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Medicine > Renal Medicine > Flashcards

Renal Medicine Flashcards

1
Q

Causes of non-visible haematuria

A

Transient: UTI, menstruation, vigorous exercise, sexual intercourse
Permanent: cancer, stones, BPH, prostatitis, urethritis, IgA nephropathy, thin BM disease

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2
Q

2-week-wait criteria for ?bladder or renal cancer

A

For bladder or renal -
>=45 AND: unexplained visible haematuria without UTI, or visible haematuria that persists after successful treatment of UTI

For bladder -
>=60 AND have unexplained non-visible haematuria and either dysuria or a raised WCC on a blood test

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3
Q

non-urgent referral for bladder cancer criteria

A

Aged >=60 with recurrent or persistent unexplained UTI

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4
Q

4 types of casts seen in urine, and the conditions that cause them

A
  • Hyaline cast: seen in normal urine, after exercise, during fever or with loop diuretics
  • Red cell cast: glomerulonephritis (nephritics)
  • White cell cast: pyelonephritis, interstitial nephritis, glomerulonephritis
  • Granular cast: CKD, acute tubular necrosis
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5
Q

Investigations for UTI

Investigations for the following groups ->

  • ?uncomplicated cystitis
  • ?complicated cystitis
  • systemically unwell
  • recurrent/atypical/male pyelonephritis
A

Non-pregnant: >=3 symptoms (or 1 severe) -> empirical abx without Ix.

Dipstick if any uncertainty (nitrites + leukocytes). Dont dipstick if pregnant or elderly.

If pregnant/male/child/failure to respond to empirical abx -> MSU

If systemically unwell -> FBC, U+E, CRP, blood culture, fasting glucose

If recurrent/atypical/male pyelonephritis -> USS and urology assessment

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6
Q

Common causative organisms of UTI

A

E coli, Staphylococcus saprophyticus, Proteus mirabilis, Klebsiella pneumonia

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7
Q

Management for UTI

  • non-pregnant cystitis
  • pregnant cystitis
  • male cystitis
  • non-pregnant pyelonephritis
  • pregnant pyelonephritis
A

Non-pregnant cystitis: 3 days trimethoprim or nitrofurantoin

  • avoid nitrofurantoin if eGFR <30
  • if failure to respond -> MSU

Pregnant cystitis: 7 days nitrofurantoin if not at term (amoxicillin or cefalexin second line)

  • avoid nitrofurantoin in tri 3
  • avoid trimethoprim in tri 1
  • avoid ciprofloxacin throughout

Male cystitis: 7 days trimethoprim or nitrofurantoin

Non-pregnant pyelonephritis: 7-10 days co-amoxiclav/ trimethoprim/ cefalexin

Pregnant pyelonephritis: admit to hospital, send MSU

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8
Q

Risk factors for UTI

A

sex, incontinence, constipation, menopause, reduced oestrogen, spermicides, dehydration, obstruction, DM, stones, immunosuppression, catheter, pregnancy, tract malformation

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9
Q

Stage 1 vs stage 2 vs stage 3 AKI

A

Stage 1: rise of serum creatinine >26.5 or 1.5-1.9x baseline, and urine output <0.5ml/kg/hour for 6-12hrs

Stage 2: serum creatinine 2.0-2.9x baseline, or UO <0.5ml/kg/hr for >12 hours

Stage 3: serum creatinine >3x baseline, or UO <0.3ml/kg/hour for >24 hours

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10
Q

Pre-renal causes of AKI

A

Renal artery stenosis, haemorrhage, D+V, pancreatitis, burns, shock, MI, sepsis, drugs (NSAIDs, ACEI), hepatorenal syndrome

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11
Q

Intrinsic causes of AKI

A

glomerulonephritis, acute tubular necrosis, drugs (gentamicin, contrast media), infection, tumour lysis syndrome, rhabdomyolysis, HUS, TTP, DIC

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12
Q

Post-renal causes of AKI

A

Stones, malignancy, stricture, clot, prostatic hypertrophy, retroperitoneal fibrosis

eg. BPH -> acute urinary retention -> bilateral hydronephrosis

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13
Q

Signs and symptoms of AKI

A

May be asymptomatic
Reduced urine output
Pulmonary and peripheral oedema (fluid overload)
There may be pain/signs of acute urinary retention if obstruction
Arrhythmias secondary to K+ and acid-base balance changes
Uraemia (pericarditis, encephalopathy)

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14
Q

Investigations for AKI

A

UEs
Urinalysis
Renal ultrasound

ABG will show acidosis and maybe hyperkalaemia

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15
Q

Management of AKI

A
  • If Pre-renal: correct fluid depletion and.or increase renal perfusion via circulatory support, treat any underlying sepsis
  • If intrinsic: refer for likely biopsy and specialist treatment of intrinsic renal disease
  • If post-renal: catheter, nephrostomy or urological intervention to relieve retention

Supportive treatment:

  • Fluid boluses
  • Careful fluid balance (catheter and UO hourly, daily weights)
  • Check K+ and treat any hyperkalaemia urgently
  • Review drug chart
  • RRT is not responding to medical management
  • Urology review if obstruction is suspected
  • Nephrology review if cause unknown or AKI severe
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16
Q

Cause and management of fluid overload

A

Caused by aggressive fluid resuscitation, oliguria and sepsis due to increased capillary permeability

Mx: O2 if needed, fluid restriction, diuretics if symptomatic, RRT

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17
Q

Management of hyperkalaemia >6.5 or any with ECG changes

A
  1. 10ml 10% calcium chloride
  2. 10units actrapid in 50ml 50% glucose infusion
  3. +/- salbutamol nebs
  4. Renal replacement therapy
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18
Q

Indications for RRT in AKI

A

fluid overload not responding to Mx, severe/prolonged acidosis, recurrent/persistent hyperkalaemia despite management, uraemia

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19
Q

ECG changes with hyperkalaemia

A

Tall tented T waves -> prolonged PR -> small/absent P -> wide QRS -> sine wave -> asystole

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20
Q

Classification of CKD

A

1: eGFR >90 with some sign of kidney damage on other tests
2: eGFR 60-89 with some sign of kidney damage on other test
3a: eGFR 45-59
3b: eGFR 30-44
4: eGFR 15-29
5: eGFR <15. ESRF. Dialysis or transplant needed.

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21
Q

Clinical features of CKD

A

Oedema, weight loss, SOB, tiredness, pruritis (uraemia), encephalopathy (uraemia), rash, N+V (uraemia), anorexia (uraemia), restless legs, muscle cramps, bone disease (osteitis fibrosa cystica, osteomalacia, osteosclerosis, osteoporosis)

Low Vit D (lack of hydroxylation)
High phosphate (lack of excretion)
Hypocalcaemia (due to low vit D and high phosphate)
Secondary hyperparathyroidism (due to hypocalcaemia)
High ALP due to bone turnover
Hyperkalaemia
Normochromic normocytic anaemia (lack of EPO)

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22
Q

Management of CKD

A

Optimise BP and DM, lifestyle

Reduce risk of complications: lifestyle, atorvastatin, low dose aspirin

CKD diet: high protein, low potassium, low sodium, low phosphate

Manage complications:
-Anaemia: erythropoietin
-Acidosis: sodium bicarb if eGFR<30 and bicarb <20
-Oedema: fluid and sodium restriction, consider loop diuretics
Bone mineral disorders: reduce phosphate in diet first line, phosphate binders, vit D (calcitriol/alfacalcidol), parathyroidectomy
-Restless legs: consider neuropathic analgesia

Renal replacement therapy

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23
Q

Indications for dialysis in CKD

A 
eGFR usually 5-10
inability to control fluid balance (pulm oedema)
Inability to control HTN
Serositis
Acide base or electrolyte disturbance
Pruritus
N+V or nutritional deterioration
Cognitive impairment
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24
Q

How does haemodialysis work

  • when is the AV fistula created
  • where is it done, how many sessions per week, how long per session
A
  • Blood passed from AV fistula into a machine over a semi-permeable membrane against a dialysis fluid. Blood is filtered and then put back in body
  • AV fistula created 8 weeks before dialysis
  • Requires at least 3 sessions/week, lasting 3-5 hours each session
25
Q

How does peritoneal dialysis work

-where is the session done

A

Dialysis solution is injected into the abdo cavity through a permanent catheter, the blood is then filtered using the peritoneum as a semipermeable membrane

26
Q

what is STEAL syndrome

A

inadequate blood flow to the limb distal to the AV fistula, causing distal ischaemia

27
Q

Haemodialysis complications

A

Site infection, endocarditis, stenosis of fistula, hypotension, stenosis thrombosis, cardiac arrhythmia, air embolus, anaphylactic reaction to sterilising agents, disequilibrium syndrome

28
Q

Peritoneal dialysis complications

A

Peritonitis, sclerosing peritonitis, catheter infection, catheter blockage, constipation, fluid retention, hyperglycaemia, hernia, back pain

29
Q

Renal transplantation complications

A
  • Surgical complications: haemorrhage, thrombosis, infection, urinary leak, hernia
  • Delayed graft function (requires dialysis)
  • Acute rejection (T cell mediated or antibody mediated -> high dose methylprednisolone or plasma exchange and IVIg)
  • Chronic rejection
  • Opportunistic infection
  • Malignancies
  • Bone marrow suppression
  • Recurrence of original disease
  • Urinary tract obstruction
  • Cardiovascular disease
30
Q

Indications and contraindications for renal transplant

A

Indications: ESRF or progressing towards ESRF

CI: active metastatic cancer, active infection, HIV, unstable CVD, heart failure

31
Q

Different types of renal transplant

A

DBD: brain death donor
DCD: circulatory death donor
Live related
Live unrelated

32
Q

Renal transplant immunosuppression

A

Monoclonal antibodies (basiliximab): selectively inhibits T cell activation to reduce risk of rejection

Calcineurin inhibitors (tacrolimus, ciclosporin): inhibits T cell activation. Narrow therapeutic index. Nephrotoxic so close monitoring required. CYP450 clearance

Antimetabolites: Mycophenolate mofetil, azathioprine

Prednisolone

33
Q

Investigations for glomerulonephritides

A

RENAL BIOPSY IS REQUIRED FOR DIAGNOSIS

Bloods - FBC, U+E, LFT, CRP, immunoglobulins, electrophoresis, complement, autoantibodies (ANA, ANCA, anti-dsDNA, anti-GBM), blood cultures, hepatitis serology, ASOT (anti-streptolysin O titre for post strep glomerulonephiritis)

Urine - MC+S, bence jones, A:CR or P:CR, RBC casts

Imaging - CXR (pulm haemorrhage), renal USS

34
Q

Examples of nephritic syndromes

A

IgA nephropathy (Bergers), Henoch-Schoönlein purpura, post-strep glomerulonephritis, anti-GBM disease (Goodpasture’s), rapidly progressive glomerulonephritis, Alport syndrome

35
Q

Examples of nephrotic syndromes

  • primary renal causes
  • secondary causes
A

Primary: Minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, membranoproliferative glomerulonephritis

Secondary: DM, SLE, myeloma, amyloid, pre-eclampsia

36
Q

IgA Nephropathy (Berger’s)

  • what is it/what happens?
  • presentation
  • associated conditions
  • progression to ESRF
  • management
A
  • Commonest cause of glomerulonephritis worldwide
  • Deposition of IgA complexes (=IgA and C3) in the mesangium
  • Young adult male with haematuria 1-2 days post URTI. Associated with high levels of complement.
  • Associated with alcoholic cirrhosis, coeliacs, and HSP
  • Renal failure may occur decades later
  • Mx: control BP (lifestyle, anti-HTN), prednisolone (prevent IgA complex formation)
37
Q

Henoch-Schönlein purpura

  • what is it
  • presentation
  • diagnosis
  • management
A

-IgA mediated small vessel vasculitis (systemic version of IgA nephropathy) -> IgA complex deposits in skin, gut, kidney, joints
-Seen in children following infection -> palpable purpuric rash over buttocks/arms/legs, abdo pain, polyarthritis, haematuria, renal failure
-clinical diagnosis. Positive immunofluorescence for IgA and C3 in skin. Renal biopsy shows IgA.
-Mx: analgesia, supportive treatment for nephropathy. (inconsistent evidence for use of steroids and immunosuppressants).
Good prognosis.

38
Q

Post-streptococcal glomerulonephritis

  • nephrotic or nephritic
  • when does it occur and in who
  • features
  • diagnosis
  • mx
A
  • causes a mixed nephritic and nephrotic picture
  • A child presents with haematuria 1-2 weeks after strep pyogenes URTI
  • features: headache, malaise, haematuria, proteinuria (<3g/day), oedema, HTN, -Diagnosis: starry sky appearance on immunofluorescence, low C3 levels, raised ASOT (anti-streptolysin O titre)
  • supportive management (manage HTN and oedema) +/- abx (penicillin)
  • good prognosis
39
Q

Nephritic syndrome clinical features

A

Haematuria, hypertension, oliguria, some oedema

40
Q

Nephrotic syndrome clinical features

A

Proteinuria (P:CR >300), hypoalbuminaemia (<30g/L), oedema, intravascular fluid depletion, hypercholesterolaemia

41
Q

Goodpasture’s syndrome (anti-GBM disease)

  • cause
  • age and gender most at risk
  • presentation
  • investigations
  • management
A

-Caused by type 4 collagen autoantibodies, which attack the GBM
- bimodal age 20-30 and 60-70, males more common
- Rapidly progressive. Within weeks/months -> pulmonary haemorrhage, haematuria, anuria, AKI, renal failure. often dialysis-dependent at diagnosis
-Ix: biopsy shows crescents in the glomerulus (linear IgG deposits along GBM)
Anti-GBM antibodies in the blood. Raised transfer factor (due to pulm haemorrhage)
-Mx: plasma exchange, steroids, cyclophosphamide

42
Q

Rapidly progressive glomerulonephritis

  • 3 types
  • management
A

Group of glomerulonephritides causing rapid reduction in renal function over days/weeks
Type 1: anti-GBM (goodpasture)
Type 2: immune-complex mediated (post-strep, SLE, IgA nephropathy, HSP)
Type 3: Pauci-immune/cANCA (wegener)/pANCA (churg-strauss), idiopathic

Mx: coricosteroids, cyclophosphamide, plasma exchnage if anti-GBM or ANCA, monoclonal ab if SLE

43
Q

Alport syndrome

  • inheritance pattern
  • what is it
  • features
  • diagnosis
  • management
A

-X-linked dominant (85%) or autosomal recessive
-Abnormal type 4 collagen (affects GBM, cochlear BM, eye BM).
Abnormal GBM is leaky -> haematuria -> protein eventually leaks through too -> GBM eventually undergoes sclerosis -> renal failure and HTN
-Features: SN hearing loss, myopia, cataracts, anterior lenticlonus (lens capsule cant maintain shape), renal failure, haematuria, proteinuria, HTN
-Diagnosis: clinical signs, FHx, renal or skin biopsy
-Mx: ACEI/ARB for proteinuria, lens replacement for anterior lenticlonus, RRT and supportive Mx for kidney failure

44
Q

Complications of nephrotic syndrome

A

VTE: due to urinary loss of anticoagulants anti-thrombin III, protein C+S) III, and increased clotting factors -> LMWH and warfarin

Infection due to urinary loss of immunoglobulins and immune mediators, and oedema fluid acting as a culture medium -> pneumococcal vaccine

Hyperlipidaemia as a result of hypoproteinaemia leading to reactive hepatic synthesis of proteins (including lipoproteins) -> atherosclerosis

Hypocalcaemia (not a true hypocalcaemia) due to low albumin

HTN due to fluid retention and reduced kidney function

Malnutrition due to oedema of the gut and ascites causing impaired absorption

45
Q

Minimal change disease

  • causes
  • features
  • management
  • prognosis/progression to ESRF
A
  • causes: idiopathic, drugs (lithium, NSAIDs), hodgkins, thymoma, infectious mononucleosis
  • only intermediate sized proteins are lost (albumin), BP normal, minimal change to glomerulus on biopsy
  • manage with steroids for 1-4 months
  • no progression to ESRF
46
Q

Focal segmental glomerulosclerosis

  • causes
  • at risk age group
  • investigations
  • management
  • prognosis/progression to ESRF
A
  • Idiopathic, secondary to other renal pathologies, HIV, heroin, alports, sickle cell
  • occurs in young adults
  • biopsy shows scarring of certain segments of glomerulus
  • Mx: ACEI/ARBS (for proteinuria and HTN), steroids, calcineurin inhibitors
  • At risk of developing renal failure
47
Q

What drug/drugs can be used to treat proteinuria?

A

ACEI/ARBs

48
Q

Membranous glomerulonephritis

  • how common
  • causes
  • Ix
  • Mx
  • prognosis/progression to ESRF
A
  • Commonest type of GN in adults, and third most common cause of ESRF
  • Causes: idiopathic (antiphospholipase A2 antibodies), hep B, malaria, syphilis, lung cancer, lymphoma, leukaemia, gold, penicilamine, NSAIDs, autoimmune (SLE, thyroiditis, RA)
  • Ix: biopsy shows thickened GBM due to subepithelial deposits of Ig
  • Mx: ACEI/ARB to reduce proteinura, combination of corticosteroids and cyclophosphamide for severe disease, consider anticoag for high risk patients
  • prognosis: rule of thirds. one third have spontaneous remission, one third remain proteinuric, one third develop ESRF
49
Q

Membranoproliferative glomerulonephritis

  • 3 types
  • management
  • prognosis
A
  • Type 1 (90%): caused by cryoglobulinaemia or hep C, shows subendothelial and mesangium deposits (tram-track appearance) on renal biopsy
  • Type 2: causes by partial lipodystrophy, factor H deficiency. Low C3 levels. Biopsy shows dense deposits (intramembranous immune complexes)
  • Type 3: caused by hep B and hep C
  • management: steroids may be effective
  • prognosis is poor
50
Q

Diabetic nephropathy

  • pathophysiology
  • features
  • investigations/screenin
  • management
A
  • Patho: hyperglycaemia -> increased growth factors, RAAS, oxidative stress -> increased glomerular capillary pressure, podocyte damage, endothelial dysfunction
  • Features: albuminuria, glomerulosclerosis, nodules, fibrosis -> reduced renal function
  • Co-existing HTN accelerates disease
  • Ix: annual A:CR screening. A:CR shows microalbuminuria
  • Mx: DM control, BP <130/80 (ACEI/ARB), statins, sodium restriction
51
Q

Lupus nephritis

  • pathophysiology
  • SLE features
  • diagnosis
  • management
A
  • Autoimmune dsDNA and ANA antibodies -> deposition -> inflammation and tissue damage
  • renal disease, malar rash, photosensitivity, serositis, ulcers, arthritis, CNS effects, cytopenia
  • diagnosis: antibody scren (ANA, ds-DNA), renal biopsy if A:CR>30 or P:CR >50
  • Mx: ACEI/ARBs, hydroxychloroquine for extra-renal disease, immunosuppression (rituximab, MMF, steroids, cyclophosphamide)
52
Q

Granulomatosis with polyangitis

  • what is it
  • features
  • investigations
  • management
  • prognosis
A
  • (wegeners) Small-medium vessel vasculitis
  • Epistaxis, saddle shaped nose, sinusitis, nasal crusting, haemoptysis, dyspnoea, proptosis, rash, rapidly progressive glomerulonephritis
  • Ix: c-ANCA, CXR (cavitating lesions), renal biopsy (epithelial crescents)
  • Mx: steroids, cyclophosphamide, plasma exchange
  • prognosis: median survival 8-9 yrs
53
Q

Eosinophilic granulomatosis with polyangitis

  • what is it
  • features
  • investigations
  • management
A
  • (churg-strauss) small-medium vessel vasculitis
  • Features: asthma, eosinophilia, pasanasal sinusitis, mononeuritic multiplex, dyspnoea
  • Leukotriene receptor antagonists may precipitate disease
  • Ix: p-ANCA, eosinophilia, CXR (vasculitic damage and eosinophil infiltration), Lung function tests (asthma), biopsies of affected tissues, ECG
  • Mx: prednisolone, inhaled steroids, cyclophosphamide/rituximab if unresponsive, azathioprine/methotrexate to allow for steroid reduction,
54
Q

Autosomal dominant polycystic kidney disease

  • mutation
  • renal clinical features
  • extrarenal clinical features
  • diagnostic criteria
  • management
A
  • Mutation in PKD1 most common (ESRF by 50y) or PKD2 (ESRF by 70y)
  • 2/3 people need transplant
  • Asymptomatic until cysts or large or they haemorrhage -> loin pain, haematuria, cyst infection, renal calculi, HTN, CKD, ESRF
  • Extrarenal features: liver cysts, intracranial aneurysm (SAH), mitral valve prolapse, ovarian cyst, diverticulosis
  • USS diagnostic criteria in patients with positive FHx: <30yrs old requires two cysts (unilateral or bilateral), aged 30-59 requires two cysts in both kidneys, aged >60 requires 4 cysts in both kidneys
  • Mx: vasopressin antagonist (tolvaptan), RRT, transplant, increased fluid intake suppresses cyst growth, BP <130/80 (ACEI/ARB)
55
Q

Autosomal recessive polycystic kidney disease

  • Which is more common, ARPKD or ADPKD?
  • Which chromosome is the defect on?
  • How is it usually diagnosed and when?
  • Associated condition
  • When does ESRF occur?
  • Other organ involvement
A

-Much less common than ADPKD, due to defect on chromosome 6 (fibrocystin)
Prenatal USS diagnosis
Associated with Potter’s syndrome secondary to oligohydramnios
ESRF in childhood
Patients also typically have liver fibrosis

56
Q

Acute interstitial nephritis

  • causes
  • features
  • investigations
  • management
A
  • Causes: drugs most common (penicillin, rifampicin, NSAIDs, allopurinol, furosemide), SLE, sarcoidosis, Sjögrens, staph infection
  • features: eosinophilia (30%), mild AKI, HTN, 10% have allergic triad (rash, fever, arthralgia)
  • Ix: sterile pyuria, white cell casts
  • Mx: treat underlying cause, steroids
57
Q

Rhabdomyolysis

  • typical presentation
  • clinical features
  • lab results
  • causes
  • management
A
  • A patient who has had a fall or prolonged epileptic seizure and is found to have AKI on admission
  • Clinical features: muscle pain.swelling, AKI, red/brown urine, history of trauma/ immobility/ dehydration
  • Lab results: AKI with disproportionately raised creatinine, elevated CK, myoglobinuria, hypocalcaemia (myoglobin binds calcium)< elevated phosphate (released from myocytes), hyperkalaemia (due to renal failure), met acidosis
  • Causes: seizure, collapse/coma, ecstasy, crush injury, statins (esp if prescribed with clarithromycin)
  • Mx: IV fluids to maintain UO, urinary alkalisation sometimes, manage hyperkalaemia, ?RRT
58
Q

Acute tubular necrosis

  • causes
  • investigations
A

Most common cause of AKI
Ischaemic causes: shock, sepsis
Nephrotoxins: gentamicin (aminoglycosides), myoglobin (rhabdomyolysis), contrast, lead
Ix: AKI (raised urea, raised creatinine, raised potassium), muddy brown casts in urine

59
Q

Renal artery stenosis features

A

HTN, CKD, flash pulmonary oedema (rapid onset pulm oedema)

Accounts for 90% of renal vascular disease, with fibromuscular dysplasia being the most common cause of the remaining 10%

Medicine (15 decks)

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