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CRRAB II Week 3 > PBL Objectives > Flashcards

PBL Objectives Flashcards

1
Q

How many children show renal manifestations in the first month after HSP? How many show renal manifestations after the third month?

A

85% - first month
95% - three months
Almost all are self limiting

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2
Q

What is evidence for further disease/shows the extent of kidney damage?

A

Degree of protein in the urine

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3
Q

What are you looking for in HSP kidney biopsy?

A

Cresents!

(Crescentic glomerulonephritis) –> indication for treatment

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4
Q

What do crescents tell us?

A

Indication of rapid progressive glomerulonephritis

–> treat because it can cause irreversible damage

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5
Q

How many children can go on to end stage kidney disease?

A

1-3% (very small percentage of kids)

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6
Q

What are the two most common treatments for HSP?

A

High dose steroids + Cyclophosphamide or daily Mycophenolate Mofetil

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7
Q

What supportive nutritional treatment should be used for HSP?

A

Reduce salt intake –> reduce edema (salt directly related to volume) but REALLY it’s just more important to get him to eat

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8
Q

How many kids with HSP will go on to have chronic HTN as adults?

A

1/3

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9
Q

What is used to treat chronic HTN in adults who were previously kids with HSP?

A

ACE inhibitors, diuretics

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10
Q

Was there an indication for dialysis in our patient? When is dialysis considered?

A

NO.

Considered when kiddo’s GFR is

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11
Q

What is a good way to calculate GFR using creatinine clearance?

A

GFR = 186.3 x (serum creatinine^-1.154)
x (age^0.203)
x 1.212 (if African American)
x 0.742 (if female)

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12
Q

Why are changes in creatinine clearance more important than absolute values in determining injury?

A

Because with changes you can compare the creatinine value at this time to the patient’s baseline (is kidney fxn improving, declining, or at baseline?)

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13
Q

How can you differentiate between acute and chronic kidney disease?

A

Looking at creatinine changes over time

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14
Q

What are two mechanisms by which blood pressure can be increased in someone with renal injury?

A
  1. Renal Artery Stenosis

2. Blood vessel damage

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15
Q

What is the general mechanism by which renal artery stenosis raises blood pressure?

A

Kidney responds to decreased blood supply like hypotension, so it raises BP even more even though BP is normal.

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16
Q

What is the detailed mechanism by which renal artery stenosis raises blood pressure?

A
  1. Stenosis decreases blood flow to the glomerulus
  2. Kidneys think there is systemic hypotension
  3. Juxtaglomerular apparatus secretes renin —> Angiotensinogen –> Angiotensin I —> Angiotensin II (angiotensin converting enzyme)
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17
Q

What does Angiotensin II effect?

A
  1. Contraction of arteriolar smooth muscle –> vasoconstriction –> increased TPR –> increased BP
  2. Stimulates release of aldosterone by adrenal gland –> increases reabsorption of Na+ in distal convoluted tubule–> water follows –> increase plasma volume –> increase BP
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18
Q

How does blood vessel damage cause increased BP?

A
  1. If vessels are damaged, they may stop removing wastes and extra fluid from the body
  2. Extra fluid in blood vessels may then raise blood pressure even more
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19
Q

How can renal damage exacerbate HTN?

A

By:

  1. Volume expansion
  2. Increased systemic vascular resistance
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20
Q

What symptoms are seen in HSP?

A
  • Abdominal pain
  • Rash on legs (red –> purple –> brown)
  • Prior influenza
  • Tired
  • Dark Stools
  • Warm/painful knee
21
Q

What are vitals like in HSP?

A
  • Hypotension

- Low grade fever

22
Q

What happens in the blood with HSP?

A
  • Elevated WBCs
  • Elevated eosinophils
  • Elevated ESR
23
Q

What other lab values are seen with HSP?

A
  • High normal creatinine & BUN
  • Low normal bicarbonate
  • Urine pH normal
  • Hematuria
  • Fecal occult blood
  • Elevated IgA
  • Leukocytoclastic vasculitis
  • Mural fibrin deposition
  • Angiocentric neutrophilic/lymphoblastic infiltrate
  • Increased mesangial matrix
  • Protein in urine
24
Q

Who is most affected by HSP?

A

90% of cases reported in children

25
Q

What time of year are HSP rates highest?

A

December to March

lowest in July and August

26
Q

What is the prevalence for HSP in children and adults?

A

20-27/100,000 children

1-2/100,000 adults

27
Q

What are the four main groups of risk factors for HSP?

A
  1. Infection
  2. Genetics
  3. Toxins
  4. Associated conditions
28
Q

What types of infections are risk factors for HSP?

A
  • Streptococcus
  • Parvo B19
  • Hep B, C
  • HIV
  • Bartonella
  • Salmonella
  • Shigella
  • Staph. aureus
  • Community exposure of strep, staph, parainfluenza
  • Many others
29
Q

What should you know about infections associated with HSP?

A
  • Peak incidence during fall and winter months in children
  • Clustering within families
  • Common prodrome of URI, especially group A beta-hemolytic Streptocossus
30
Q

What are the genetic risk factors for HSP?

A
  • Increased occurrence in family members
  • HLA DRB*01 allele increased susceptibility
  • Decreased frequency in HLA-DRB*07 allele
  • Increased chance of nephritis in HLA-B35 positive patients
  • Increased occurrence in children with Familial Mediterranean Fever
  • HSP nephropathy associated with HLA-B35 and HLA-DQA1
  • Increased risk of HSP associated with polymorphisms of 2 renin-angiotensin system genes
31
Q

What toxins pose a risk for HSP?

A
  • ACE Inhibitors
  • ARBs (Aldosterone receptor blockers)
  • Antibiotics
  • NSAIDs
32
Q

What are associated conditions for HSP?

A
  1. Familial Mediterranean Fever

2. Inflammatory Bowel Disease

33
Q

What is the main histopathologic sign of IgA vasculitis?

A

Leukocytoclastic vasculitis with or without fibrinoid necrosis

34
Q

What will you see in HSP with immunofluorescence?

A

Perivascular IgA deposition

35
Q

What is seen upon renal histology of HSP?

A

Diffuse hypercellularity, focal and segmental proliferation, mesangial proliferation, minimal change to severe cresenteric glomerulonephritis, segmental sclerosis fibrosis, mononuclear cell infiltration, mesangial/subendothelial/subepithelial deposits, diffuse glomerular deposits of IgA/C3/fibrin/IgG, IgA deposits in mesangium

36
Q

What do severe cases of HSP show in renal histology?

A

-Diffuse proliferation with infiltration of neutrophils and circumferential crescents in glomeruli

37
Q

What leads to blood vessel necrosis in HSP?

A

[Immune-mediated process]

  1. IgA complexes form and are deposited in different places in the body resulting in inflammatory responses
  2. This inflammation results in leukocytoclastic (destroying WBCs) vasculitis (inflammation of blood vessels) ultimately leading to blood vessel necrosis
38
Q

How does TNF alpha influence HSP pathophysiology?

A

Elevated TNF alpha –> antigenic reactions in endothelial cells –> increases affinity for IgA binding

39
Q

What does vessel necrosis lead to in HSP?

A

It allows “stuff” to leak out into the tissues.

  1. When stuff leaks, circulating cells, inflammatory mediators, and plasma proteins pass through the capillary wall into the Bowman space.
  2. Since there is no mechanism to reabsorb blood and plasma proteins, this passes into the urine and is found on a UA
40
Q

What does IgA deposition in the abdominal tract result in?

A

Abdominal pain associated with leakage of blood and interstitial fluid into intestinal lumen from peritoneal or visceral purpuric lesions or GI hemorrhage

41
Q

What does IgA cause in mesangial cells?

A
  • Mesangial cells proliferate when they take up Ig’s via endocytosis
  • This leads to decreases ability to filter (lower GFR)
  • Body responds to lower GFR like it does to a decrease in BP (sensed by decreased filtrate at the Macula Densa)
  • Body responds by secreting Renin to raise BP
42
Q

What is seen in NEPHROTIC syndrome?

A
  • MASSIVE PROTEINURIA
  • Hypoalbuminemia (peeing out albumin)
  • Edema
  • Hyperlipidemia/hyperlipiduria
43
Q

What is seen in NEPHRITIC syndrome?

A
  • Hematuria
  • Oliguria (small amt of urine)
  • Azotemia (elevated BUN and serum creatinine)
  • Hypertension
  • Less severe than nephrotic syndrome
  • Inflammatory lesions causing increased cellularity within the glomeruli + leukocytic infiltrate
  • Inflammation in capillaries –> RBCs in urine
  • Hemodynamic changes –> decreased GFR –> oliguria, azotemia
44
Q

What does inflammation in the capillaries cause?

A

RBC in urine

45
Q

What do inflammatory lesions cause?

A

Increased cellularity within the glomeruli & leukocytic infiltrate

46
Q

What do hemodynamic changes cause?

A

Decreased GFR –> oliguria, azotemia

47
Q

What are the most common physical exam findings in HSP?

A
  • Low grade fever
  • Palpable purpuric rash
  • Nonmigratory arthritis (most common in knees and ankles)
  • Arthralgia
  • Occult blood in stool
48
Q

What are the most common physical exam findings in HSPN?

A

-Hypertension
-Edema
-Pulmonary edema w/increased respiratory rate and possible rales
[these are in addition to the HSP exam findings!]

CRRAB II Week 3 (10 decks)

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