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MSRA > Nephrology > Flashcards

Nephrology Flashcards

1
Q

What is the function of the kidneys?

A
  • Regulation of pH, volume and composition of blood, and elimination of nitrogenous waste
  • Secretion of erythropoetin

Via juxtamedullary (long LOH) and cortical nephrons (short LOH)

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2
Q

Describe the blood supply of the kidney

A

Aorta > renal artery > afferent arteriole
Afferent arteriole supplies glomerulus
Efferent arteriole EXITs glomerulus
This then forms the vasa recta (capillaries) which follow the nephron to allow reabsorption
Vasa recta > renal vein > IVC

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3
Q

What is reabsorbed in the PCT?

What is secreted in the PCT?

A

a) Sodium, chloride, potassium, glucose, amino acid, urea, bicarbonate water

b) Creatinine, drugs, hydrogen (via sodium hydrogen transpoter and sodium potassium ATPase pump)

PCT is a very important regulator of acid base balance!

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4
Q

What is reabsorbed in the loop of henle?

A

a) Descending loop - WATER
Ascending loop - sodium, chloride, potassium

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5
Q

What is reabsorbed in the distal convoluted tubule?

What is secreted in the DCT?

A

a) Sodium, chloride, potassium, calcium, magnesium, bicarbonate

b) Hydrogen, potassium (via transporter where diuretics have effet?

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6
Q

What is reabsorbed in the collecting duct?

A

Sodium, chloride, urea, water

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7
Q

What are the pre-renal causes of acute kidney injury?

A

Sudden and severe reduction in BP due to interruption of blood flow to the kidneys from severe injury or illness:
- Blood loss
- Dehydration
- Heart failure
- Sepsis
- Vascular occlusion

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8
Q

What are the intrinsic renal failures of AKI?

A

Direct injury to the kidneys due to:
- Glomerulonephritis
- Acute tubular necrosis (drugs, toxins, prolonged hypotension)
- Acute interstitial nephritis
- Vascular

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9
Q

What are the post-renal causes of AKI?

A

Sudden obstruction of urine flow dur to enlarged prostate, kidney stones, bladder injuury or tumour:
- BPH
- Cervical cancer
- Prostate cancer
- Meatal stenosis/phimosis
- Retroperitoneal fibrosis
- Prostate cancer
- Urinary calculi

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10
Q

What is acute tubular nephrosis ?

A

Most common cause of infrarenal AKI - caused by ischaemic or nephrotoxic injury to renal tubular epithelial cells. As a result you get cell death from apotosis/necrosis and necrotic cell debris will build up causing backleak of urine.

Investigations show:
- Low urine osmolality
- High urinary sodium

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11
Q

What is acute glomerulonpehritis? What are the symptoms?

A

Acute inflammation of the glomerulus due to strep throat, SLE, goodpastures syndrome, wegeners disease, polyarteritis nodosa

Symptoms include:
- Puffiness of the face
- Blood in the urine or brown urine
- Decreased urine production
- Shortness of breath due to fluid in the lungs
- Hypertension

This can eventually lead to nephrotic or nephritic syndrome.

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12
Q

What is nephrotic syndrome?

A

A condition involving the loss of significant volumes of protein via the kidneys which results in hypoalbuminaemia.

Defined as:
- Proteinuria >3.5g in a day
- Serum albumin <30g

Symptoms include:
- Peripheral oedema (adults), facial oedema (children) - due to low oncotic pressure
- Frothy urine
- Fatigue
- Poor appetite
- Recurrent infections
- Venous/arterial thrombosis due to hypercoagulability
- Hyperlipidemia

Causes include:
Primary - MCD, focal segmental glomerulosclerosis, membranous nephropathy
Secondary - Hep B, SLE, diabetes, sarcoid, syphylis, malignancy,obesity, drugs

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13
Q

How is nephrotic syndrome managed?

A

Depends on the cause! do bloods and urine and a renal biopsy for adults.

In children, most cases are caused by minimal change disease so biopsy is not needed. Treate with oral steroids.

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14
Q

What is minimal change disease?

A
  • T cell and cytokine mediated damage to the GBM causing increased glomerular permeability to serum albumin
  • Nearly always presents as nephrotic syndrome accounting for 75% of cases in children and 25% in adults
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15
Q

What causes minimal change disease?

A

Majority of cases are idiopathic, in around 10-20% a cause is found:
- Drugs: NSAIDs, rifampicin
- Hodgkins lymphoma, thymoma
- Infectious mononucleosis

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16
Q

What are the features of MCD?

A
  • Nephrotic syndrome with highly selective proteinuria
  • Normotension

Renal biopsy shows normal glomeruli
Electron microscopy shows fusion of podocytes and effacement of foot processes

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17
Q

How is MCD treated?

A

1st - Oral corticosteroids
2nd - Cyclophosphamide

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18
Q

What is nephritic syndrome?

A

A condition involving haematuria, mild to moderate proteinuria (<3.5g/day), hypertension, oliguria and RED CELL CASTS in the urine

Symptoms include:
- Haematuria
- Oedema
- Hypertension
- Oliguria (<300ml/day)
- Encephalopathy due to electrolyte imbalance

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19
Q
A
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20
Q

What are the features of chronic glomerulonephritis?

A

Slow (and often silent) development eventually leading to:
- Haematuria and proteinuria
- Hypertension
- Oedema
- Polyuria
- Frothy urine

This may be hereditary but often no cause is found. There is no specific treatment but your doctor may tell you to:
- Keep a low protein/salt/potassium diet
- Control blood pressure
- Take diuretics for oedema
- Take calcium supplements
(essentially same as treatment for CKD)

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21
Q
A
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22
Q

What are the features of acute interstitial nephritis? What does renal biopsy show?

A
  • Characterised by the presence of inflammatory infiltrates and oedema within the interstitum, usually associated with an acute deterioration in renal function
  • Usually due to a hypersensitivity reaction to medications (>250 known)
  • Also AI and infective causes
  • Characteristic presentation of AKI +/- hypersensitivity triad (fever, rash, eosinophilia)
  • Renal biopsy shows interstitial immune infiltrate, eosinohpils and tubulitis
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23
Q

How is AIN managed?

A
  • Discontinue triggering medication
  • Corticosteroid therapy
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24
Q

What are the vascular causes of AKI?

A
  • Renal artery stenosis
  • Renary artery thrombosis
  • Renal vein thrombosis
  • Renal artery aneurysm
  • Atheroembolic renal disease
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25
Q

What are the signs and symptoms of renal artery stenosis?

A
  • Hypertension refractory to 3 or more medications
  • Increased urea
  • Unexplained kidney failure
  • Sudden kidney failure on starting ACEi
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26
Q

How is renal artery stenosis managed?

A

Medical - antihypertensives (not ACEis), statins
Surgical - angioplasty, stent insertion, bypass

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27
Q

What are the diagnostic criteria for AKI?

A
  • Rise in creatinine of 26 or more in 48h OR
  • > 50% rise in creatinine over 7 days OR
  • Fall in UO to <0.5ml/kg/h for 6h OR
  • > 25% fall in eGFR in children/young adults in 7 dats
28
Q

When should patients in AKI be referred to a nephrologist?

A
  • Renal transplant
  • ICU patient with unknown cause
  • Vasculitis/glomerulonephritis/tubulointerestitial nephritis/myeloma
  • Unknown cause
  • Inadequate response to treatment
  • Complications of AKI
  • Stage 3
  • CKD 4/5
  • Qualify for renal replacement hyperkaelamia, metabolic acidosis, complications of uraemia, fluid overload
29
Q

How do you differentiate between AKI and CKD?

A

Renal USS - patients with CKD have bilateral small kidneys (exceptions included - PKD, diabetic nephropathy, amylodiosis, HIV nephropathy)

You also see hypocalcemia on bloods due to low vit D

30
Q

Which 2 pathologies cause renal disease following URTI?

A
  1. IgA nephropathy (at the time)
  2. Post-streptococcal glomerulonephritis (1-2 weeks post infection)
31
Q

What are the features of IgA nephropathy (aka Berger’s disease)? What do investigations show?

A
  • Develops 1-2 days after URTI
  • Common in young males
  • Presents as macroscopic haematuria without proteinuria
  • Associated with alcoholic cirrhosis, coeliac disease, HSP
  • Histology shows mesangial hypercellularity, positive immunofluoresnce for IgA and C3
  • If reduced GFR; treat with ACEi or steroids. Otherwise no treatment needed.
32
Q

What are thre features of post-streptococcal glomerulonephritis? What do investigations show?

A
  • Occurs 1-2 weeks post URTI
  • Caused by immune complex (IgG, IgM, C3) deposition in glomeruli
  • Usually from strep pyogenes or other group A beta-haemolytic infection
  • Common in young children
  • Associated haematuria, proteinuria and oedema
  • Bloods show raised anti-streptolysin O titre and low C3
  • Renal biopsy shows diffuse glomerulonephritis, neutrophils
  • Electron microscopy shows HUMPS (lumpy complex deposits)
  • Immunofluoresence shows starry sky appearance
33
Q

What are the features of Henoch-Schonlein purpura?

A
  • IgA mediated smal vessel vasculitis that overlaps with Bergers
  • Palpable purpuric rash with localised oedema over buttocks and extensor surfaces of arms and legs, abdo pain, polyarthritis, features of IgA nephropathy
  • Managed with analgesia and supporitve care.

VERY GOOD PROGNOSIS

34
Q

What are some causes of haematuria?

A

Transient:
- UTI
- Menstruation
- Vigorous exercise
- Sexual intercourse

Persistent:
- Cancer (bladder, renal, prostate)
- Stones
- BPH
- Prostatitis
- Urethritis (eg. chlamydia)
- Renal (IgA neprhopathy, post strep glom, thin basement membrane disease, goodpastures)

35
Q

How is haematuria investigated?

A
  • Urine dipstick (do 3 samples 2-3 weeks apart = 2/3 is diagnostic)
  • Renal function/ACR/PCR
  • Urine microscopy
36
Q

When should you 2WW patients with haematuria?

A

Aged 45 with unexplained visible haematuria or haematuria which persists after treatment of UTI

Aged 60 with unexplained nonvisible haematuria and dysuria or raised WCC on blood test

37
Q

What are the features of Goodpasture’s syndrome (Anti-GBM disease)?

A
  • Autoimmune disease involving production of antibodies against the lungs and kidneys
  • May be tiggered by viral infections, smoking, solvent inhalation or genetics
  • Causes glomerulonephritis and bleeding into lungs
38
Q

How is Goodpasture’s syndrome managed?

A
  • Cyclophosphamide
  • Corticosteroids
  • Plasmapheresis 2-3 weeks

If very unwell may need urgent dialysis or intubation

39
Q

What are the features of Alport’s syndrome?

A
  • Inherited X-linked dominant disease causing a defect in the gene which codes for Type 4 collagen (COL4A5)
  • Leads to an abnormal GBM
  • Symptoms include microscopic haematuria, progressive renal failures, deafness, lenticonus, retinitis pigmentosa
  • More severe in males
  • Renal biopsy shows splitting of lamina densa on electron microscopy ‘basket eave appearance’
40
Q

What are the features of thin basement membrane nephropathy?

A
  • Familiar disorder of type 4 collagen (COL4A3/4A4)
  • Overlaps with Alport syndrome
  • Characterised by thin basement membrane WITHOUT extra renal pathology
  • Much better prognosis as low risk of progression to renal failure
  • Renal biopsy shows diffuse GBM thinning
41
Q

How are Alport’s syndrome and TBMN managed?

A

No specific cure

42
Q

What are the features of haemolytic uraemic syndrome?

A
  • Triad of AKI + microangiopathic haemolytic anaemia + thrombocytopenia
  • Secondary is most common; usually secondary to shiga-toxin producing E. coli infection, pneumococcal infection, HIV
  • Primary (atypical) is due to complement dysregulation
  • Investigations show anaemia, low platelets, schistocytes/helmet cells, AKI, shiga toxins on stool culture
43
Q

How is HUS managed?

A
  • Supportive (fluids, transfusion, dialysis)
  • Plasma exchange only if severe and not associated with diarrhoea
  • ECULIZUMAB in adults atypical infection
44
Q

What are the features of rhabdomyolysis?

A
  • Breakdown of muscle tissue, releasing proteins and electrolytes into the blood
  • High CK (5x upper limit of normal) following long lie or prolonged seizure
  • Associated high phosphate/potassium, low calcium, metabolic acidosis and myoglobinuria
  • Manage with IV fluids and urinary alkalinization
45
Q

What are the features of AD polycystic kidney disease?

A
  • Most common inherited form of kidney disease
  • Involves formation of numerous fluid filled cysts in the kidneys which replace the kidney leading to failure
  • Presents at 30/40yo with palpitations, hypertension or haematuria
  • Extra renal features include liver cysts, berry aneurysms, valve dysfunction

Two types:
1. ADPKD T1 - chromosome 16 (85% of cases)
2. ADPKD T2 - chromosome 4

46
Q

How is ADPKD diagnosed?

A

Ultrasound diagnosis criteria (in patients with positive family history):
- Two cysts (unilateral or bilateral), if aged <30 years
- Two cysts in both kidneys if aged 30-59 years
- Four cysts in both kidneys if ages >60 years

47
Q

How is ADPKD managed?

A

Tolvaptan (vasopressin receptor 2 antagonist) an be used only if:
- CKD 2/3 at start of treatment
- Evidence of rapidly progressing disease

Otherwise, SUPPORTIVE CARE

48
Q

What are the common causes of CKD?

A
  • Diabetic nephropathy
  • Chronic glomerulonephritis
  • Chronic pyelonephritis
  • Hypertension
  • Adult PKD
49
Q

How is CKD classified?

A

1 - eGFR >90 with kidney damage on other tests
2 - eGFR 60-90 with kidney damage on other tests
3a - eGFR 45-59
3b - eGFR 30-44
4 - eGFR 15-29
5 - eGFR<15, likely to need dialysis or kidney transplant

50
Q

How is CKD managed?

A

Conservative - diet, exercise, smoking cessation
Medical - control BP with ACEi/ARB (often need both), furosemide if eGFR <45 (stop if AKI)
Other - Stage 5 CKD may require RRT (haemodialysis, haemofiltration, haemodiafiltration, peritoneal dialysis, kidney transplant)

May also need epo, antiplatelets, iron therapy, phosphate binders (sevalemer, calcium acetate), potassium binders (eg. lokelma, patiromer), vitamin D

51
Q

Which variables are required for the Modification of Diet in Renal Disease (MDRD) equation?

A

CAGE:
Creatinine
Age
Gender
Ethnithicity

This formulation is used to calculate eGFR in CKD (as creatinine is not accurate0

52
Q

What are the different types of dialysis?

A
  1. Haemodialysis/haemofiltration - where the blood is filtered outside of the body using a dialysis machine. 4h 3x weekly
  2. Peritoneal - where the persons abdominal lining is used to filter the blood 30 minute exchanges 4x weekly
53
Q

How does peritoneal dialysis work?

A
  • Dialyse fluid is infused into the abdomen using the peritoneum as a membrane
  • When the dialysate has absorbed waste metabolites, it is drained and replaced by fresh fluid (this is called an exchange)
  • Uses a peritoneal dialysis catheter (does not need AV fistula)

Types include continuous ambulatory PD and automated PD

54
Q

What is the difference between haemofiltration and haemodialysis?

A

Dialysis - relies on diffusion of small solutes along their concentration gradients
Pros: less expensive
Cons: cerebral oedema, haemodynamic lability

Filtration - relies on convection through a larger pome hemofilter ie. does not use a dialysate (think filtration in glomerulus)
Pros: more physiologic (con control BP), allows toxin removal, user friendly
Cons: requires patient immobilization, prolonged anticoagulation, more expensive

Dialysis tends to be used for CKD pts whereas filtration is used more in ICU for acute renal failure

55
Q

What are the indiciations for acute haemodialysis/filtration in an ICU setting?

A

AEIOU

A - intractable acidosis
E - electrolyte derangement
I - intoxication
O - volume overload
U - uraemic symptoms

56
Q
A
57
Q

What immunosuppression should be given following a renal transplant?

A

Initial: ciclosporin/tacrolimus with monoclonal antibody

Maintenance: ciclosporin/tacrolimus with mycophenolate mofetil or sirolimus

Add steroids if more than one steroid responsive acute rejection episode

58
Q

What monitoring is required for those on long term immunosuppresion post transplant?

A

Cardiovascular - due to hyperlipidaemia hypertension and hyperglycaemia associated with tacrolimus

Renal - due to nephrotoxic effects of tacrolimus and ciclosporin

Malignancy - due to risk of SCC and BCC

59
Q

What are the different types of transplant rejection?

A
  1. Hyperacute - extremely rare, caused by pre-formed antibodies directed against ABO or HLA antigens on the donor kidney cells. Occurs within minutes to hours and leads to widespread thrombosis, ishcaemia and necrosis. Treat with removal.
  2. Acute - due to mismatched HLA, cell-mediated. Usually asymptomatic but picked up with high creat, pyuria, proteinura. Can be due to CMV. Occurs <6 months, may be reversible with steroids and immunosuppresants.
  3. Chronic - antibody and cell-mediated mechanisms causing fibrosis to the transplanted kidney. Occurs > 6 months.
60
Q

What are the complications of a renal transplant?

A
  • ATN of graft
  • Vascular thrombosis
  • Urine leakage
  • UTI
  • Rejection
  • Cardiovascular
  • Malignancy
61
Q

What are HLA genes?

A

Human leukocyte antigens are genes in MHCs that help code for proteins to differentiate between self and non-self. They are located on chromosome 6.

HLAs are the major cause of organ transplant rejection!

62
Q

What is the effect of increased adrenaline and angiotension II on the kidneys?

A

Increase arteriolar resistance and decrease renal blood flow

63
Q

What are the two methods by which the kidney autoregulates its blood flow over a range of BPs?

A
  1. Myogenic mechanism - smooth muscle contracts when stretched
  2. Tubuloglomerular mechanism - macula densa cells secrete adensoine which makes efferent arteriole constrict in response to low GFR
64
Q

What are the features of renal cell carcinoma?

A
  • Originates from proximal renal tubular epithelium
  • RF are smoking, obesity, con Hippel Lindau disease
  • Classical triad of haematuria, loin pain and loin mass
  • May have VARICOCELE
  • Classical cannoball secondaries in the lungs (mets)
65
Q
A

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