37
Q

Give 4 medications used to treat UTIs

A

Uncomplicated: Cefalexin or nitrofurantoin.
Male: cefalexin or ciprofloxacin
Pyelonephritis/ urosepsis: co-amoxiclav

38
Q 
What is polycystic kidney disease?
What is the inheritance pattern?
How does the patient present?
What family history may be a factor?
Give 4 examination findings.
Give 3 investigation findings
A
  • Fluid filled cysts grow on kidney.
  • Autosomal dominant
  • Acute loin pain, stone formation, abdominal discomfort, signs of renal failure.
  • FHx or SAH- berry aneurysms.
  • HTN, renal enlargement, abdominal pain, haematuria
  • Raised Hb, haemturia, deranged U&E
39
Q

What is the classic triad of renal cell carcinoma signs?
Give 2 other symptoms.
What testicular presentation may there be?
What is the ratio of male to female patients?

A
  • Haematuria, loin pain, abdominal mass
  • Pyrexia of unknown origin, night sweats.
  • Varicocele due to compression of left testicular vein by invasion of left renal vein.
  • M:F 2:1.
40
Q

Give 5 risk factors and 3 associated inherited syndromes for renal cell carcinoma

A
  • Age, smoking, obesity, hypertension, dialysis.

- Von Hippel-Lindau syndrome, tuberous sclerosis, familial papillary renal cell carcinoma.

41
Q

Give 5 investigation findings for renal cell carcinoma

A
  • Increased BP
  • RBCs in urine
  • Polycythaemia or Iron deficiency anaemia
    (bleeding cysts)
  • ALP- bone metastases
  • Cannon ball mets
  • Filling defect/ calcification on imaging.
42
Q

What is the pathophysiology of renal failure due to artery stenosis?

A
  • Atherosclerosis (80%) or fibromuscular dysplasia (10%, young F) causes stenosis, renal hypo perfusion.
  • Leads to increased angiotensin II and aldosterone.
  • Leads to increased blood pressure.
  • Leads to fibrosis, glomerulosclerosis and renal failure.
43
Q

What two medications are strongly contraindicated in renal artery stenosis?

A
  • ACEi and ARBs- remove efferent arterial tone, causing hypo perfusion.
44
Q

Give examination findings of renal artery stenosis

A
  • Hypertension
  • Abdominal/ renal artery bruits
  • Signs of bilateral renal failure
  • Weak leg pulses.
45
Q

What change in kidney size is expected in renal artery stenosis?

What is the gold standard imaging technique?

A
  • US shows smaller kidney.
  • CT angiogram or MR angiography- risk of nephrotoxicity.
  • Digital subtraction renal angiography is gold standard but invasive.

Yr 3 MedEd (31 decks)

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