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Clinical Med II Exam 3 (Annie and Lauren) > Glomerulonephritis And PCKD 🥤 > Flashcards

Glomerulonephritis And PCKD 🥤 Flashcards

1
Q

Can nephritic and NephrOtic diseases overlap?

A

Yes

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2
Q

What is the difference between focal and diffuse glomerular diease?

A

Focal: typically <50% of glomeruli are involved

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3
Q

What is the difference between primary and secondary glomerular disease?

A

Primary: glomerular injury limited to kidney

Secondary: renal abnormalities result from a systemic disease

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4
Q

What is the definition of glomerulonephritis

A

A term given to those diseaseS that present in the nephritic spectrum and usually signifies and inflammatory process causeing renal dysfunction

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5
Q

What is the most common cause of glomerulonephritis?

A

Deposition of immune complexes in the glomerulus

antibody+antigen= immune complex

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6
Q

What are the clinical findings of nephritic syndrome?

A

“Glomerular” hematuria- dysmorphic RBCs, RBC casts, cola/smoke colored

Proteinuria- less than <3.0g/day

Elevated creatinine

Oliguria

Edema

HTN

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7
Q

What would you expect to see in the urine of someone with nephritic syndrome

A

Dysmorphic RBCs**** (Mickey mouse shaped)

RBC casts***

Cola/smoke colored

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8
Q

What condition is the most severe and clinically urgent end of the nephritic spectrum?

A

Rapidly Progressive Glomerulonephritis

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9
Q

What is Rapidly Progressive Glomerulonephritis?

A

Progressive loss of renal function over a comparatively short period of time

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10
Q

What is the characteristic sign you will see when you look at the glomeruli in someone with Rapidly Progressive Glomerulonephritis?

A

Crescent Formation

🐝🐝

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11
Q

What is a crescent formation?

A

Nonspecific response to severe injury to the glomerular capillary wall

Seen in Rapidly Progressive Glomerulonephritis

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12
Q

Which one has hematuria: nephritic or nephrotic

A

Nephritic

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13
Q

What are the 3 diseases that are listed under the nephritic spectrum on the chart she put in the slides a bunch of times

A

asymptomatic glomerular nephritis

Nephritic syndrome

Rapidly progressive glomerulonephritis

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14
Q

So your patient comes in and says he’s pissing blood. What kind of findings would you expect if it was an extraglomerular source (aka NOT glomerular hematuria)

A

Red or Pink

Clots maybe

No proteinuria

Normal RBC morphology

No RBC casts

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15
Q

Your patient is pissing blood. What findings would make you suspect a glomerular source?

A

Cola colored

No clots

Proteinuria maybe

RBCs are dysmorphic **🐝

RBC casts may be present

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16
Q

What medication should you consider giving your patients with glomerulonephritis for antiproteinuric therapy

A

ACE/ARB

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17
Q

Should we immediately hospitalize patients with glomerulonephritis

A

Yes for acute nephritic syndrome and RPGN

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18
Q

What are the characteristic of nephritic syndrome that ms Herrick listed on her summary slide

A

Glomerular hematuria- RBC casts, dysmorphic RBCs

Proteinuria

Increased creatinine or decreased GFR

HTN

Edema

Cola colored urine

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19
Q

What is the other name for IgA nephropathy that might not be on the test but might help you find YouTube videos

A

Berger Disease

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20
Q

What is the most common cause of ~primary~ GN in the world

A

IgA nephropathy

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21
Q

What age usually gets IgA nephropathy?

A

2nd and 3rd decades of life (young adults)

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22
Q

What is the pathogenesis of IgA nephropathy

A

IgA complex deposits in the glomerular mesangium -> inflammatory response***

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23
Q

Why will a patient come to see their PA if they have IgA Nephropathy

A

They will have an episode of Gross Hematuria a few days after a URI

(Remember the kidney damage is from the deposition of immune complexes in the mesangium)

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24
Q

What end of the nephritic spectrum are patients with IgA Nephropathy going to be at

A

Can present anywhere along the spectrum

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25
Q

How do you confirm the diagnosis of IgA Neprhopathy

A

Kidney biopsy (only done for severe disease)

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26
Q

What is the prognosis for IgA nephropathy

A

Spontaneous remission in 1/3 of pts

Progression to ESRD in 20-40%

Remaining may have chronic microscopic hematurua and stable creatinine

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27
Q

Do you treat every patient with IgA Nephropathy

A

Only the ones who have:

Proteinuria >1g ***

Decreased GFR

HTN

(The ones at higher risk of profressing to ESRD)

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28
Q

How do you treat IgA Nephropathy? (If you decided to treat)

A

ACE/ARB

Maybe glucocorticoids/immunosuppressive

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29
Q

What kind of infection leads to poststreptococcal GN?

A

group A beta-hemolytic strep lol

Specifically pharyngitis or impetigo (strep skin infection)

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30
Q

Who is more likely to get post streptococcal GN?

A

males *twice as common

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31
Q

What is the pathophysiology of poststreptococcal GN?

A

Immune mediated:

An immune complex containing a streptococcal antigen is deposited in glomerulus➡️complement activation and inflammation

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32
Q

How long after a GAS infection will post streptococcal GN present?

A

1-3 WEEKS after infection ***

IgA nephropathy was only 1-2 days after onset of URI sx

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33
Q

What will you find in the serum in post streptococcal GN?

A

Elevated streptococcal antibodies (ASO titers)

Low complement

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34
Q

How do you treat post streptococcal GN?

A

Supportive care

Kids do better, and recurrence is rare

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35
Q

What is Anti-GBM disease?

A

Antibodies attack the glomerular basement membrane (GBM)

(The target antigen is also found in the alveolar basement membrane*** when antibodies attack those too it’s called GoodPasture)

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36
Q

What is the difference between Anti-GBM disease and Goodpasture Syndrome?

A

Anti-GBM: anti-GBM antibodies plus glomerulonephritis (KIDNEY ONLY)

Goodpasture: glomerulonephritis AND Pulmonary hemorrhage (LUNG AND KIDNEY)

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37
Q

_____________accounts for 10-20% of patients with acute rapidly progressive GN

A

Anti-GBM disease

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38
Q

What age and genders get anti-GBM/Goodpasture

A

First peak: 30yo, males, more lung involvement

Second peak: 60yo, females

39
Q

What causes anti-GBM/Goodpasture?

A

Idiopathic usually

40
Q

What pulmonary sx will you see in Goodpasture syndrome

A

Overt hemoptysis pulmonary hemorrhage

Cough

Dyspnea

41
Q

How do you diagnose anti-GBM/Goodpasture syndrome

A

anti-GBM antibodies in serum/kidney biopsy

ANCA will be positive in 40%***

(If they have anti-GBM ~and~ ANCA, it will help confirm your diagnosis)

42
Q

What is the other name for Systemic Lupus Erythematosis (SLE) Nephritis

A

Lupus Nephritis

43
Q

What kind of antibodies will be present in Lupus Nephritis?

A

Anti-ds DNA antibodies

44
Q

What is the treatment for anti-GBM/Goodpasture

A

Urologist will do plasmapheresis and give immunosuppressants

45
Q

What will initially make you suspect that your patient has Lupus Nephritis

A

Abnormal urinalysis

High creatinine

Confirmed with renal biopsy

46
Q

What is the other name for IgA Vasculitis

A

Henoch-Schonlein Purpura (HSP)

47
Q

What is the characteristic pathology of IgA Vasculitis (HSP)

A

Tissue deposition of IgA-containing immune complexes

48
Q

Who is most likely to get IgA Vasculitis (HSP)

A

Children post URI

49
Q

What is the CLASSIC TETRAD of IgA Vasculitis (HSP)

A

Rash (Palpable* purpura)

Abdominal Pain

Arthralgias

Renal disease
🐝🐝🐝

50
Q

Which kidney problems show up after other illnesses?

A

Poststreptococcal GN: 1-3 weeks post GAS

IgA nephropathy: 1-2 days post URI

IgA Vasculitis: post URI

51
Q

How do you treat IgA Vasculitis (HSP)

A

Supportive care

52
Q

Name that dx:

8 year old boy

Red-brown urine this morning

Sore throat resolved last week

A

Postinfectious GN

53
Q

Name that dx:
20year old male

Gross hematuria 2 days after URI

A

IgA Nephropathy

Due to age and 2 days post URI

54
Q

What is Pauci-Immune Glomerulonephritis?

A

Systemic ANCA-associated Vasculitis (GPA, MPA, or EGPA) cause vascular and tissue damage.

BUT there is an Absence or paucity of immune deposits on kidney biopsy

55
Q

What are the systemic ANCA-associated vasculitides

A

Granulomatosis with polyangitis (GPA)

Microscopic polyangitis (MPA)

Eosinophilic GPA (EGPA)

56
Q

What are the hallmark features (not symptoms) of GPA

A

Necrotizing granulomatous inflammation**

Pauci-immune Vasculitis of small-medium vessels

57
Q

What parts of the body are affected by GPA

A

Upper AND Lower respiratory tracts

Kidneys

58
Q

What are the pulmonary symptoms of GPA

A

Chronic sinusitis

Saddle nose deformity

Otitis media

Ocular involvement

Cough, dyspnea, hemoptysis

59
Q

What are the RENAL manifestations of GPA

A

Glomerulonephritis- crecentic necrotizing glomerulonephritis** (RPGN)

60
Q

What is the difference between MPA and GPA

A

MPA:
Absence of granuloma formation

UPPER respiratory tract is SPARED (no chronic sinusitis in MPA**)

61
Q

When does GPA typically present vs MPA

A

GPA: 35-55yo

MPA: 50yo

62
Q

What is Eosinophilic GPA?

A

ANCA-associated Vasculitis that is associated with asthma and eosinophilia*🐝

63
Q

What are the 3 disease phases of EGPA?

A
  1. Prodrome- allergic disease (asthma/allergic rhinitis)
  2. Eosinophilic/tissue infiltrative phase
  3. Vasculitis- necrotizing Vasculitis of the small-medium vessels
64
Q

Which Pauci-Immune GN do you think your patient has if they have asthma, are corticosteroid dependent and have nasal polyps

A

EGPA

65
Q

How do you treat Pauci-Immune GN (GPA, MPA, and EGPA)

A

Immunosuppressants- corticosteroids and cytotoxic agents

Referral to nephro/neuro/rheum/pulm etc

66
Q

Of the 3 Pauci-Immune GNs, which ones have more C-ANCA and which ones have more P-ANCA

A

C-ANCA: GPA

P-ANCA: MPA and EGPA

67
Q

What kind of glomerulonephritis do patients with Anti-GBM usually present with

A

RPGN

68
Q

What kind of glomerulonephritis do patients with Pauci-immune GN typically present with

A

RPGN

69
Q

Name that dx:
30 yr old male

Presents with acute RPGN

Has GN + pulmonary hemorrhage

+anti-GBM antibodies

A

Goodpasture syndrome

70
Q

Name that dx:

50 year old male

Hx of recurrent URIs and chronic sinusitis

Presents with acute RPGN

+ C-ANCA

A

GPA

71
Q

When are most simple kidney cysts found

A

Incidentally on ultrasound

72
Q

You’re doing an ultrasound and WHOA you found a cyst on their kidney. What do you need to do now?

A

You need to do an ultrasound and a CT to differentiate it from malignancy, abscess, or polycystic kidney disease

73
Q

What will you see on CT of a benign, harmless simple cyst

A

Smooth thin walls that are sharply demarcated

Does NOT enhance with contrast*****

74
Q

Do you get polycystic kidney disease from your parents?

A

Yes it can be autosomal dominant or autosomal recessive

75
Q

What are the 2 types of polycystic kidney disease

A

Autosomal dominant (ADPKD)

Autosomal recessive (ARPKD)

76
Q

What is the most common genetic cause of CKD?

A

Autosomal Dominant PKD

77
Q

Which two genes account for most cases of ADPKD

A

PKD1

PKD2

78
Q

Does PKD affect one or both kidneys

A

ALWAYS BOTH

79
Q

Is a “progressive decline in kidney function” seen in ADPKD, ARPKD, or both

A

Both

80
Q

For most patients with ADPKD, renal function remains intact until the ________ decade of life

A

4th

81
Q

What causes the decline of renal function in ADPKD

A

Cysts accumulate fluid ➡️ enlarge*➡️compress neighboring renal parenchyma➡️progressively compromising renal function

82
Q

What is the mechanism that the kidneys use to try to compensate in ADPKD

A

“Hyperfiltration.”

83
Q

What are the RENAL manifestations of ADPKD

A

HTN ***** might be presenting sx

Abdominal/flank pain (big bois squishing)

Palpable kidneys

Hematuria

+/- proteinuria

Hx of UTIs and nephtolithisis

84
Q

What are the EXTRArenal manifestions of ADPKD?

A

Intracranial aneurysms (“worst headache of my life”)

Hepatic Cysts*****

Heart valve probs (midsystolic click)

85
Q

What is the Initial modality used for the screening and diagnosis of ADPKD?

A

Ultrasound ***

86
Q

What is the management of ADPKD?

A

Strict BP control, low salt diet, statins🧂

Avoid caffeine? ☕️

Pain control

Tolvaptan ***(vasopressin receptror antagonist)

Dialysis/transplant

87
Q

What is the only disease modifying medication for ADPKD/

A

Tolvaptan

ADH receptor antagonist- though that ADH may make it worse

88
Q

Who gets Autosomal recessive PKD?

A

Infants and children (they are born with big kidneys and liver probs)

89
Q

What gene is mutated in autosomal recessive PKD

A

PKHD1

90
Q

Are the kidneys the only thing affected by ARPKD

A

No. Hepatobiliary tract is affected big time

91
Q

What are the characteristic findings of ARPKD

A

Bilateral markedly enlarged kidneys

HTN (in babies!)

Congenital hepatic fibrosis

Portal HTN (ascites in a baby!)

92
Q

Which kind of PKD can be detected before birth on ultrasound after 24 weeks

A

ARPKD

93
Q

What is the treatment for ARPKD?

A

One health

Clinical Med II Exam 3 (Annie and Lauren) (5 decks)

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