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Nephritis Roop/Raja Flashcards

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1
Q

What does PCN stand for?

A

penicillin

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2
Q

Define oliguria

A

abnormal, small amounts of urine

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3
Q

What are RBC casts?

A

RBC that has been pushed through the nephron and ureter and is shaped like a “cast” of the blood vessel (blood should not be here)

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4
Q

What is an ASO titer lab study looking for?

A

Antistreptolysin O titer (antibodies for strep)

In children ASO titer SHOULD be under 100 todd units/mL (anything higher indicates strep antibodies)

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5
Q

What does low serum complement C3 and C4 levels mean?

A

Immune complex diseases

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6
Q

What does low CH50 levels mean?

A

lab study is looking for the integrity of classical pathway

low values indicate infection, lupus, glomerulonephritis, etc.

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7
Q

What is an Anti-DNase B lab test?

A

a blood test looking for antibodies for a substance (protein) produced by group A streptococcus

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8
Q

What do high BUN levels mean?

A

Low kidney function

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9
Q

What is the “triad of signs and symptoms” for post-streptococcal glomerulonephritis

A

-edema
-HTN
-oliguria

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10
Q

What is the first step in urine formation

A

filtration

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11
Q

What are the 3 Starling forces controlling urine formation?

A

1) Oncotic pressure (from albumin, keeps fluid in, also called blood colloid osmotic pressure)
2) Glomerular blood hydrostatic pressure (moving fluid out)
3) Capsular hydrostatic pressure

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12
Q

Normally, ____ Starling forces are at work in glomerular filtration

A

3

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13
Q

Are blood cells and protein normal components of urine? Why or why not?

A

no

if present, then it’s coming from the glomerulus

What are the 3 layers?
1) Endothelium of the capillaries (RBC cannot/should not get past this layer)
2) Basement membrane (proteins cannot/should not get past this layer)
3) Podocytes

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14
Q

How does a strep infection affect the glomerulus and how is this reflected in the patient’s lab results?

A

Destroying the glomerulus layers → protein and RBC leaking

Antibody complexes → glomeruli increases in size
-Antibodies traveling to the kidneys OR can be detected in the kidneys and make immune complexes there

Humps = IgG + C3 accumulate in area, causes podocytes to breakdown and increase inflammation in bowman’s space due to neutrophils

Podocytes are breaking down (causing filtration barrier to breakdown)

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15
Q

Will GFR be reduced or increased? How is this reflected in the lab studies?

A

decreased

-High creatinine
-Low urine output
-Proteinuria
-RBC in urine

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16
Q

Explain the peripheral edema

A

Oncotic pressure and hydrostatic pressure is not balanced
-No oncotic pressure (lack of albumin) → moving fluid out
-Fluid entering into bowman’s space
-Simple squamous lines bowman’s space
-Fluid leaves easily

RAAS system triggered
-Aldosterone → sodium reabsorption
-Water always follows

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17
Q

What is the treatment for post-strep glomerulonephritis for the 5 y/o pt?

A

-Restart antibiotics
-Change diet (decrease sodium and fluid intake)
-LAST RESORT: in hospital, put them on meds

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18
Q

Immune response to an infection often involves multiple pathways. What are the 3 we talked about?

A

1) innate immunity (including complement pathway)
2) cellular immunity (antibody production against infectious agent)
3) autoimmunity (antibody production against self)

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19
Q

Innate immunity can see PRRs (pattern recognition receptors) on the surface of…..

A

neutrophils and macrophages

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20
Q

How do PRRs (pattern recognition receptors) in innate immunity work?

A

they have to bump into the foreign invader to notice it

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21
Q

Innate immunity has complement proteins ranging from C__ - C___ and are made in the _________

A

C1-C9

liver

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22
Q

Which complement protein is floating in the body constantly? Is it active or inactive

A

C3 in low levels, inactive

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23
Q

What is the point for having C3 floating around in the body constantly?

A

if C3 gets activated then it can quickly make C3 convertase, start inflammation (MAC), and increase vascular permeability

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24
Q

What are the 3 pathways in innate immunity?

A

1) classical
2) alternative
3) mannose binding lectin (MBL) pathway

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25
How is the classical pathway initiated?
by the presence of an immune complex (antigen bound to antibody)
26
How is the alternative pathway initiated?
increased levels of C3 → LPS can increase levels of C3, amplifying existing low levels of C3, foreign entity with no mannose or your body doesn’t have immune complexes against it
27
How is the MBL pathway initiated?
bacterial cell walls have more mannose sugars; while our cell walls have more sialic acid differentiates self from nonself MBL can also come from liver
28
With glomerulonephritis, which innate immune pathways are activated?
all 3!!!!!
29
cellular immunity relies on _____ cells and ____ cells
B cells and T cells
30
Cellular immunity has B cells generating antibodies against antigens. What is the function/purpose of generating antibodies?
it causes a tagging system → “there is a foreign entity here and we need to get rid of it”
31
Cellular immunity has macrophages and ______ that will get rid of tagged foreign entity
RBCs
32
What are the complement receptors on the surface of macrophages called in cellular immunity?
CR1 receptors
33
Macrophages carry ____ receptors
Fc
34
Macrophages carry Fc receptors. They MUST also have ____ receptor for _____ to bind. This is an added checkpoint so that macrophages are engulfing what it should
C5a, C5a
35
Macrophages carry Fc receptors. They MUST also have C5a receptor for C5a to bind. This is an added checkpoint so that macrophages are engulfing what it should. They also need to have ____ bound to foreign entity
C3b
36
Macrophages have a number of receptors on it to ensure what?
that the antigen will attach
37
What is the typical pathway for when a macrophage receptor has an antigen bind (specifically C3b)?
C3b will be on the surface of the foreign entity → kidney → spleen
38
If macrophages cannot clear the foreign entity then what happens?
immune complexes are floating around to help
39
Autoimmunity is where the antibody production is against self, this is known as.....
"self attacking"
40
When infection is cleared or when the foreign microorganism is gone, inflammation and complement will continue or stop?
stop
41
The lectin pathway, or mannose-binding lectin (MBL) and ficolins recognize and bind ________ on pathogen surface
carbohydrates
42
Classical pathway has _____ that interacts with pathogen surface or with antibodies bound to the surface
C1q
43
Alternative pathway has ____ that undergoes spontaneous hydrolysis to C3(H2) to initiate eventual deposition of C3 convertase on microbial surfaces
C3
44
All 3 pathways generate a _____ convertase, which cleaves C3, leaving C3b bound to the microbial surfaces and releasing C3a
C3
45
After all 3 pathways generate a C3 convertase, C3a and C__a recruit phagocytic cells to the site of infection and promote inflammation
C5a
46
After all 3 pathways generate a C3 convertase, phagocytes with receptors for ____ engulf and destroy the pathogen
C3b
47
After all 3 pathways generate a C3 convertase, completion of the complement cascade leads to the formation of a ________________, which disrupts cell membrane and causes cell lysis
membrane attack complex (MAC)
48
How does the immune system dispense of complexes containing antibodies and small, soluble antigens from our blood?
Fc receptors and complement -Fc receptors on phagocytes play some role -Complement plays a more important role
49
What are the 3 general steps of the complement system?
1) C3b can bind to antibodies that have bound soluble antigen into a complex 2) The C3b then binds to CR1 on the surface of a RBC 3) RBC circulates and ends up at the liver and spleen (complexes are stripped off their surface and immediately get degraded by local phagocytes) note: there are TONS of RBCs in our blood and few phagocytes
50
Ingestion of complement-tagged pathogens by _________ is mediated by receptors for the bound complement proteins
phagocytes
51
Ingestion of complement-tagged pathogens by phagocytes is mediated by receptors for the bound complement proteins. What are the 3 steps?
1) bacterium is coated with C3b 2) when only C3b binds to CR1, bacteria are not phagocytosed 3) C5a must also be there to activate macrophages to phagocytize via CR1 (C5a binds to a GPCR on surface)
52
Glomerular deposition of preformed circulating immune complexes (antibodies directed against bacterial antigens). These bacterial antigen-antibody immune complexes can activate the _____________ and ______________ complement pathways
alternative and classical (both pathways are kicked up because of excessive inflammation)
53
autoimmunity from antibodies directed to intrinsic glomerular antigens via.....
molecular mimicry
54
Cross-reactivity between foreign molecules on pathogens and self molecule can lead to _______ responses and _______________ disease
antiself, autoimmune
55
Molecular mimicry between bacterial antigens and glomerular basement membrane molecules, such as......
collagen, laminin, and heparan sulfate
56
Strep has molecular mimicry to human cells (it carries a lot of entities that humans have). What does it resemble?
basement membrane of glomerulus
57
Autoimmune syndromes involving molecular mimicry = _________________ that follows streptococcal infection: antibodies against bacterial cell surface can cross react with _________ ________
rheumatic fever, heart valves
58
Activation of Complement: circulating bacterial antigens that can activate complement through the ________ or ____________ pathways, independent of immunoglobulin.
lectin, alternative (this happens when the body is unable to to clear everything out in time)
59
Nephrotic syndrome can result from an abnormality of glomerular permeability that may be primarily due to an intrinsic renal disease in the kidneys or secondary due to.....
1) congenital infections 2) diabetes 3) systemic lupus erythematosus 4) neoplasia 5) certain drug use.
60
What is the most common cause of nephrotic syndrome in children?
minimal change glomerulonephritis
61
In white adults, nephrotic syndrome is most frequently due to ____________ ____________, whereas in populations of African ancestry, the most common cause of the nephrotic syndrome is ________ _______________ ______________.
membranous nephropathy, focal segmental glomerulosclerosis
62
What are the 4 primary causes of nephrotic syndrome?
1) minimal change nephropathy 2) focal glomerulosclerosis 3) membranous nephropathy 4) hereditary nephropathies
63
What are the 6 secondary causes of nephrotic syndrome?
1) Diabetes mellitus (DM) 2) Lupus erythematosus 3) viral infections (hep B, hep C, HIV) 4) amyloidosis and paraproteinemias 5) preeclampsia 6) allo-antibodies from enzyme replacement therapy
64
Can nephrotic syndrome be secondary to something else?
yes
65
What are the S&S of nephrotic syndrome?
1) proteinuria 2) low serum albumin 3) edema 4) frothy urine due to protein
66
Nephrotic syndrome affects who?
1) children + adults 2) both sexes equally 3) any race
67
What is the first sign of nephrotic syndrome in children?
edema of the face
68
What is the first sign of nephrotic syndrome in adults?
dependent edema (usually in the legs)
69
What are the 3 main types of nephrotic syndrome?
1) minimal change glomerulonephritis 2) membranous nephropathy 3) focal segmental glomerulosclerosis (FSGS)
70
Minimal change glomerulonephritis is most prominent in who?
children
71
Minimal change glomerulonephritis is usually ___________ but can also be secondary to what?
idiopathic secondary: -tuberculosis -leukemia -NSAIDs
72
Minimal change glomerulonephritis causes damage to the ____________
glomeruli
73
nephrotic syndrome causes swelling in body parts like....
legs, ankles, or around the eyes (edema)
74
Minimal change glomerulonephritis causes proteinuria, this is because there is a loss of what?
loss of protein in blood
75
Patients with minimal change glomerulonephritis will have _______ levels of fat or lipids in the blood (high cholesterol)
high
76
Membranous nephropathy is most prominent in who?
white adults
77
Membranous nephropathy is caused by what?
thickening of a part of the glomerular basement membrane (thickened glomerular membrane does not work normally)
78
Is membranous nephropathy autoimmune?
potentially
79
What are the 4 pathological stages of membranous nephropathy?
1) presence of scattered or more regularly distributed small immune-complex-type electron-dense deposits in the subepithelial zone. 2) projections of basement membrane material around the subepithelial deposits. 3) the new basement membrane material surrounds the deposits. 4) the loss of electron density of the deposits, which often results in irregular electron-lucent zones within an irregularly thickened basement membrane
80
There are two kinds of membranous nephropathy (MN). What are they?
1) idiopathic (also known as primary MN, more common than secondary MN) 2) Secondary MN (caused by another disease or drug (Hep B, NSAIDs, Lupus))
81
Membranous nephropathy causes what 5 S&S?
1) weight gain 2) fatigue 3) proteinuria 4) high cholesterol 5) edema
82
Focal segmental glomerulosclerosis (FSGS) is most prominent in who?
African ancestry
83
What is focal segmental glomerulosclerosis (FSGS)?
rare disease in which scar tissue develops on the glomeruli, the small parts of the kidneys that filter waste from the blood. small section of glomeruli = FOCAL
84
What are the 3 types of focal segmental glomerulosclerosis (FSGS)?
1) primary 2) secondary 3) genetic
85
What happens to the podocytes in focal segmental glomerulosclerosis (FSGS)?
the podocytes are damaged and do not regenerate
86
Where does focal segmental glomerulosclerosis (FSGS) get its name?
Sclerosis → cannot filter bc of the scar tissue
87
Focal segmental glomerulosclerosis (FSGS) can be caused by a variety of conditions, such as....
-diabetes -sickle cell disease/anemia -other kidney diseases -obesity -infection (HIV) -drug toxicity -meds (interferons or bisphosphonates) -drugs such as heroin or anabolic steroids (substances used to enhance muscle growth) (A rare form of FSGS is caused by inherited abnormal genes)
88
With focal segmental glomerulosclerosis (FSGS), it is common to see weight gain due to what?
extra fluid build up in the body
89
What are the 4 S&S for focal segmental glomerulosclerosis (FSGS)?
-proteinuria -high cholesterol -weight gain -edema
90
What is the best way to diagnose focal segmental glomerulosclerosis (FSGS)?
kidney biopsy
91
What are the metabolic consequences of proteinuria?
1) infection due to loss of immunoglobulins and edema fluid acting as a culture medium 2) liver compensates by increasing production of proteins, including lipoproteins resulting in hyperlipidemia
92
What is a classic feature of nephrotic syndrome?
hyperlipidemia!!!!!!!
93
What are the complications of proteinuria?
-venous thrombosis -pulmonary embolism -hypercoagulability caused by the loss of anticoagulant proteins along with simultaneous increase of clotting factors
94
Several mechanisms promote thrombosis in patients with nephrotic syndrome. What are they?
-increased urinary conc. of proteins that prevent thrombosis (antithrombin III and possibly protein C and S) -increased synthesis of factors that promote thrombosis (factors V and VIII, von Willebrand factor, alpha-2-plasma inhibitor, plasminogen activator inhibitor 1, and fibrinogen)
95
What is the treatment for nephrotic syndrome?
-treat cause -lipid-lowering meds (statins) -corticosteroids are the first-line therapy for idiopathic nephrotic syndrome in children with most patients going into remission following treatment -for patients with membranous nephropathy, approximately 30% undergo spontaneous remission -generally patients with focal-segmental glomerulosclerosis (FSGS), will progress to an end-stage renal disease (ESRD) requiring dialysis and kidney transplant. 25-30% of patients with FSGS develop ESRD within 5 years
96
What is the nephrotic syndrome tree?
tree diagram that shows the trunk w/ increasing proteinuria and the branches (other S&S) represent other components that appear when proteinuria crosses the nephrotic range threshold -proteinuria (multifactorial, partially resolved) -hyperlipidemia (hypertriglyceridemia and hypercholesterolemia) -lipiduria (urinary loss of plasma lipids) -hypoalbuminemia (albuminuria, inadequate liver synthetic comp.) -edema (increased sodium retention and increased peripheral permeability)
97
‘___________ ___________’ to intrinsic glomerular antigens, leading to subepithelial deposits and activation of the alternative complement pathway
Molecular mimicry
98
The bacterial antigens cause glomerular injury through multiple potential mechanisms. What are they?
-The resultant complement activation leads to the generation of chemotactins C3a and C5a, recruitment of neutrophils and monocytes, and leukocyte-mediated injury in glomeruli. -In addition, locally activated plasmin degrades the glomerular basement membrane directly or through the activation of metalloproteinases and may promote inflammation. Predisposing host factors such as genetic susceptibility and dysregulation of the alternative complement pathway may contribute to pathogenesis.

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