Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Nephrology 2 > Nephrotic Syndrome > Flashcards

Nephrotic Syndrome Flashcards

1
Q

What are the key features of Nephrotic Syndrome?

A
  • proteinuria ( greater than 3.5g/24hrs)
  • edema
  • hypoalbunimemia (less than 3.0g/dL)
  • hyperlipidemia/hyperlipiduria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Etiologies of Nephrotic Syndrome:

  • Adults
  • Children
A

Adults:

  • DM
  • HIV
  • Amyloidosis
  • SLE
  • NSAIDS
  • Minimal Change Dz
  • Segmental Focal Glomeruloscerlosis
  • Membranous Nephropathy

Children:
-minimal change dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Nephrotic Syndrome Pathophysiology

A

-glomerular damage leads to increased permeability of the glomerular capillaries to protein….proteinuria (greater than 3.5g/24hrs), leads to hypoproteinemia (albumin less than 3g/100ml.) Hypoproteinemia reduces the plasma oncotic pressure thereby decreasing the plasma volume leading to decreased GFR, increased aldosterone secretion, and fluid retention. Decreased plasma oncotic pressure also favors fluid movement into the tissues, both resulting in edema.

Hypoproteinemia can lead to compensatory synthesis of proteins by the liver, resulting in hyperlipidemia that then damages the glomerulus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What proteins are typically lost in proteinuria?

A

albumin

clotting factors (more likely to bruise)

transferrin

imunoglobulins (immunocompromised)

Vit D binding protein (reduced vit D decreases serum calcium levels thereby increasing PTH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is lipiduria?

A

presence of oval fat bodies in urine, they are fat taken up by Mfs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Minimal Change dz:

  • common in who?
  • microscopic findings
A
  • 90% of dz in children, may occur in adults secondary to NSAIDS
  • cannot see abnormalities on normal microscope, requires electron microscope to see the destroyed podocytes and mesangial cell proliferation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Etiologies of Minimal Change Dz

A
  • infection (viral and bacterial)
  • Drugs: NSAIDS, Lithium, Ampicillin
  • Tumors: hodgkinds, leukemia
  • Allergies: food, bee stings, pollens
  • Other dz: allogenic stem for leukemia, hematopoietic cell transplantation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Tx of Minimal Change Dz

-what are the SE of the tx

A

Steroids.

Short term: GI upset, psychosis, increased BS, HTN, insomnia

Long term: osteoporosis, immunosuppression, cataracts, ulcers, adrenal axis suppression, weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Focal Segmental Glomerulosclerosis:

  • common in who?
  • characterized by what?
  • what are the primary and secondary causes?
A

common in adults, most common lesion found in those with idopathic nephrotic syndrome.

Characterized by the presence of mesangial collapse and sclerosis in SOME areas (segments) of the glomeruli.

Primary: idiopathic
Secondary: HIV infection, Obesity, Lupus, Diabetes, Meds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Membranous Nephropathy

  • characterized by?
  • primary and secondary causes?
A

-characterized by basement membrane thickening w/ little infiltration, deposition of immune complexes on basement membrane, this causes damage and leakage of proteins.

Primary: idiopathic d/t autoabys

Secondary: Hep B antigenemia and also Hep C

  • Lupus, Cancer
  • Drugs: Gold, Catopril, NSAIDS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the most common cause of nephrotic syndrome in adults?

A

Membranous Nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Nephrotic Syndrome: -Complications

-dx

A

Complications:

  • edema
  • hypovolemia**
  • hypertension (as it advances and kidney function goes south, you get more RAAS involved leading to HTN)
  • acute renal failure
  • protein malnutrition
  • infection
  • Deficiency of Vit D and hypocalcemia
  • increased risk of atherosclerosis
  • thromboembolism ( losing volume so they are hypercoaguable)

Dx:

  • 24hr urine (excreting more than 3.5g/24hr)
  • renal bx for definitive dx
  • Serologic studies: ANA(anti-nuclear abys), Complement, Serum/urine protein electrophoresis(IgG, Multiple myeloma), syphilis, Hep B/C, cryoglobulins, antistreptococcal abys
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Nephrotic Syndrome:

-CI to bx

A

CI Bx:

  • uncorrectable bleeding diathesis
  • small kidneys (indicating chronic irreversible dz)
  • uncontrolled, severe HTN
  • Bil. Cystic Kidneys or renal tumor
  • hydronephrosis
  • renal or pre-renal infection
  • uncooperative pts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Nephrotic Syndrome Tx for:

  • proteinuria
  • edema
  • hyperlipidemia
  • hypercoaguability
A

Proteinuria:

  • ACEi/ARB; start low and slow b/c BP is already low, monitor SCr and K+. These decrease intraglomerular pressure so youre not forcing out so much protein.
  • best first step*

Edema:

  • dietary Na restriction
  • loop diuretics

Hyperlipidemia:

  • statins
  • may resolve with resolution of dz

Hypercoagulability:
-do not anticoagulate unless they have DVT; then give LMWH (Lovenox) subQ bridging with warfarin until INR is therapeutic and then you drop lovenox.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Nephrotic Dz from SYstemic Disorders

A
  • Amyloidosis
  • Diabetic Nephropathy
  • HIV associated Nephropathy
  • SLE
  • Hep C
  • Multiple Myeloma
  • Sickle Cell dz
  • TB
  • Gout
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Amyloidosis

  • what is this?
  • what are primary and secondary causes of amyloidosis
  • where does amyloid deposit?
  • Tx
A

what; deposition of proteins(amyloid) in organs leading to their destruction and ultimately the death of the patient.

Primary: deposition of light chain Ig or deposition of heavy chain Ig

Secondary: primarily autoimmune disorders and some cancers

Amyloid deposits in the mesangium of capillary loops, obliterate the glomerulus.

Tx:

  • dialysis
  • Mephalan (chemo drug, will destroy BM) then autologus hematopoietic cell transplant
  • remission can happen if the inciting agent is removed in secondary AA.
  • Primary progresses to ESERD in 2-3years, 5 year survival is less than 20% with death secondary to ESRD and heart dz.
17
Q

Diabetic Nephropathy

  • most common cause of what?
  • screening
A

Most common cause of ESRD in the US.

Screening:

  • initial screening should always include microalbuminuria!!
  • 20-30% will have this after 15years
  • -24hrs urine collection is the accepted standard to CONFIRM.
18
Q

Proteinuria normal, microalbuminuria, macroalbuminuria values in Diabetic Neuropathy screening

A

Normal: less than 30

Microalbuminuria: 30-299

Macroalbuminuria: greater than 299 (shows up on standard dipstick)

19
Q

Diabetic Nephropathy:

-pathophys

A

Patho: Intraglomerular HTN and ischemic injury result in glomerulosclerosis.

Hyperglycemia can induce direct mesangial expansion and damage

Production of cytokines, inflammation and endothelial growth factors destroy the capillary walls and results in nephropathy

20
Q

Tx diabetic nephropathy

A
  • Tight glycemic control
  • BP control with ACEI/ARB (NOT TOGETHER)
  • Na+ restriction/ addition of diuretic sometimes
  • weight loss if obese
  • control hyperlipidemia
21
Q

HIV Associated Nephropathy

  • dx
  • pathology
  • tx
A

Dx: need renal bx to confirm

Pathology: shows focal segmental glomerulosclerosis

Tx: Highly active retroantiviral therapy (HAART) for prolonged course, steroids w/ cyclosporine(immunosuppressant) and ACEI

22
Q

Systemic Lupus (SLE)

  • presentation
  • dx
  • tx
A

Presentation: usually nephritic type

Dx: need UA and chem panels, if positive findings do renal bx

Tx: ACEi, maybe loop diuretic and statins for hyperlipidemia, close monitoring, renal bx to make dx after you confirm high proteinuria

23
Q

WHO classification of SLE

A
  • Type 1: normal
  • Type 2: mesangial proliferative
  • Type 3: focal and segmental
  • Type 4: diffuse and proliferative
  • Type 5: Membranous Nephropathy
24
Q

Hepatitis C

  • normal presentation?
  • indications for tx
  • tx
A

Normally presents as nephrtic (membranoproliferative glomerulonephritis), but you will see mixed nephrotic/nephritic.

Indication for Tx:

  • poor renal function
  • nephrotic syndrome
  • new/worse HTN
  • fibrosis on bx
  • progressive dz

Tx:
-interferon 9mo, this may result in suppression of viremia and help improve hepatic function.

25
Q

Multiple Myeloma

  • what is this?
  • characterized by
  • dx
  • Tx
A

What; malignancy of plasma cells

Characterized by light chain immunoglobulins (Bence Jones Protein) in urine.
-hypercalcemia and hyperuricemia frequent

Dx:
serum protein electrophoresis

Tx:

  • correct hypercalcemia
  • volume repletion
  • chemotherapy to treat malignancy
26
Q

Sickle Cell dz

  • how does this cause renal dysfunction?
  • characterized by?
  • tx
A

Ho: sickling of RBC in medulla, congestion and stasis lead to hemorrhage, interstitial inflamm, and papillary infarcts.

Characterized by:

  • hematuria
  • isothenuria (urine osmolality equal to that of serum)
  • papillary necrosis
  • proteinuria

Tx:
hydration and control sickle cell dz

27
Q

TB

  • classic renal manifestation of TB is the presence of what in the urine?
  • dx
  • tx
A

Classic renal manifestation is the presence of microscopic pyuria with a sterile urine culture -STERILE PYURIA

Dx:
-urine cultures are Gold standard , first morning, mid-stream voided specimens for 3-6 cultures

Tx: Adequate drug therapy for TB will resolve renal manifestations

28
Q

Gout:

  • how does this cause nephrotic syndrome?
  • tx
A

How; kidney primary organ for excretion of uric acid, pts with PCT dysfunction have decreased excretion of uric acid, deposition of crystals can occur in the tubules, interstitium, or urinary tract.

Tx: Avoid food and drugs that cause hyperuricemia:

  • bacon, sardines, liver, sweetbreads, bread, wine, diuretics, theophylline, ascorbic acid.
  • aggressive hydration
  • Allopurinol and colchicine to reduce serum uric acid levels.

Nephrology 2 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions