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MBBS VI - Medicine Final Summary > Nephrological system > Flashcards

Nephrological system Flashcards

1
Q

What is the definition of CKD?
What is ESRD?

A
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2
Q

What is the classification of CKD by GFR and albuminuria?

A
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3
Q

Compare the features of acute kidney injury vs chronic kidney disease?

  • Clinical
  • Biochemical
  • Radiological
A
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4
Q

What are common causes of CKD?

A
  • DM nephropathy (45%)
  • Hypertension/ Renal artery stenosis (RAS) (27%)
  • Glomerulonephritis (10%)
  • Interstitial disease (5%)
  • Polycystic kidney disease (2%)
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5
Q

What are prerenal, renal and post renal causes of chronic kidney disease?

A
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6
Q

What are general SS for CKD
What SS related to uremiea?

A
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7
Q

What history taking done for CKD?
- Medical
- Drug
- Family

A
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8
Q

What Ix done for chronic kidney disease and why?

A
  • CBC with DC: normochromic normocytic anemia: decreased EPO secretion (decreased renal function + anemia of chronic disease)
  • Lipid profile: hypertriglyceridemia due to increased synthessi of lipoproteins in liver due to hypoalbuminemia
  • Electrolyte profile and serum Ca2+ and PO4- level:
    HypoNa: inability to excrete free water in patients with advanced renal failure leads to water retention and development of hypoNa
    HyperK: due to metabolic acidosis
    Develops in patients who is oliguric or has additional problems e.g. increased tissue breakdown, reduced aldosterone secretion or responsiveness. Impaired cellular uptake of K+ due to diminished Na+K+ ATPase pump also contributes to hyperK
    HypoCa: hyperP leading to hypoCa. Decreased synthesis of calcitriol in kidneys –> muscle cramps, tetany
    Hyperphosphatemia: decreased renal excretion of PO4
  • ABG: metabolic acidosis and increased anion gap. Excretion of acid and regeneration of HCO3- is impaired in low GFR
    Increased H+ production in lactic acid or ketoacids in sepsis and trauma
    Decreased HCO3- due to loss from diarrhea or renal tubular acidosis
  • Serum PTH level: increased PTH level due to secondary hyperparathyroidism (decreased Ca due to decreased calcitriol production from kidneys)
  • RFT: increased urea/BUN and creatinine level, decreased GFR
  • Urinanalysis: microalbuminuria, proteinuria >3.5g/day
  • Renal biopsy: indicated if creatinine is markedly elevated or worsened over course of days
  • Autoimmune markers: ANA/anti-dsDNA/C3/4/ANCA/anti-GBM –> membranous nephropathy (adults) (nephrotic pattern)
  • LFT: hepatorenal syndrome, increased ALP level
  • HBV and HCV serology: urgent HBsAg if haemodialysis is anticipated
  • Serum/urine protein electrophoresis with immunofixation (suspicious of light chain nephropathy)
  • Serum free light chain assays
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9
Q

What imaging done for kidney disease and what is expected results?

A

 KUB
 USG renal
* Evaluate for polycystic kidney disease and obstruction
* Radiological features of CKD
o Small kidneys due to dysplasia, scarring or shrunken in CKD
o Large kidneys in polycystic kidney disease or amyloidosis (infiltration)
o ↑ Renal parenchymal echogenicity

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10
Q

What is the general treatment for chronic kidney disease?

A
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11
Q

What are the management of common complications of chronic kidne ydisease?

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12
Q

In chronic kidney disease what mineral is most concerned that will affect bones
What is the management?

A
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13
Q

What are the cardiovascular complications of chronic kidney disease
How are they managed?

A
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14
Q
A

 Chronic renal failure
* Presence of renal disease for at least 6 years
* Presence of uremic complexion
* Biochemical parameters of hypocalcemia and phosphate retention
* USG evidence of bilateral small and coarsened kidneys
* Absence of notable causes of acute renal failure
o UTI
o Urinary tract obstruction
o Nephrotoxic drug consumption
 Another possibility is acute-on-chronic renal failure secondary to accelerated hypertension

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15
Q

How would you assess renal function in this patient?

A
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16
Q

What accounts for cafe au lait appearance in chronic kidney diseae?

A

 Coexistence of anemia and retention of β-melanocyte-stimulating hormone
 Pigment deposition (urochromogens)

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17
Q

What are the indications for emergency dialysis?

A
  • Respi: Acute pulmonary edema
  • CVS: Uremic pericarditis or cardiac tamponade
  • CNS: Uremic encephalopathy
  • Endo: Severe metabolic acidosis
  • Endo: Hyperkalemia
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18
Q

How to classify the causes of acute kidney injury?

A
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19
Q

Acute kidney injury is classified into prereneal, renal and post renal causes, what are they?

A
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20
Q

What are the lab Ix for acute kidney injury?

A
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21
Q

How to interpret urinanalysis results of acute kidney injury?

  • Proteinuria + haematuria + dysmorphic RBC + RBC casts
  • Heavy proteinuria + NO haematuria
  • Granular of epithelial cell casts + renal tubular epithelial cells
  • Pyuria
A
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22
Q

How to interpret plasma urea to creatinine ratio/plasma BUN to creatinine ratio? (increased and decreased ratio causes)
GFR
Urine albumin to creatinine ratio (ACR)/urine albumin level

A
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23
Q

What are SS of acute kidney injury?

A
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24
Q

What biochemical tests and results in acute kidney injury?

A
  • CBC with DC
  • Electrolyte profile and serum Ca2+ and Po43-
    HypoNa (inability to excrete free water in patients with advanced renal failure leads to water retention and hypoNa)
    HyperK: occurs due to presence of metabolic acidosis
    HypoCa: decreased synthesis of calcitriol (vit D) in kidneys –> muscle cramps, tetany, perioral paresthesia and carpopedal spasm
    HyperP: decreased renal excretion of PO43-
  • ABG: metabolic acidosis adn increased anion gap. Excretion of acid and regeneration of HCO3- is impaired in low GFR. Increased H+ in lactic acid or ketoacids in sepsis and trauma
  • RFT: increasewd urea/BUN and creatinine level
  • Urinanalysis: albuminuria, 24 hour urine and MSU for microscopy and culture with sensitivity testing
  • Renal biopsy
  • Autoimmune markers: ANA/anti-dsDNA/C3/C4/ANCA/anti GBM
  • LFT: hepatorenal syndrome
  • HBV and HCV serology: urgent HBsAg if haemodialysis is anticipated
  • Serum/urine protein electrophoresis with immunofixation
  • Serum free light chain assays
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25
Q

What is general approach to manage acute kidney injury?

A
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26
Q

What are the indication of renal replacement therapy in acute kidney injury?

A
  • A = Acidosis: Refractory metabolic acidosis with HCO3- < 10 mmol/L
  • E = Electrolyte disturbance: Uncontrolled hyperkalemia > 6 mmol/L
  • I = Intoxication: Alcohol/ NSAIDs/ acetaminophen/ metformin
  • O = Oedema: Refractory fluid overload/ Uncontrolled pulmonary edema
    o Uncontrolled pulmonary edema related to renovascular hypertension (chronic hypertension and Na+ and H2O retention due to RAAS activation)
  • U = Uremia: Uremic pericarditis/ Uremic encephalopathy/ Intractable uremic symptoms
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27
Q

How to manage complications of acute kidney injury?
Volume depletion
Volume overload
Electrolye and acid base disturbances

A
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28
Q

How to classify glomerulonephritis?

A
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29
Q

What are the causes of glomerulonephritis (proliferative (nephritic) and non proliferative (nephrotic))?
Primary and secondary causes

A
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30
Q

What is the structures in a glomerulus?

A
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31
Q

What is general features of IgA nephropathy?
Clinical course?
Dx?
Treatment?
Etiology?
Morphology?

A

Primary nephritic syndrome (disease process isolated to kidneys)

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32
Q

What is general features of membranoproliferative glomerulonephritis (MPGN)?
Clinical course?
Dx?
Treatment?
Etiology?
Morphology?

A

Secondary nephritic syndrome (renal disease as a component of systemic disorder)

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33
Q

What is general features of post streptococcal glomerulonephritis (PSGN)?
Clinical course?
Dx?
Treatment?
Etiology?
Morphology?

A

Secondary nephritic syndrome

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34
Q

What is general features of lupus nephritis?
Clinical course?
Dx?
Treatment?
Etiology?
Morphology?

A
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35
Q

What is general features of minimal change disease
Clinical course?
Dx?
Treatment?
Etiology?
Morphology?

A

Primary nephrotic syndrome

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36
Q

What is general features of focal segmental glomerulosclerosis (FSGN)?
Clinical course?
Dx?
Treatment?
Etiology?
Morphology?

A

Primary nephrotic syndrome (non proliferative)

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37
Q

What is general features of membranous nephropathy?
Clinical course?
Dx?
Treatment?
Etiology?
Morphology?

A

Primary nephrotic syndrome (non proliferative)

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38
Q

What is the clinical manifestation of nephritic syndrome?

A
  • present in nephritic but uncommon in nephrotic syndrome
39
Q

What is clinical manifestation of nephrotic syndrome?

A
40
Q

What is the pathogenesis of rapidly progressive glomerulonephritis
What clinical features?

A

Clinical syndrome and not a specific etiology of GN
RPGN = crescentic GN –> progressive loss of urine function over a short period of time ~6 weeks

41
Q

What are the main causes of rapidly progressive glomerulonephritis?

A
42
Q

What biochemical tests for nephritic/nephrotic syndrome?

A
43
Q

What is tested in urinanalysis for nephrotic/nephritic syndroome?

A

Gross appearance
Turbidity: infection, chyluria (filariasis) or presence of precipitated crystals
Red to brown urine
Smoky brown and coca cola urine
White urine: pyuria, chyluria or presence of phosphate crystals

Chemical (urine dipstick)
Heme: dx of haematuria requiures microscopy
Proteinuria: most sensitive to albumin –> suggests glomerular disease and glomerular haematuria. Cannot detect microalbuminemia (30-300mg/day). Insensitive to other non albumin proteins such as Ig light chains
Glucose: glycosuria due to inability of kidney to reabsobred filtered glucose –> DM, SGLT2i, generalized proximal tubular dysfunction (fanconi syndrome)
Nitrite: indicates bacteriuria (enterobacteriaceae express nitrate reductase which converts urinary nitrate into nitrite)
Leukocyte esterase: indicates pyuria (released by lysed neutrophils and macrophages and is a marker for the presence of WBC)
Urine pH: useful in metabolic acidosis and renal tubular acidosis
Special gravity: weight of the solution compared with weight of an equal volume of distilled water

Microscopic
RBC (haematuria)
Blood clots: signs of non glomerular bleeding. Glomerular bleeding is usually a diffse capillary process in which minute amount of blood is added to large volume of glomerular filtrate. Presence of urokinase and tissue type plasminogen activator in glomeruli and tubules makes clot formation unlikely
WBC: neutrophils (suggests UTI if associated with bacteriuria, non bacterial infections (TB), nephrolithiasis and interstitial nephritis if urine culture is -ve (Sterile pyuria)
Microorganisms: bacteriuria
Epithelial cells: indicates contamination by genital secretions
Casts: RBC casts (signs of glomerular bleeding)
Crystals: uric acid crystals. Calcium oxalate crystas. Magnesium ammonium phosphate crystals
Lipiduria: diagnostic of glomerular disease because of the apparent requirement for increased of glomerular permeability. Suggestive of nephrotic syndrome

44
Q

What tests for renal biopsy can be done?
Contraindications to percutaneous renal biopsy?

A
45
Q

What is values of 24 hour urine albumin, protein
Urine dipstick
Albumin to creatinine ratio

A
46
Q

What is classical clinical features of nephrotic syndrome?

A
  • Heavy proteinuria
  • Hypoalbuminemia
  • Edema
  • Hyperlipidemia and Lipiduria
47
Q

What is lab definition of nephrotic syndrome?

A
48
Q

What are the terms used to classify and describe nephrotic syndrome?

A
49
Q

What are the causes of primary nephrotic syndrome?
Most common cause in children and adults?

A
50
Q

What are the causes of secondary nephrotic syndrome?

A
51
Q

What is the clinical manifestation of nephrotic syndrome?

A
52
Q

What are the biochemical test and expected results for nephrotic syndrome?

A
53
Q

What is gold standard procedure to determine cause of proteinuria? and what tests done
Indications of pre steroid renal biopsy in children?
What is pre biopsy evaluation?

A
54
Q

What are absolute contraindicaitons, relative contraindications to renal biopsy?
What are the complications?

A
55
Q

What is general management of nephrotic syndrome?

A
56
Q

What is the specific treatment for nephrotiv syndrome in children?

A
57
Q

What is complication and treatment of nephrotic syndrome?

A
58
Q

Nephrotic syndrome patients prone to what kinds of infection, most common agents
Treatment and prevention?

A
59
Q

What is the mechanism of renal insufficiency and anasarca in nephrotic syndrome?
How to manage these diseases?

A
60
Q

What are the general features of acute interstitial nephritis?

A

 Immune-mediated tubulointerstitial injury primarily triggered by medications (most common), infection or autoimmune disease
* Also known as acute tubulointerstitial nephritis (ATIN)
 Characterized by inflammatory infiltrate in the kidney interstitium
 Classically presents as acute kidney injury (AKI) with rapid decline in renal function as measured by elevated creatinine and blood urea nitrogen (BUN)

61
Q

What are the drug causes of acute interstitial nephritis?

A
62
Q

What are the systemic causes of acute interstitial nephritis?

A
63
Q

What is the SS of acute interstitial nephritis?

A
64
Q

What are the Ix done for acute interstitial nephritis?

A
65
Q

What is treatment for acute interstitial nephritis?

A
66
Q

What is the epidemiology of acute tubular necrosis?

A

MOST common cause of AKI in hospitalized patients
* Two major causes of AKI in hospital are prerenal disease and acute tubular necrosis (ATN) and should be distinguished from one another

67
Q

What are the ischemic causes that can cause acute tubular necrosis?

A
68
Q

What are the nephrotoxic causes that can cause acute tubular necrosis?

A
69
Q

What are the ix for acute tubular necrosis?

A
70
Q

What is management of acute tubular necrosis?

A
71
Q

What is RTA?

A

RTA is a hyperchloremic metabolic acidosis with normal anion gap caused by renal tubular dysfunction in the presence of a relatively normal GFR

72
Q

What is the classification of RTA?

A
73
Q

What are primary and secondary causes of type 1 (distal RTA) and type 2 (proximal) RTA?

A
74
Q

What are the causes of type 4 (hyperkalemic RTA)?

A
75
Q

What are the causes of Fanconi syndrome?

A

 Hereditary causes
* Cystinosis (most common)
* Wilson’s disease
* Galactosemia
* Tyrosinemia
* Lowe syndrome
 Acquired causes
* Multiple myeloma
* Amyloidosis
* Malignancy
* Hypergammaglobulinemia

76
Q

What is the SS of RTA?

A
77
Q

What are the Ix for renal tubular acidosis?

A
  • CBC with DC
  • Electrolyte profile: hyperCl in all types of RTA, hyperK in Type 4 (hyperK) RTA, HypoK in type 1(distal RTA) + 2 (proximal) RTA
  • RFT: serum urea and creatinine to assess renal function
  • Urinananlysis: uirne dipstick can be used to screenin o furine pH but is unreliable
  • ABG: metabolic acidosis in RTA. Base excess (non respiratory pH disturbances). Positive base excess = metabolic alkalosis. Negative base excess = metabolic acidosis =proceed to anion gap to determine the cause of metabolic acidosis
78
Q

What are the acid base abormalities in RTA?
What is plasma K, urine anion gap

A
79
Q

What is treatment of tyep 1 (distal) RTA?

A

 Alkali replacement
* Sodium bicarbonate
* Sodium citrate
* Potassium citrate
o Alkalinizing K+ salts that can be utilized when hypokalemia persist o Contraindicated in hyperkalemic forms of Type 1 (Distal) RTA

80
Q

What is treatment of type 2 (proximal) RTA?

A
81
Q

What is treatment of type 4 (hyperK) RTA?

A
82
Q

What are the general features of polycytic kidney disease?

A
83
Q

What is the ddx of polycystic kidney disease?

A
84
Q

What are the SS of polycystic kidney disease?

A
85
Q

What is the diagnostic criteria of polycystic kidney disease?

A
86
Q

What is history taking and PE of polycystic kidney disease?

A
87
Q

What Ix doen for polycystic kidney disease?

A
88
Q

What is medical treatment for polycystic kidney disease?

A
89
Q

What is surgical treatment for polycystic kidney disease?

A
90
Q

What are renal complications for polycystic kidney disease?

A

 Kidney stones (Nephrolithiasis)
* Occurs in up to 25% of patients
* Most of the stones are composed of uric acid and the remaining is calcium oxalate
 End-stage renal disease (ESRD)
* Requires renal replacement therapy such as hemodialysis or renal transplantation

91
Q

What are the extrarenal complications of polycystic kidney disease?

A
92
Q

What are the complications of renal cysts in PCKD?

A

 Infected renal cysts and pyelonephritis
* Second most common cause of death in patients with ADPKD
* Correlates with the structural abnormality of the renal parenchyma
 Rupture and hemorrhage of renal cysts
* Presents with hematuria

93
Q

What is prognosis of PKD?

A

 Most patients die from cardiac causes
* Cardiac hypertrophy and coronary disease accounts for majority of cases

MBBS VI - Medicine Final Summary (20 decks)

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