Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
65 Cards in this Set
- Front
- Back
|
What are the 3 layers involved in glomerular filtration?
|
Capillary endothelium
Glomerular BM Visceral epithelium (podocytes) |
|
|
What is the overall goal of the glomerulus?
|
To filter the blood of molecules we don't need while keeping those we do need in the blood.
|
|
|
Describe the structure of the podocytes. How are they involved in filtration?
|
The podocytes are located on the side of the glomerulus closest to the urinary (Bowman's) space. The slits in between the podocytes are lined with proteins that filter material based upon size and charge.
|
|
|
What factors determine whether a molecule is filtered at the glomerulus?
|
Size & charge
neutral and cationic molecules are filtered better, as well as small molecules |
|
|
What are 3 indicators of glomerular injury?
|
-decreased GFR
-proteinuria -hematuria |
|
|
Why would a person with glomerular injury have decreased GFR?
|
-due to clogging of the capillary with immune cells
-decreased ultrafiltration coefficient due to due to defect with mesangial cells |
|
|
How does hematuria occur?
|
Misshaped RBC's move through capillary endothelium and are thus filtered.
|
|
|
What is the one definitive indicator of glomerular damage?
|
RBC casts
|
|
|
How does proteinuria occur?
|
There is neutralization of the negative charges on proteins (which usually prevents filtration of proteins).
-injury to glomerular epithelium -hemodynamic factors: vasoconstriction of the efferent arteriole forces the gomerulus to filter proteins. |
|
|
What are 3 ways that the immune system can cause glomerular injury?
|
-Ab's binding to the glomerulus
-Ab-Ag complexes clogging the mesangial cells and the capillary -Immune cells releasing factors that damage the kidney. |
|
|
What is an example of an immune disease where Ab's bind to the glomerulus? What does it bind to?
|
Goodpasture's disease --> IgG binds to the type 4 collagen found in the glomerular BM
|
|
|
What is an example of an immune disease that has the circulation of immune complexes that damage the kidney?
|
SLE
|
|
|
What is an example of a disease that causes damage due to the action of factors released by T-lymphocytes?
|
Minimal change disease
|
|
|
What are categories of non-immune diseases that cause damage to the kidney?
|
-Deposition diseases (i.e. amyloidosis)
-Genetic diseases: Alport's disease (mutation in the type 4 collagen in the BM)/Fabry's buildup of alpha-galactidases/Familial Nephrogenic disease where there is a defect in the nephrin protein of the filtration slits. |
|
|
Define focal and diffuse. What is this describing?
|
These terms describe ALL of the glomeruli:
-focal: <50% of the glomeruli are affected -diffuse: >50% of the glomeruli are affected. |
|
|
Define global and segmental. what are these terms describing?
|
These terms are describing ONE glomeruli.
Global: the entire glomerulus is affected segmental: only the glomerular tuft is affected |
|
|
What is the difference between the primary and secondary glomerulopathy?
|
Primary: we don't know what causes these diseases
Secondary: associated with a systemic disease (post-strep glomerulonephtitis) |
|
|
What defines proteinuria?
|
if you have > 150mg of protein/24hr.
|
|
|
What are the different categories of proteinuria? What are the levels of protein found within each category?
|
Isolated proteinuria: less than 3.5g of protein
Nephrotic range proteinuria: > 3.5 g protein Nephritic range proteinuria: <3.5 g protein |
|
|
What are the 3 diseases associated with primary glomerulopathy (nephrotic syndrome)?
|
Minimal Change disease
Focal Segmental glomerulosclerosis Membranous GN |
|
|
What microscope is necessary to identify minimal change disease? What is the pathology associated with this disease?
|
You must use an EM to identify this disorder because nothing can be detected with a light microscope
Change in the charge selectivity in the filtration slits so that now albumin is now able to be reabsorbed. |
|
|
What does focal segmental GM telling you about the nature of the disease?
|
<50% of the glomeruli are affected and only a certain portion is affected.
|
|
|
What is the pathology of membranous GM?
|
The deposition of proteins in the glomerular BM
|
|
|
What is the source of secondary GN?
|
The secondary conditions are due to other infections (diabetes, SLE)
|
|
|
What would the lab results look like for someone with nephritis vs. nephrotic syndrome with protein, blood in the urine, and urine sediment?
|
nephrotic syndrome: > 3.5g protein, bland sediments
nephritic syndrome: < 3.5g protein; hematuria, RBC casts |
|
|
Describe the effects of GFR, HTN, and Edema in nephritic and nephrotic syndromes?
|
Nephrotic --> GFR might be slightly affected, but not drastically, edema present, no HTN
Nephritic --> decreased GFR, HTN, no edema |
|
|
What histolo-pathological structure is associated with RPGN?
|
Cresents!!
|
|
|
What is a clinical feature of RPGN?
|
rapid decrease in GFR
|
|
|
What diseases are associated with primary GN and secondary GN?
|
Primary:
Crescent formation Membranoproliferative GN IgA nephropathy 2ndary: SLE Post-GN Hep B & C |
|
|
What are the 3 layers of the glomeruli from the outer most to the innermost? Describe their arrangement around the capillary?
|
the visceral epithelium (podocytes)
the glomerular BM the capillary endothelium the visceral epithelium and the BM do not fully circumvent the the capillary but reflect over the capillaries and the mesangial cells --> THEY DO NOT FULLY REFLECT AROUND THE CAPILLARY |
|
|
The Bowman capsule is surrounded by ____________ epithelium.
|
Parietal epithelium (attached to the visceral epithelium).
|
|
|
What is nephrin and where is it found? What is its function?
|
Nephrin is located between the filtration slits and is a series of proteins that acts as a barrier to proteins that are filtrated. Also has charge associated for filtration.
|
|
|
Between what 2 layers are subendothelial and subepithelial deposits located? What is an intramembranous deposit?
|
Subendothelial: between the fenestrated endothelial and the basement membrane
subepithelium: beneath the epithelium and above the BM Intramembranous: within the BM |
|
|
What is the difference in appearance of immunoflorescence signals of Ab's that bind to the glomerulus vs. immune complexes that get caught in the glomerulus during filtration?
|
Ab's binding to the glomerulus alone will show a smooth coating on immunoflorescence
Ab-Ag deposition will have a lumpy bumpy appearance |
|
|
What are 2 major histological features of the primary phase of progressive renal damage?
|
Focal segmental glomerulosclerosis
Or tubulointerstitial fibrosis |
|
|
What are the changes associated with the secondary phase of progressive renal damage?
|
Compensatory glomerular hypertrophy and hypertension causing further damage to other glomeruli.
|
|
|
List ways that the tubules can be injured?
|
-ischemia in an upstream tubule may cause a decrease in blood flow to the tubule and cause necrosis, acute and chronic inflammation in the adjacent interstitium, damage to peritubular capillaries, and to proteinuria which may directly injure tubular epithelium.
|
|
|
tubular injury may eventually lead to ___________. What occurs in this situation?
|
Tubular interstitial fibrosis --> scarring of the tubules; great indicator of just how long a kidney has to function.
|
|
|
What would the laboratory findings for a nephrotic syndrome show?
|
Proteinuria, Hypercholesterolemia, low albumin levels.
|
|
|
What age group is most susceptible to minimal change disease? What is the DOC?
|
The young; predinisone
|
|
|
What treatment can you use to definitively diagnose a patient with Minimal Change disease?
|
Predinisone...if prednisone successfully treats the symptoms of prednisone, its confirmed as minimal change disease.
|
|
|
What microscope is necessary for detection of MCD? What is seen upon seeing the slide?
|
EM; effacement of the visceral epithelium and we have loss of charges necessary to act as a barrier to filtration and this allows for proteinuria.
|
|
|
Are there deposits associated with MCD? What is the primary structure affected in MCD
|
NO deposits
Podocytes are mostly affected in MCD |
|
|
What are the secondary causes of MCD?
|
NSAIDs
Tumors --> lymphoma Vaccinations |
|
|
What drug can be used to diagnose MCD?
|
predinisone/steroids -->RELAPSES
|
|
|
MCD has a _______ onset?
|
RAPID
|
|
|
What are the symptoms of focal segmental Glomerulosclerosis?
|
This is a nephrotic syndrome, so it would be the typical symptoms low albumin, high cholesterol, proteinuria.
|
|
|
What are the histological features of FSGS?
|
Fibrosis of the glomerulus which closes capillary loops/basement membrane collapse/trapping of plasma proteins/effacement of visceral epithelial (like MCD)/ NO COMPLEXES!!!
|
|
|
What is the etiology of the primary and secondary FSGS?
|
primary: we don't know
secondary: HIV, heroine, sickle cell, obesity Genetic: in the proteins needed for filtration (nephrin, podo |
|
|
What is the most common primary nephrotic syndrome in African americans? What is the prognosis of this disease?
|
FSGS; prognosis isn't good because 50-80% of patients will progress to ESRD. This disease can RELAPSE
|
|
|
What is the treatment for primary FSGS? What are the stipulations for treatment?
|
steroids or immunosuppressive therapy but ONLY in the PRIMARY stage can you treat FSGS
|
|
|
what drug can be used in primary and secondary disease?
|
ACE inhibitors
|
|
|
What is the difference in onset between MCD and FSGS?
|
MCD has a much more RAPID onset than FSGS. and has a poor response to drugs
|
|
|
What are the characteristics of clinical finding in nephrotic syndrome?
|
protein in urine
hypercholesterolemia low albumin |
|
|
Where do complexes form in Membranous GN? What does this cause?
|
in the subepithelial area which causes BM thickening.
|
|
|
What is the pathogenesis of membranous GN?
|
there is the deposition of immune complexes: either Ab directed against the BM or Ag-Ab complexes that get stuck --> this activates complement which brings in other inflammatory cells that damage the podocytes.
|
|
|
What are the primary and secondary forms of Membranous GN?
|
primary: Ab that binds to the BM
secondary: immune complexes that get stuck during filtration. |
|
|
What is the most common nephrotic syndrome in Caucasian adults?
|
Membranous GN
|
|
|
What are the secondary causes of membranous GN?
|
-medications
-tumors (solids) -infections (syphillis, Hep B) -autoimmune: SLE, rheumatoid arthritis |
|
|
What is the prognosis of Membranous GM? What are the predictors of poor outcome?
|
the rule of thirds:
1/3: -without treatment --> spontaneous remission -slow remission with no progression -aggressive course with ESRD Predictors of poor outcome: -fibrosis seen on histological slide -elevated creatine -HTN -old age heavy proteinuria If they have one of these factors, you should prob treat! |
|
|
What is the explanation behind the "tram-tracking", and what glomerular disease is it associated with?
|
This is the appearance of a splitting of the BM due to the laying down of new BM
MPGN |
|
|
FSGN is associated with what other diseases/lifestyle behaviors?
|
HIV
Obesity Sickle cell |
|
|
Where does the tram-tracking occur relative to the BM??
|
SUB-endothelially whereas with membranous GN it occurs sub-epithelially.
|
|
|
Primary MPGN is seen mostly in ___________ while secondary is mostly seen in ____________.
What diseases is the secondary form associated with? |
kids, adults
SLE, leukemia, Hep C |
|
|
What are the clinical characteristics of MPGN?
How do you treat MPGN? |
Pt. will have characteristics of nephrotic and nephritic syndromes
Decreased levels of complement Few remissions 50% will have ESRD |
