Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Med Year 3 > Glomerulonephritis and PCKD > Flashcards

Glomerulonephritis and PCKD Flashcards

(58 cards)

Start Studying
1
Q

what is interstitial nephritis

A

inflammation of space between cells and tubules = interstitium

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

what is glomerularsclerosis

A

pathological process of scarring of tissue in glomerulus, caused by GN or obstructive uropathy

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

what is IgA nephropathy

A

bergers disease = most common cause of glomerulonephritis

  • peak age: 20
    IgA deposits in mesangium
    overalps with HSP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how does IgA nephropathy present and how is it managed?

A

classically: macroscopic haematuria in young people following an UPPER RESP TRACT INFECTION

manage with monitoring 6-12 months, ACE-I if hypertensive

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

what is nephrotic syndrome?

A

when basement membrane in glomerulus becomes highly permeable to protein so leaks into urine

damaged podocytes, so loss of albumin (main protein that keeps blood in blood vessels)

low albumin = increased lipids by liver

loss of anti-thrombin 3= hypercoaguable

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

what is the classic triad of nephrotic syndrome?

A

low serum albumin
high urine protein +3 on dipstick
oedema

= also may have hypercholesterolaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what causes nephrotic syndrome?

A

minimal change disease in children

in adults: focal segmental glomerularsclerosis (presents in young adults, due to idiopathic reasons, HIV, renal path, heroin etc)

secondary causes: HSP, diabetes, infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how do you manage nephrotic syndrome?

A 
high dose steroids for 4 weeks 
low salt diet
diuretics 
fluid restriction: 1-1.5L
albumin infusions
antibiotic prophylaxis 
anti-coag?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is nephritic syndrome?

A

inflammation of kidney = group of symtpoms

 antibody meets antigen to form immune complex
 this complex will lodge itself in capillary and cause an IR against capillary and antigens
 WCC are recruited (hence on FBC, high WCC)
 Areas become inflamed, and breakdown
 Allows RBC and WBC to pour through the opening
• Hence protein gets through as well

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

what are the features of nephritic syndrome?

A

peripheral oedema
proteinuria
serum albumin <25

oliguria
high BP
granular casts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what would you see on a urine dip for nephritic?

A

proteins, bloods, WC

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

what are the causes of nephritic syndrome?

A

minimal change disease
focal segmental

primary: IgA, post-strep GN, GPS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

main difference between nephritic and nephrotic?

A

only protein in urine = nephrotic

protein, sediments and extra cells = nephritic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is glomerulonephritis, and what are some examples?

A

conditions that cause inflammation of or around glomerulus and nephron

o	Minimal change disease
o	Focal segmental glomerulosclerosis
o	Membranous glomerulonephritis
o	IgA nephropathy (AKA mesangioproliferative glomerulonephritis or Berger’s disease)
o	Post streptococcal glomerulonephritis (AKA diffuse proliferative glomerulonephritis)
o	Mesangiocapillary glomerulonephritis
o	Rapidly progressive glomerulonephritis
o	Goodpasture Syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the pathophysiology of GN

A

immunoglobulin and complement activation within glomeruli

antigens may be trapped and deposited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is membranous GN

A

most common type
- ages 20 and 60
IgG deposits in basement membrane
idiopathic

secondary to malignancy, NSAIDs, rheumatic disorders

management: ACE-I, immunosuppression if svere (ccs and cyclophosphamide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the prognosis of membranous GN

A

o 1/3 recover spontaneously, 1/3 remain proteinuric, 1/3 develop ESRF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is membranoproliferative GN

A

= same as membranous but deposits also in mesangium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is post-strep GN?

A 
patients <30 years 
presents as:
- 1-3 weeks after a strep infection
-develops as acute nephritic syndrome 
- malaise, haematuria, proteinuria, hypertension, oliguria

caused by: immune complex depositition in glomeurli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what causes post-strep GN and what are the investigations?

A

immune complex deposition in glomeruli

- low C3 on bloods, renal biopsy, starry sky appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is GPS?

A

small cell vasculitis

  • anti-GBM antibodies attack glomerulus and pulmonary basement membrane

= GN and pulmonary haemorrhage

  • more common in men, age 20 and 60
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are the tests and management for GPS

A

linear IgG deposits and CO transfer factor is raised

management: plasma exchange, steroids, cyclophosphamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what differential could you give for GPS

A

wegeners (ANCA vasculitis may present with wheeze and sinus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is rapidly progressive GN

Study These Flashcards
A

very acute illness w sick patients

secondary to GPS often
nephritic syndrome features

treated with BP control and steroids

25
what is vasculitis
inflammation of the blood vessles, diff sizes
26
what type of vasculitis affects small vessels?
Henoch=schonlein purpura Eosinophilic granulomaosis with polyangiitis (churg-strauss syndrome) Microscopic polyangiitis = main feature is renal failure Granulomatosis with polyangiitis (wegener’s granulomatosis)
27
what type of vasculitis affects medium sized vessels?
Polyarteritis nodosa Churg-strauss syndrome Kawasaki disease
28
what type of vasculitis affects large vessels?
GCA and takayasu's arteritis
29
what is the main complication of GCA?
blindness
30
what are some generic presentations of vasculitis?
``` purpura, joint and muscle pain peripheral neuropathy renal impairment anterior uveitis and scleritis GI disturbance and bleeding hypertension ```
31
what are the systemic manifestations of vasculitis
fever, fatigue, WL, anaemia
32
how do you test for vasculitis?
CRP and ESR raised | ANCA blood test
33
what is HSP?
IgA vasculitis = affects children presents as rash on legs and bum inflammation bc of IgA deposits on BV of affected organs often triggered by URTI most common in children under age of 10 rash due to leaking from small BV
34
what are the features of HSP and how do you treat it?
purpura, joint pain, abdo pain, renal involvement = analgesia and hydration
35
explain the ANCA system
Antineutrophil cytoplasmic antibodies (ANCA) are a group of autoantibodies produced when a person's immune system mistakenly targets and attacks its own neutrophil proteins. Two of the most commonly targeted proteins are myeloperoxidase (MPO) and proteinase 3 (PR3)
36
what are p-anca and c-anca?
p-ANCA: also called anti-MPO antibodies --> microscopic polyangiitis and churg-strauss syndrome typical pattern of peri-nuclear staining, specific for myeloperoxidase enzyme c-ANCA also called anti-PR3 antibodies --> wegener’s granulomatosis diffuse cytoplasmic staining both enzymes are stored in neutrophil granules
37
what is churg strauss syndrome?
small and medium vasculitis lung and skin problems presents with severe asthma in late teens eleveated eosinophils on FBC
38
what is granulomatosis with polyangitis?
wegeners CLASSIC SIGN: saddle shaped nose small vessel affects resp and kidneys (epistaxis, crusty secretions), cough, wheeze, haemoptysis with consolidation on CXR leads to rapidly progressing GN
39
what is the pathogenesis of ANCA vasculitis
expression of auto-antigeon on surface due to cytokines binding = activation of neutrophils cytotoxic injury to vessel wall apoptosis and necrosis of neutrophils and endothelial cells
40
how do you diagnose ANCA vasculitis?
history and examination, ANCA blood test, kidney biopsies, CXR, CO transfer factor differentiates between pulm oedema and presence of blood in alveoli
41
how do you manage ANC vasculitis?
Induction of remission: cyclophosphamide and steroids Maintenance of remission: azathioprine & CCS
42
what is polyarteritis nodosa?
Medium vessel Most associated with hep B = clear cause or hep C and HIV Affects skin, GI tract, kidneys and heart Renal impairment, strokes and myocardial infarction Usually ANCA negative
43
how does PAN present and how is it treated?
Presentation: GI bleed, bowel infarction, HTN, renal artery aneurysms Livedo reticularis = mottled, purplish, lace like rash Diagnosis: angiogram Treatment: if hep B neg, give CCS and cyclophosphamide If hep b positive: antiviral and CCS
44
what is kawasaki disease?
Medium vessel vasculitis Common in oriental world • Young children <5 years Clinical features: -Persistent high fever >5 days -Erythematous and desquamation of palms and soles -Strawberry tongue (red tongue with prominent papillae)
45
how do you treat kawasaki disease and what is the key complication?
Treatment: symptomatic but IV immunoglobulins are used for severe form Key complication = coronary artery aneurysm
46
what is takayasu's arteritis?
large vessel aorta, pulmonary arteries can swell and form aneurysms or can become narrow and blocked = AKA pulseless disease
47
how does takayasus present and how is it treated?
fever, malaise, muscle aches, claudication or syncope CT, MRI angio or doppler of US carotids treatment: steroids
48
what is polycystic kidney disease
genetic condition where kidneys develop multiple fluid filled cysts two types are autosomal dominant and autosomal recessive
49
how does ADPKD present?
= chromosome 16 or 4 - extra renal: cerebral aneurysms, cysts on liver, spleen, pancreas etc - issues with cardiac valve and colonic diverticula
50
what is the USS diagnostic criteria for ADPKD?
Two cysts, unilateral or bilateral, if aged <30 years 2 cycts in BOTH kidneys if 30-59 4 cysts in both kidneys if aged >60 years - Also, use CT scans to diagnose
51
what are complications of ADPKD?
``` Chronic loin pain Hypertension Cardiovascular disease Gross haematuria if cyst ruptures Renal stones (common in patients with PKD) ESRD at age 50 ```
52
what is ARPKD?
gene on chromosome 6 rarer and more severe presents in childhood/infancy = presents in pregnancy with oligohydraminos as fetus doesn't produce enough urine
53
how else does ARPKD present?
- may require dialysis in first few years of life dysmorphia = ears are low set, flat nasal bridge ESRD before adulthood
54
what does a renal biopsy show for ARPKD?
multiple cylindrical lesions at RA to cortical surface
55
how do you manage polycystic kidney disease?
tolvaptan = vasopressin receptor antagonist slows the development of cysts and progression of RF if CKD stage 2 or 3 - nephrectomy if poor prognosis otherwise supportive: anti-hypertensivem analgesia, AB, drainage of INFECTED cysts
56
what is von hippel lindau disease?
autosomal dominant condiiton on chromosome 3 (encodes TSG protein) presents in 20s or 30s with malignancies in retina, CNS, kidneys renal manifestations: cortical renal cysts, renal cell carcinoma treatable by surgical intervention screening in genotype confirmed patients is annual USS and CT every 3 years (for fam members CT too)
57
what are simple cysts
non genetic cause of cystic disease more common with age Unilocular and located in the cortex Kidneys do not get enlarged by these cysts Over the age of 30 Unlikely that on its own this will cause haematuria or pain
58
what is acquired renal cystic disease?
Patients who have had a long duration of dialysis can develop acquired renal cysts Tend to have shrunken kidneys and a negative family history of cystic diseases

Med Year 3 (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions