Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology (Guide) > Histopathology - Renal Pathology > Flashcards

Histopathology - Renal Pathology Flashcards

1
Q

What two syndromes arise from issues with the glomerulus?

A
  • Neprhotic syndrome
  • Nephritic syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are some primary causes of nephrotic syndrome?

A
  • Minimal change disease
  • Membranous glomerular disease
  • Focal segmental glomerulosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are some secondary causes of nephrotic syndrome?

A
  • DIABETES
  • Amyloidosis
  • SLE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are some causes of nephritic syndrome?

A
  • Acute-post infectious (e.g. Post-streptococcal)
  • IgA Nephropathy (e.g. Berger Disease)
  • Rapidly progressive glomerulonephritis
  • Alport’s Syndrome (e.g. Hereditary nephritis)
  • Thin Basement Membrane Disease (e.g. Benign Familial Haematuria)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are some conditions that affect the tubules and interstitium?

A
  • Acute tubular necrosis
  • Tubulointerstitial nephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are some conditions that affect the renal blood vessels?

A

Thrombotic Microangiopathies
- HUS
- TTP

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

What is the triad of nephrotic syndrome?

A
  • Proteinuria (>3g/24hr) / PCR >300mg/mmol
  • Hypoalbuminaemia
  • Peripheral oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are other characteristic features of nephrotic syndrome?

A
  • Hyperlipidaemia
  • Thrombotic disease (increased cholesterol + clotting tendency)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some key words associated with nephrotic syndromes?

A
  • Swelling (classically periorbital in children)
  • Frothy urine (due to proteinuria)
  • ISSUE WITH PODOCYTES (filtration barrier)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the general management for nephrotic syndromes?

A

Steroids

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

What is the epidemiology, prognosis + general features of minimal change disease?

A

Epi:
- Most common in children
- Second peak in elderly

Features:
- Possible trigger = recent allergic Rx
- A/w: eczema, asthma

Px:
- <5% ESRF

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

What are the investigative findings for minimal change disease?

A

Light microscopy:
- No change

Electron microscopy:
- Loss of podocyte foot processes

Immunofluorescence:
- No immune deposits

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

What is the management and response for minimal change disease?

A
  1. Steroids
  2. Cyclosporin

90% response to steroids

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

What is the epidemiology, prognosis + general features of membranous glomerulonephritis?

A

Epi:
- Common in adults

Features:
- Primary or secondary
- Secondary causes: SLE, Drugs, Malignancy
- Abs against Phospholipase A2 present in 75%

Px:
- 40% ESRF >2-20yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the investigative findings of membranous glomerulonephritis?

A

Light microscopy:
- Diffuse glomerular basement membrane thickening

Electron microscopy:
- Loss of pdocyte food processes
- Subepithelial deposits = spikey

Immunofluorescence:
- Immune complex deposits along entire GBM

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

What is the management and response of management for membranous glomerulonephritis?

A
  • Steroids
  • ACEi/ARB to control BP

Response to steroids = poor

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

What is the epidemiology, prognosis and general features of focal segmental glomerulosclerosis?

A

Epi:
- Common in adults
- Common in Afro-Caribbean people

Features:
- Primary or secondary
- Secondary causes: OBESITY, HIV, drugs (lithium, heroin), lymphoma

Px: 50% ESRF in 10yrs

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

What are the investigative findings of focal segmental glomerulosclerosis?

A

Light Microscopy:
- Focal + segmental glomerular consolidation + scarring
- Hyalinosis

Electron Microscopy:
- Loss of podocyte foot processes

Immunofluorescence:
- No immune deposits

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

What is the management and response to management of focal segmental glomerulosclerosis?

A
  1. Steroids + ACEi/ARB (to control BP)
  2. Calcineurinin inhibitors

50% response to steroids

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

What is seen on renal histology of diabetes?

A
  • Diffuse glomerular basement membrane thickening
  • Mesangial matrix nodules (KIMMELSTIEL WILSON NODULES)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is seen on histology of amyloidosis?

A

Apple green birefringence with Congo red stain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are some key points to nephrotic syndrome in diabetic patients?

A
  • Classically found in Asians
  • First presents with microalbuminaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are some key features of amyloidosis?

A

AA (Acute Phase Protein) Amyloidosis:
- A/w: Chronic inflammation (e.g. RA, TB)

AL (Light Chain) Amyloidosis:
- Most common from multiple myeloma

Clinical Features:
- Maroglossia
- Heart Failure
- Hepatomegaly

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

How is a nephrotic syndrome diagnosed?

A

Urine Dip:
- Proteinuria
- NO haematuria

Urine PCR:
- >300mg/mmol

Serum Albumin:
- Low

Total cholesterol:
- High

Immunoglobulins:
- Low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the diagnostic investigation of choice in an adult with nephrotic syndrome?

A

Renal biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is nephritic syndrome?

A

A manifestation of glomerular inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the triad for nephritic syndrome?

A
  • Hypertension
  • Haematuria
  • Peripheral oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the characteristic features of nephritic syndrome?

A

PHAROH
- P: Proteinuria (less than nephrotic)
- H: Haematuria (coke-coloured urine)
- A: Azootemia (high urea + creatinine)
- R: Red Cell Casts (in urine)
- O: Oliguria
- H: Hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are general features of post-streptococcal glomerulonephritis and what is its cause?

A
  • 1-3wks post-streptococcal throat infection/impetigo
  • Usual cause = Strep. pyogenes (Group A strep)

Glomerular damage due to immune complex deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What clinical features are seen for post-streptococcal glomerulonephritis?

A
  • Haematuria (red cell casts)
  • Proteinuria
  • Oedema
  • HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the investigative findings for post-streptococcal glomerulonephritis?

A

Bloods:
- Increased ASOT Titre
- Decreased C3

Biopsy:
- Light microscope = Increased cellularity of glomeruli
- Fluorescence = Granular deposits of IgG + C3 in GBM
- Electron microscope = Subendothelial humps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the management for post-streptococcal glomerulonephritis?

A
  • Supportive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the general features of IgA nephropathy, and what is it?

A
  • Commonest GN worldwide
  • More common in East/South asian populations
  • Presents 1-2 days after URTI
  • Presents with frank haematuria
  • Can progress to ESRF

Deposition of IgA immune complexes in glomeruli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the clinical features of IgA nephropathy?

A
  • Persistent/recurrent frank haematuria
  • Asymptomatic microscopic haematuria
  • Other Sx of nephritic syndrome not seen
  • Can present with vasculitic rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the investigative findings of IgA nephropathy?

A

Bloods:
- Increased IgA

Biopsy:
- Immunofluorescence = granular deposition of IgA + C3 in mesangium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the rule of thirds associated with IgA nephropathy?

A
  • 1/3 = asymptomatic
  • 1/3 = develop CKD
  • 1/3 = develop progressive CKD requiring dialysis/transplantation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the most aggressive form of glomerulonephritis?

A

Rapidly progressive (crescenteric) GN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are some general + clinical features of rapidly progressive glomerulonephritis?

A
  • Can cause ESRF in weeks
  • Regardless of cause, all types characterised by presence of crescents in glomeruli
  • Classification based on immunological findings

Presentation:
- Nephritic syndrome
- Oliguria + renal failure more pronounced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are crescents?

A

Proliferation of macrophages + parietal cells in Bowman’s space which pushes glomerulus to one side

40
Q

What are the different types of rapidly progressive glomerulonephritis?

A
  • Type1 = Anti-GBM antibody (Goodpastures Syndrome)
  • Type 2 = Immune complex mediated
  • Type 3 = Pauci-immune/ANCA-associated
41
Q

What is the pathogenesis and some causes of type 1 rapidly progressive glomerulonephritis + which other organs are involved

A

Path:
- Anti-GBM antibody (against collagen Type IV)

Causes:
- Goodpasture’s syndrome
- HLA-DRB1 association

Organ involvement:
- Lungs = pulmonary haemorrhages

42
Q

What is seen on microscopy of type 1 rapidly progressive glomerulonephritis?

A

Light:
- Crescents

Fluorescence:
- Linear deposition of IgG in GBM

43
Q

What is the pathogenesis and some causes of type 2 rapidly progressive glomerulonephritis + which other organs are involved

A

Path:
- Immune complex mediated

Causes:
- SLE
- IgA nephropathy
- Post-infectious GN
- HSP
- Alport’s syndrome

Organ involvement:
- Often limited (except in SLE)

44
Q

What is seen on microscopy of type 2 rapidly progressive glomerulonephritis?

A

Light:
- Crescents

Fluorescence:
- Granular (lumpy bumpy)
- IgG immune complex deposition on GBM/mesangium

45
Q

What is the pathogenesis and some causes of type 3 rapidly progressive glomerulonephritis + which other organs are involved

A

Path:
- Pauci-immune (e.g. lack of anti-GBM/immune complex)

Causes:
- c-ANCA = Wegener’s granulomatosis
- p-ANCA = Microscopic polyangitis

Organ involvement:
- Vasculitis (skin rashes + pulmonary haemorrhages)

46
Q

What is seen on microscopy of type 3 rapidly progressive glomerulonephritis?

A

Light:
- Crescents

Fluorescence:
- Lack of/scanty immune complex deposition

47
Q

What are some features of hereditary nephritis (Alport’s Syndrome)?

A
  • Hereditary glomerular disease caused by mutation in Type IV collagen α 5 chain
  • X-LINKED
  • Nephritic syndrome + bilateral sensorineural deafness + eye disorders (lens dislocation + cataracts)
  • Presents at 5-20yrs with nephritic syndrome progressing to ESRF
48
Q

What are some features of thin basement membrane disease (benign familial haematuria)?

A
  • Rarely causes nephritic syndrome (usually asymptomatic haematuria)
  • Diffuse thinning of GBM caused by mutation in Type IV collagen α 4 chain
  • AUTOSOMAL DOMINANT
  • Prevalence = ~5%
  • Incidental Dx with microscopic haematuria
  • Excellent prognosis
49
Q

What are three differentials for asymtomatic haematuria?

A
  • Thin Basement Membrane Disease (Benign Familial Haematuria)
  • IgA Nephropathy (Berger Disease)
  • Alport Syndrome
50
Q

What are some clinical differences between IgA Nephropathy + Benign Familial Haematuria?

A
  • IgA = more common in asian population
  • IgA = frank haematuria
  • IgA = Change in renal function Cr raised
51
Q

What is acute tubular injury (acute tubular necrosis)?

A
  • Damage to tubular epithelial cells leads to cells being shed + blocking tubules as casts
  • Causes reduced flow + increased haemodynamic pressure in nephron
  • Leasd to reduced pressure gradient across BM, causing acute renal failure
  • Tubular glomerular feedback reduces blood supply to kidney further as a result of AKI
52
Q

What is the most common cause of acute renal failure?

A

Acute tubular necrosis

53
Q

What are the causes of acute tubular necrosis and how do they work?

A

Hypovolaemia
- Causes pre-renal ARF leading to ischaemia of nephrons

Nephrotoxins:
- Drugs (Aminoglycosides (gentamicin), NSAIDS)
- Radiographic contrast agents
- Myoglobin (secondary to rhabdomyolysis)
- Heavy metals

54
Q

What is seen on histology for acute tubular necrosis?

A

Necrosis of short segments of tubules

55
Q

What is seen on microscopy of urine for acute tubular necrosis?

A

Muddy brown casts

56
Q

What is tubulointerstitial nephritis?

A

A group of renal inflammatory disorders that involve the tubules + interstitium

57
Q

What are the different conditions that cause tubulointerstitial nephritis?

A
  • Acute pyelonephritis
  • Chronic pyelonephritis + reflux nephropathy
  • Acute interstitial nephritis
  • Chronic interstitial nephritis / Analgesic nephropathy
58
Q

What is acute pyelonephritis, its causes, how it presents and what is seen on urineanalysis?

A
  • Bacterial infection of the kidney, usually a result of an ascending infection
  • Common cause = E. coli

Presentation:
- Fever
- Chills
- Sweats
- Flank pain
- Renal angle tenderness
- Leukocytosis
+/- Frequency, dysuria + haematuria

Urine:
- Leukocytic casts

59
Q

What is chronic pyelonephritis + reflux nephropathy and its causes?

A
  • Chronic inflammation + scarring of parenchyma caused by recurrent + persistent bacterial infection

Causes:
- Chronic obstruction (posterior urethral valves, renal calculi)
- Urine reflux (= reflux nephropathy)

60
Q

What is acute interstitial nephritis, its causes how it presents and its histological findings?

A
  • A hypersensitivity reaction
  • Causes: usually drugs (Penicillins, NSAIDs, diuretics) (presents days after drug exposure)

Presents:
- Fever
- Skin rash
- Haematuria
- Proteinuria
- Eosinophilia
- Urine = white cell casts = sterile pyuria

Histo:
- Inflammatory infiltrate with tubular injury, eosinophils + granulomas

61
Q

What are the features and symptoms of chronic interstitial nephritis/analgesic nephropathy?

A
  • Seen in elderly with long-term analgesic consumption (NSAIDs + Paracetamol)

Sx (only in late disease):
- HTN
- Anaemia
- Proteinuria
- Haematuria

62
Q

What are two types of thrombotic microangiopathies that affect the kidneys?

A
  • HUS
  • TTP
63
Q

What is the epidemiology and characteristics of HUS?

A
  • CHILDREN

Triad:
- MAHA
- Thrombocytopenia
- (progressive) renal failure

64
Q

What is the epidemiology + characteristics of TTP?

A
  • ADULTS

PENTAD:
- MAHA
- Thrombocytopenia
- Renal failure
- Fever
- Neurological Sx (LOC, decreased vision)

65
Q

What is the pathophysiology of HUS?

A
  • THROMBI CONFINED TO KIDNEYS
  1. A/w: E. coli O157:H7 = Gastroenteritis cause
  2. Endothelial damage
  3. Thrombosis, platelet consumption + fibrin strand deposition (leads to low plts)
  4. Destruction of RBCs (leads to schistocytes + low Hb)
66
Q

What is the pathophysiology of TTP?

A
  • Genetic/acquired deficiency of ADAMTS13
  • THROMBI OCCUR THROUGHOUT CIRCULATION (esp. in CNS)
67
Q

What is ADAMTS13 MoA?

A
  • Usually cleaves vWF (protease)
  • Deficiency leads to formation of giant vWF multimers
  • Causes platelet aggregation + fibrin deposition
68
Q

What are the signs and symptoms of a thromboti microangiopathy (HUS + TTP)?

A
  • Low plts = bleeding (petechiae, haematemesis, melena)
  • MAHA = pallor + jaundice
69
Q

What does HUS usually involve?

A

Renal failure

70
Q

How are thrombotic microangiopathies (HUS + TTP) diagnosed?

A
  • Low Hb + plts
  • Signs of haemolysis = increased bilirubin + reticulocytes + LDH
  • Fragmented RBCs (SCHISTOCYTES) on blood smear (RBCs sheared as they pass through clots)
  • Negative Coomb’s test
71
Q

What is acute renal failure and what sign is observed as a result?

A
  • Acute decline in renal function
  • Low urine output
  • Rapid loss of renal function
  • Manifests as increased serum Cr + Urea
72
Q

What are the complications of acute renal failure?

A
  • Metabolic acidosis
  • Hyperkalaemia
  • Fluid overload
  • HTN
  • Low Ca
  • Uraemia
73
Q

What are the three different types of acute renal failure?

A
  • Pre-renal
  • Renal
  • Post-renal
74
Q

What is the most common cause of acute renal failure?

A

Pre-renal

75
Q

What is pre-renal acute renal failure and its causes?

A
  • Decrease in flow to kidneys

Causes:
- Renal Hypo-perfusion (hypovolaemia, sepsis, renal artery stenosis, ACEi, CCF, burns, acute pancreatitis)

76
Q

What are renal causes of acute renal failure and how do they cause renal failure?

A
  • Direct damage to nephrons
  • Acute tubular necrosis
  • Acute glomerulonephritis
  • Thrombotic microangiopathy
77
Q

What is the second most common cause of AKI?

A

Post-renal causes of acute renal failure

78
Q

How do post-renal causes of acute renal failure work, and what are they?

A
  • Physical blockade to outflow
  • Obstruction of urine flow

Causes:
- Stones
- Tumours
- Prostate causes (hypertrophy)
- Retroperitoneal fibrosis

79
Q

What is chronic renal failure and what is it due to?

A
  • Progressive, irreversible loss of renal function
  • Characterised by prolonged Sx of uraemia (fatigue, itching, anorexia, confusion)
  • Due to progressive damage
80
Q

What are the commonest causes of chronic renal failure in the UK?

A
  • Diabetes (20%)
  • Glomerulonephritis (15%)
  • HTN + Vascular Disease (15%)
  • Reflux nephropathy (chronic pyelonephritis) (10%)
  • PCKD (9%)
  • Obstruction
  • ATN
81
Q

How is chronic renal failure measured + staged?

A

By using GFR

82
Q

What are the different stages of chronic renal failure and the GFR ranges for each stage?

A
  1. Kidney damage with normal renal function = >90
  2. Mildly impaired = 60-98
  3. Moderately impaired = 30-59
    - A = 45-49
    - B = 30-44
  4. Severely impaired = 15-29
  5. Renal failure = <15
83
Q

What is adult polycystic kidney disease?

A

A part of a heterogenous group of disorders characterised by renal cysts + numeroud systemic extra-renal manifestations

84
Q

What is the inheritance of polycystic kidney disease?

A

AUTOSOMAL DOMINANT
- 85% = PKD1 mutations (Chr 16 - encodes polycystin-1)
- 15% = PKD2 mutations (Chr 4 - encode polycystin-2)

85
Q

What are the pathological features of polycystic kidney disease?

A
  • Large multicystic kidneys with destroyed renal parenchyma, liver cysts (PKD1) + BERRY ANEURYSMS (leads to SAH + HTN)
86
Q

What are the clinical features of polycystic kidney disease?

A

MISHAPES:
- M: abdmominal Mass
- I: Infected cysts + Increased BP
- S: Stones
- H: Haematuria
- A: Aneurysms (berry)
- P: Polyuria + nocturia
- E: Extra-renal cysts
- S: Systolic murmur (mitral valve prolapse)

87
Q

How is PCKD diagnosed and what is the diagnostic criteria?

A

Via USS of kidneys
- 15-39yrs = 3+ cysts
- 40-59yrs = >2 cysts in each kidney
- >60yrs = 4 cysts in each ovary

88
Q

What is the mainstay of Tx for PCKD?

A

RRT (renal replacement therapy)

89
Q

What is lupus nephritis?

A

Kidney damage relating to lupus

90
Q

What is seen on histology of lupus nephritis?

A
  • Immune complex deposition in capillaries = WIRE LOOP CAPILLARIES
  • Deposition of immune complexes + complement in GBM (LUMPY, BUMPY GRANULAR FASHION)
91
Q

What are the six classes of lupus nephritis?

A
  1. Minimal meangial disease (near normal on light microscopy)
  2. Mesangial proliferative disease
  3. Focal subendothelial deposits
  4. Diffuse subendothelial deposits
  5. Subepithelial immune deposits (membranous disease)
  6. Advanced sclerosis (>90%)
92
Q

What are the types of renal cell carcinoma?

A
  • Clear cell carcinoma (well differentiated)
  • Papillary carcinoma (Commonest in dialysis-associated cystic disease)
  • Chromophobe renal carcinoma (pale, eosinophilic cells)
93
Q

What are the RFs for developing a renal cell carcinoma?

A
  • Smoking
  • Obesity
  • HTN
  • Unopposed oestrogen
  • Heavy metals
  • CKD
94
Q

What are the clinical features of a patient with a renal cell carcinoma?

A
  • Costovertebral pain
  • Palpable mass
  • Haematuria
95
Q

What is paraneoplastic syndrome?

A
  • Polycythaemia
  • Hypercalcaemia
  • HTN
  • Cushing’s syndrome
  • amyloidosis
96
Q

What is seen on a kidney biopdy of a patient with multiple myeloma?

A

Amyloid deposition

Pathology (Guide) (84 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions