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BiB Midterm 3 & Final > Nephritic and Nephrotic Syndrome > Flashcards

Nephritic and Nephrotic Syndrome Flashcards

1
Q

How does Nephrotic syndrome present clinically?

A 
Periorboital and Peripheral Edema
Frothy Urine
Massive Proteinuria (>3.5g/day
Hypoalbuminemia
Hyperlipidemia
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2
Q

Why are patients with nephrotic sydrome susceptible to infection and a hypercoaguable state?

A

Defective glomerulus causes the leakage of anti-clotting proteins (C and S) as well as immunoglobulins.

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3
Q

What is the difference between IgA Nephropathy and IgA Vasculitis?

A

IgA Nephropathy only affects the kidneys. IgA Vasculitis is a more systemic disease.

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4
Q

The glomerulus is supplied blood by the..

A

afferent and efferent arterioles

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5
Q

Which layer in the glomerulus is fenestrated and highly permeable to water and small solutes?

A

The endothelium

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6
Q

Which layer in the glomerulus is the charge barrier?

A 
The glomerular basement membrane
Negatively charged (due to proteoglycans)
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7
Q

Which layer in the glomerulus has a slit diaphragm, acting as a size barrier?

A

The visceral epithelial cells (Podocytes)

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8
Q

Define Azotemia

A

An increase in the level of nitrogenous waste in the blood (urea and creatinine) due to renal insufficiency

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9
Q

Signs of Nephritic Syndrome Include: (6)

A 
Hematuria
Hypertension
Oliguria
Azotemia
Variable proteinuria (potential hypoalbuminemia)
Edema
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10
Q

What diseases can cause mixed nephrotic and nephritic syndrome?

A

Lupus Nephritis

Membrano-proliferative glomerulonephritis (MPGN)

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11
Q

______ is the best diagnostic tool for a glomerular disease.

A

A Renal Biopsy

Triple approach: Light Microscopy, Immunoflorescence, Electron Microscopy

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12
Q

Define Olguria and Anuria

A

Oliguria - Low urine output (500mL/24hrs)
Anuria - Basically no urine output (<100mL/24 hrs)

500 mL is the minimum amount of fluid needed to be excreted to clear waste from blood.

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13
Q

Define Uremia

A

A variety of symptoms due to organ dysfunction caused by renal failure.
(Symptomatic renal failure)

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14
Q

In acute Kidney Injury, a fall in GFR can lead to (2)

A

Rise in serum creatinine (waste products)

Decreased urine output (sometimes)

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15
Q

Which type of AKI is the most common?

A

Pre-renal AKI (Decreased Renal Perfusion)

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16
Q

What is the classic triad of findings for acute interstital nephritis?

A

Fever
Rash
Eosinophilia

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17
Q

What is the equation used to calculate the Fractional Excretion of sodium in Acute Kidney Injury (AKI)?

A

FE(NA) = [(Urine Na / Plasma Na) / (Urine Creatinine / Plasma Creatinine)] x 100%

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18
Q

What is the equation used to calculate the Fractional Excretion of urea in Acute Kidney Injury (AKI)?

A

FE(urea) = [(Urine urea / BUN) / (Urine Creatinine / Plasma Creatinine)] x 100%

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19
Q

Acute Kidney Injury is defined as a…

A

…rapid (< 2 week) decline in the Kidney GFR.

Body retains waste products and urine output is decreased (not always.

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20
Q

Why does serum creatining have to be measured at multiple different times in order to diagnose an acute kidney injury (AKI)?

A

In order to set a baseline creatinine level so that we can determine if there is a rise in creatinine levels over time, which would indicate AKI.

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21
Q

____ allows for constriction of efferent arterioles and is blocked by____.
____ allows for dilation of afferent arterioles and is blocked by ___.

A

angiotensin II, ACE/ARBs

prostaglandins, NSAIDs

22
Q

A low cardiac output could lead to what type of acute kidney injury? (pre, intra, or post)

A

Pre-renal AKI

23
Q

What are the two types of Uretal Obstructions?
What are the two types of Bladder Obstructions?
What is the a type of Urethral Obstruction?

A

Extra (cervical cancer) and Intra (stones) Ureteral

Structural (bladder cancer) and Functional (anticholinergics, diabetes)

Prostate cancer, BPH

24
Q

Which part of the nephron tubule system is most susceptible to toxins? Which is most susceptible to ischemia?

A 
Toxins = The proximal convoluted tubule
Ischemia = the loop of henle (medulla is an already hypoxic environment)
25
Q

Radiocontrast, aminoglyosides, pigments (ie myo or hemoglobin), cisplatinum, & amphotericin B are likely to cause…?

A

Tubular acute kidney inury (AKI)

26
Q

Acute Tubular Necrosis causes a decrease in the GFR. How?

A

Tubuloglomerular feedback. An obstruction can occur in the luminal space which will lead to vasoconstriction of the afferent arteriole.

27
Q

The most likely complication of Acute Tubular Necrosis that can lead to death is…?

A

Infection!

Arrhythmias and GI hemorrhages are other complications

28
Q

Describe the pathophysiology of acute/allergic interstitial nephritis.

A

A hypersensitivity reaction to drugs (penicillin), infection, or systemic disease (lupus) leading to inflammation of the interstitial nephron space.

29
Q

What would you expect to see in the urinalysis of fa patient with Acute Interstitial Nephritis (AIN)?

A

WBCs
WBC Casts
Eosinophils (could also be high in blood)

30
Q

How can you treat Acute Interstitial Nephritis?

A

Remove offending agent (ie. drug)

Use corticosteroids

31
Q

Two blood vessel related complications that could lead to AKI are…

A

Renal Artery Thrombosis

Thrombotic Microangiopathy

32
Q

Diuretic use, burns, or hemorrhage are items that could lead to…
Pre-renal AKI?
Intrinsic AKI?
Post-renal AKI?

A

Pre-Renal AKI

33
Q

Infection, surgery, or toxin exposure could lead to…
Pre-renal AKI?
Intrinsic AKI?
Post-renal AKI?

A

Intrinsic AKI

34
Q

Anuria and history of pelvic malignancies could lead to… Pre-renal AKI?
Intrinsic AKI?
Post-renal AKI?

A

Post-Renal AKI

35
Q

A distended bladder is a big indicator of…
Pre-renal AKI?
Intrinsic AKI?
Post-renal AKI?

A

Post-Renal AKI

36
Q

What two useful tools in diagnosing a post-renal AKI?

A

Renal ultrasound

Bladder catheter or scan

37
Q

How should you treat pre-renal AKI?

A

Fix Volume!

Give IV fluids, Increase CO

38
Q

How should you treat post-renal AKI?

A

Remove the obstruction.

39
Q

How should you treat intrinsic AKI?

A

Treat the underlying issue.

  • avoid nephrotoxin, hypotension
  • maintain metabolic balance
  • good nutrition (1.5g protein, 35 kcals)
40
Q

What are the indication for dialysis in the treatment of acute kidney injury (AKI), more specifically acute tubular necrosis?

A

A E I O U

Acidosis (hyperkalemia), Electrolyte Imbalance, Intoxiation (symptoms), vOlume overload, Uremia

41
Q

Describe the pathophysiology of Goodpasteur’s Syndrome or Anti GBM Disease.

A

Rare autoimmune disease characterized by circulating antibodies against the alpha-3 chain of type IV collagen present in the glomerular basement membrane and pulmonary capillary basement membranes. Leading to crescentic nephritis.

42
Q

Antigens can be present in the glomerulus in what 3 ways?

A

Antigens can be native to the glomeruli, “planted” in the glomeruli, or an immune complex can travel into the glomeruli.

43
Q

Do immune complexes cause nephritis?

Do “planted antigens cause nephritis?

A

Yes, yes they do. (glomerulonephritis)

No, it leads to glomerulopathy (nephrotic)

44
Q

Why do immune complexes lead to inflammation of the glomerulus?

A

They activate the complement system

45
Q

What is the difference between the classical and alternative pathway complement activation

A

classical - complement is activated by an immune complex

alternative - complement is activated without immune complex (due to antibody against C3 activation regulator)

46
Q

A disease caused by a mutation in the “nephrin” gene which maintains the podocyte “slit diaphragm” leading to overall podocyte effacement and proteinuria (nephrotic syndrome)

A

Congenital Congenital Nephrotic Syndrome of the Finnish Type

Typically presents as at infancy

47
Q

This gene is responsible for maintaining the “slit diaphragm” of podocytes. It hold the slit diaphragm together through disulfide bonds which prevent macromolecule escape.

A

Nephrin

48
Q

Nephrin is mutated in what congenital disease?

A

Congenital Nephrotic Syndrome of the Finish Type

49
Q

What are the 3 types of Rapidly Progressive Glomerulonephritis (RPGN)?

A
  1. Anti-GBM - 10%
  2. Immune complex mediated (IgA Nephropathy, Post infectious GN) - 40%
  3. Pauci Immune Vasculits (Glomerulonephritis with associated vasculitis) - 50%
50
Q

All RPGN’s can have have cellular crescents. True or False?

A

True All RPGN’s are capable to have cellular crescents.

BiB Midterm 3 & Final (10 decks)

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