Brainscape's Knowledge GenomeTM

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


See full index

Renal > Clinical > Flashcards

Clinical Flashcards

1
Q

definition of chronic kidney failure?

A

reduced GFR and/or evidence of kidney damage

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

definition of chronic kidney failure?

A

reduced GFR and/or evidence of kidney damage

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

what creatinine a product of?

A

muscle breakdown

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

stage 1 CKD?

A

GFR>90ml/min with evidence of kidney disease

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

stage 2 CKD?

A

GFR 60-90ml/min, with evidence of kidney damage

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

what things count as evidence of kidney damage?

A
  • proteinuria
  • haematuria
  • abnormal imaging
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

stage 3A CKD?

A

GFR- 45-60ml/min

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

stage 3B CKD?

A

GFR- 30-44ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

stage 4 CKD?

A

GFR- 15-30 ml/min

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

stage 5 CKD?

A

GFR

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

what association does proteinuria have on progression of CKD?

A

more proteinuria - faster progression

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

what are the common causes of CKD? (7)

A
  • diabetes
  • hypertension
  • vascular disease
  • chronic glomerulonephritis
  • reflux nephropathy
  • polycystic kidneys
  • unknown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

commonest cause of established renal failure?

A

diabetes

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

when do symptoms due to reduced GFR occur?

A

late. GFR

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

how can CKD cause anaemia?

A

erythropoiten is produced in the kidney and production declines in CKD

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

what does erythropoiten do?

A

stimulates bone marrow to produce red blood cells

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

if patient is still anaemic after IV iron, what can you give them?

A

regular erythropoiten (Epo) injections

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

how often are Epo injections given?

A

every week or fortnight

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

what is the target Hb when giving treatment for anaemia?

A

105-125 g/l

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

how can CKD lead to bone disease?

A
  • vit D hydroxylated in kidney, reduced in CKD

- leads to reduced calcium absorption, leading to secondary hyperparathyroidism

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

what happens to phosphate levels in advanced CKD?

A

increased serum phosphate

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

biochemistry of bone disease in severe CKD?

A

high phosphate and high calcium

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

what affect dose high calcium and phosphate have on vessels?

A

vascular calcification

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

management of bone disease in CKD?

A
  • alfacalcidol
  • phosphate
  • phosphate binders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is alfacalcidol?

A

hydroxylated vit D - doesnt need activation by kidneys

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

what is a patients GFR when they are given patient education on dialysis?

A

about 20ml/min

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

how long after the procedure can a arteriovenous fistula be used?

A

needs 6 weeks to mature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

when are patients referred to the vascular surgeons for arteriovenous fistula?

A

when GFR is about 15ml/min

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

when can patients be listed for cadaveric transplantation?

A

when they are within 6 months of requiring dialysis

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

functions of the kidneys? (8)

A
  • excretion of nitrogenous waste
  • fluid balance
  • electrolyte balance
  • acid-base balance
  • vit D metabolism/phosphate excretion
  • production of erythropoiten
  • drug excretion
  • barrier to loss of proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what can a build up of urea in the blood lead to?

A

pericarditis, encepalopathy, neuropathy, gastritis

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

what affect do NSAIDS have on the kidney?

A

can cause an allergic reaction within kidney and they also reduce GFR

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

what antibiotics should you ask about in a drug history for a renal history?

A

gentamicin, trimethoprim, penicillins

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

what investigation can lead to acute kidney injury?

A

radiology contrast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what GI drug can damage the kidneys?

A

PPI

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

what must diastolic BP be above to classify as accelerated hypertension?

A

120 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what can be seen in the eyes in accerlerated hypertension?

A

papilloedema

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

what is the usual distribution of Henoch-Schonlein Purpura?

A

often on extensor surfaces and on the buttocks

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

what mediates Henoch-Schonlein purpura ?

A

IgA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is present in urine when it is a smoky brown colour?

A

myoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

how does myoglobin end up in the urine?

A

breakdown of muscle causing a release of myoglobin which is deposited in kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what does it suggest if there is isomorphic RBCs present in urine?

A

the blood is coming from lower down the renal tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what does it suggest if there is dysmorphic red blood cells in urine?

A

that they are coming from upper renal tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is acute kidney injury defined as?

A

decline in GFR over hours/days/weeks with or without oliguria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

definition of oliguria?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what 3 things defines nephrotic syndrome?

A
  • proteinuria > 3g/day
  • hypoalbuminaemia
  • oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is nephrotic syndrome often associated with?

A

hypercholesterolaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what is the renal function often like in nephrotic syndrome?

A

often normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

where do patients get oedema in nephrotic syndrome?

A

periorbital oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

do patients with nephrotic syndrome get pulmonary odema?

A

no but can get pleural effusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

signs in nephritic syndrome?

A
  • acute kidney injury
  • oliguria
  • oedema/fluid retention
  • hypertension
  • active urinary sediment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what creatinine a product of?

A

muscle breakdown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

stage 1 CKD?

A

GFR>90ml/min with evidence of kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

stage 2 CKD?

A

GFR 60-90ml/min, with evidence of kidney damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what things count as evidence of kidney damage?

A
  • proteinuria
  • haematuria
  • abnormal imaging
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

stage 3A CKD?

A

GFR- 45-60ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

stage 3B CKD?

A

GFR- 30-44ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

stage 4 CKD?

A

GFR- 15-30 ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

stage 5 CKD?

A

GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what association does proteinuria have on progression of CKD?

A

more proteinuria - faster progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what are the common causes of CKD? (7)

A
  • diabetes
  • hypertension
  • vascular disease
  • chronic glomerulonephritis
  • reflux nephropathy
  • polycystic kidneys
  • unknown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

commonest cause of established renal failure?

A

diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

when do symptoms due to reduced GFR occur?

A

late. GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

how can CKD cause anaemia?

A

erythropoiten is produced in the kidney and production declines in CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what does erythropoiten do?

A

stimulates bone marrow to produce red blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

if patient is still anaemic after IV iron, what can you give them?

A

regular erythropoiten (Epo) injections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

how often are Epo injections given?

A

every week or fortnight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what is the target Hb when giving treatment for anaemia?

A

105-125 g/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

how can CKD lead to bone disease?

A
  • vit D hydroxylated in kidney, reduced in CKD

- leads to reduced calcium absorption, leading to secondary hyperparathyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what happens to phosphate levels in advanced CKD?

A

increased serum phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

biochemistry of bone disease in severe CKD?

A

high phosphate and high calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what affect dose high calcium and phosphate have on vessels?

A

vascular calcification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

management of bone disease in CKD?

A
  • alfacalcidol
  • phosphate
  • phosphate binders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

what is alfacalcidol?

A

hydroxylated vit D - doesnt need activation by kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

what is a patients GFR when they are given patient education on dialysis?

A

about 20ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

how long after the procedure can a arteriovenous fistula be used?

A

needs 6 weeks to mature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

when are patients referred to the vascular surgeons for arteriovenous fistula?

A

when GFR is about 15ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

when can patients be listed for cadaveric transplantation?

A

when they are within 6 months of requiring dialysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

functions of the kidneys? (8)

A
  • excretion of nitrogenous waste
  • fluid balance
  • electrolyte balance
  • acid-base balance
  • vit D metabolism/phosphate excretion
  • production of erythropoiten
  • drug excretion
  • barrier to loss of proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

what can a build up of urea in the blood lead to?

A

pericarditis, encepalopathy, neuropathy, gastritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what affect do NSAIDS have on the kidney?

A

can cause an allergic reaction within kidney and they also reduce GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

what antibiotics should you ask about in a drug history for a renal history?

A

gentamicin, trimethoprim, penicillins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

what investigation can lead to acute kidney injury?

A

radiology contrast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

what GI drug can damage the kidneys?

A

PPI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

what must diastolic BP be above to classify as accelerated hypertension?

A

120 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

what can be seen in the eyes in accerlerated hypertension?

A

papilloedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

what is the usual distribution of Henoch-Schonlein Purpura?

A

often on extensor surfaces and on the buttocks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what mediates Henoch-Schonlein purpura ?

A

IgA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

what is present in urine when it is a smoky brown colour?

A

myoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

how does myoglobin end up in the urine?

A

breakdown of muscle causing a release of myoglobin which is deposited in kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

what does it suggest if there is isomorphic RBCs present in urine?

A

the blood is coming from lower down the renal tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

what does it suggest if there is dysmorphic red blood cells in urine?

A

that they are coming from upper renal tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

what is acute kidney injury defined as?

A

decline in GFR over hours/days/weeks with or without oliguria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

definition of oliguria?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

what 3 things defines nephrotic syndrome?

A
  • proteinuria > 3g/day
  • hypoalbuminaemia
  • oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

what is nephrotic syndrome often associated with?

A

hypercholesterolaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

what is the renal function often like in nephrotic syndrome?

A

often normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

where do patients get oedema in nephrotic syndrome?

A

periorbital oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

do patients with nephrotic syndrome get pulmonary odema?

A

no but can get pleural effusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

signs in nephritic syndrome?

A
  • acute kidney injury
  • oliguria
  • oedema/fluid retention
  • hypertension
  • active urinary sediment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

definition of acute kidney injury?

A

an abrupt (26.4 umol/l

  • OR increase in creatinine by >50%
  • OR a reduction in urine output
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

3 main pre-renal causes of AKI?

A
  • hypovolaemia
  • hypotension
  • renal hypoperfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

what drugs can cause renal hypoperfusion?

A
  • NSAIDS/COX-2

- ACEi/ARBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

what is oliguria defined as?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

when should ACEi be stopped?

A

if patient is vomitting/diarrhoea as this can lead to severe dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

how can ACEi cause a reduction in GFR?

A

angiotensin II mediates arteriolar vasoconstriction therefore increasing GFR. ACEi block angiotensin II so can cause a fall in GFR by causing efferent arteriole vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

what does untreated pre-renal AKI lead to?

A

acute tubular necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

what is the commonest form of AKI in hospital?

A

acute tubular necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

common causes for acute tubular necrosis?

A

sepsis and severe dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

causes of vascular renal AKI?

A

vasculitits, renovascular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

what can happen at thr glomerular that causes AKI?

A

glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

what things can cause interstitial nephritis?

A
  • drugs
  • infection eg TB
  • systemic eg Sarcoid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

what is tubular injury due to ischaemia due to?

A

prolonged renal hypoperfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

what drugs are nephrotoxic and can cause acute tubular necrosis?

A
  • antibiotics eg gentamincin, penicillin
  • NSAIDS
  • occasionally PPIs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

what scan can cause acute tubular injury in AKI?

A

CT contrast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

what condition associated with myoglobin being present in urine causes tubular injury?

A

rhabdomyolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

symptoms of AKI?

A
  • non specific symptoms
  • nausea and vomitting
  • itch
  • oedema, SOB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

signs of AKI?

A
  • fluid overload- oedema, effusions
  • uraemia
  • oliguria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

what would eosinophilia in AKI make you think of?

A

interstitial nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

if CK is high in AKI, what would you be thinking of?

A

rhabdomyolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

initial investigations in AKI?

A
  • U&Es
  • FBC and coag screen
  • Urinalysis
  • USS
  • Immunology
  • Protein electrophoresis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

what small kidneys on US suggest?

A

CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

what else do you look for on US?

A

obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

what would abnormal clotting suggest in AKI?

A

?sepsis

? disseminated intravascular coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

what could anaemia suggest in AKI?

A
  • CKD

- ?myeloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

what would you look for in immunology in AKI?

A
  • ANA (SLE)
  • ANCA (vasculitits)
  • GBM (Goodpastures)
127
Q

what is protein electrophoresis and bens-jones protein used to look for?

A

myeloma

128
Q

who should receive a myeloma screen in AKI?

A

everyone over 50

129
Q

what is a renal biopsy send to the lab for?

A
  • light microscopy
  • electron microscopy
  • immunofluorescence
130
Q

how can trimethoprim cause AKI?

A

causes a rise in creatinine and potassium

131
Q

what is post renal AKI due to?

A

obstruction of urine flow leading to back pressure (hydronephrosis) and thus loss of concentrating ability

132
Q

causes of obstruction?

A
  • calculi
  • tumours
  • strictures
  • extrinsic pressure
133
Q

what is the normal range of potassium?

A

3.5-5.0

134
Q

what is hyperkalaemia classed as?

A

K> 5.5

135
Q

what is life threatening hyperkalaemia classed as?

A

K> 6.5

136
Q

if potassium is 6-7, what will the ECG look like?

A

peaked T waves

137
Q

what happens as potassium goes up on the ECG?

A
  • peaked T waves

- flattened P wave, prolonged PR interval, depressed ST segment, widened QRS etc

138
Q

what should be given initially in acute hyperkalaemia?

A

10mls 10% calcium gluconate (over 2-3mins)

139
Q

why should calcium gluconate be given immediately in acute hyperkalaemia?

A

it stabilised and protects the myocardium and reduced risk of arrythmias. does not lower potassium

140
Q

what should be given after calcium gluconate to lower the potassium levels?

A

insulin (actrapid 10 units) with 50mls 50% dextrose

141
Q

what does calcium resonium do?

A

prevents reabsorption of potassium in the GI tract

142
Q

what are the urgent indications for dialysis in AKI?

A
  • hyperkalaemia (>7)

- severe acidosis (pH40, pericardial rub/effusion

143
Q

40 year old male presenting with general malaise and haemoptysis. urea 28, creatinine 600, eleveated ant-GBM?

A

Goodpastures syndrome

144
Q

25 year old IVDU found collapsed at home? high creatinine, urea and CK?

A

Rhabdomyolosis

145
Q

82 year old man admitted with hypotension, tachycardia, potassium high, urea high, CRP 250, CXR shows left basal consolidation?

A

Acute tubular necrosis

146
Q

does furosemide cause hyperkalaemia?

A

no it is potassium sparing

147
Q

risk factors for developing AKI?

A

age, diabetes, CKD, co-morbidity eg liver failure, heart failure etc

148
Q

what is the most common cause of end stage renal failure?

A

diabetic nephropathy

149
Q

what is the 2nd most common cause for end stage renal disease?

A

chronic glomerulonephritis

150
Q

what is glomerulonephritis?

A

immune-mediated disease of the kidneys affecting the glomeruli (with secondary tubulointerstital damage)

151
Q

how can the humoral response cause GN?

A
  • antibody-mediated
  • antigen intrinsic to the glomeruli or a planted antigen from circulation gets stuck in glomeruli causing antibody response and deposition of circulating immune complexes
152
Q

what type of immune cell can cause GN?

A

T cells

153
Q

what is the capillary lumen of the glomerulus lined by?

A

endothelium

154
Q

what layer of the glomerulus capillary is the podocytes on?

A

epithelial layer

155
Q

what separates the endothelial layer and the epithelial layer of glomerulus capillary?

A

the thick basement membrane

156
Q

what is Bowmans space between?

A

the visceral and parietal epithelium

157
Q

what does GN do to the glomerular capillary wall?

A

disruption of barrier leads to haematuria and/or proteinuria

158
Q

what does damage to endothelial or mesangial cells lead to?

A

a proliferative lesion and red cells in urine

159
Q

what does damage to podocytes lead to?

A

non-proliferative lesion and protein in urine

160
Q

what classes as microalbuminuria?

A

30-300mg albuminuria/day

161
Q

what classes as asymptomatic proteinuria?

A
162
Q

what classes as heavy proteinuria?

A

1-3 g/day

163
Q

how much protein must be in urine to be nephrotic syndrome?

A

> 3 g/day

164
Q

what is the criteria for nephritic syndrome?

A
  • acute renal failure
  • oliguria
  • odema/fluid retention
  • hypertension
  • active urinary sediment
165
Q

what type of process is occuring in nephritic syndrome?

A

a proliferative process

166
Q

what type of process is occuring in nephrotic syndrome?

A

non proliferative process

167
Q

where is the site on damage in nephrotic syndrome?

A

podocytes on epithelial layer

168
Q

complications of nephrotic syndrome?

A
  • infections
  • renal vein thrombosis
  • PE
  • volume depletion
  • vit D defiency
  • subclinical hypothyriodism
169
Q

why is there an increased of infection in nephrotic syndrome?

A

there is a loss of opsoning antibodies from circulation (due to loss of fluid from ICF)

170
Q

what causes volume depletion in nephrotic syndrome?

A

overaggressive use of diuretics

171
Q

what causes the majority of GN?

A

primary - idiopathic

172
Q

secondary causes of GN?

A
  • infections or drugs

- associated with malignancy or part of systemic diease eg ANCA-associated vasculitis, SLE, Goodpastures,HSP

173
Q

what investigations are done in suspected GN?

A
  • renal biopsy

- light microscopy, immunofluoresence, electromicroscopy

174
Q

what is meant by focal GN?

A
175
Q

what is meant by diffuse GN?

A

more than 50% of glomeruli affected

176
Q

what is meant by global GN?

A

all of glomerulus affected

177
Q

what is meant by segmenal GN?

A

part of glomerulus affected

178
Q

what causes crescent in the GN?

A

epithelial cell extracapillary proliferation

179
Q

2 routes of treatment options for GN?

A
  • non-immunosuppressive

- immunosuppressive

180
Q

what is the non-immunosuppressive treatment for GN?

A
  • anti-hypertensives
  • statins
  • ?anticoagulants
  • ?omega 3 fatty acids/fish oil
181
Q

what is used as antihypertensives in GN?

A
  • ACEi/ARBs

- diuretics

182
Q

when should anticoagulants be used in GN?

A

if patient is profoundly hypoalbuminaemic

183
Q

when would you use LMWH in GN?

A

if albumin is less than 20

184
Q

immunosuppression drugs that can be used in GN?

A
  • corticosteroids
  • azathioprine
  • alkylating agents
  • calcineurin inhibitors
  • mycophenolate mofetil
185
Q

examplesof corticosteroids used in GN?

A
  • prednisolone PO

- MethylPred IV

186
Q

what is azathioprine?

A

an old anti-prolferative agent

187
Q

examples of alkylating agents used in GN?

A
  • cyclophosphamide

- chlorambucil

188
Q

examples of calcineurin inhibitors in GN?

A

cyclosporin and tacrolimus

189
Q

when is plasmapharesis used in GN?

A

in situations where there is a high volume of antibody

190
Q

what antibody based treatments are there for GN?

A
  • IV immunoglobulin

- monoclonal T or B cell antibodies

191
Q

general treatment of nephrotic patients?

A
  • fluid restriction
  • salt restriction
  • diuretics
  • ACEi/ARBs
  • ?anticoagulation
192
Q

when would you give IV albumin in a nephrotic patient?

A

only if they are volume depleted

193
Q

definite treatment of the nephrotic patient?

A

immunosuppression

194
Q

what is complete remission of nephrotic syndrome classed as?

A

proteinuria

195
Q

what is partial remission of nephrotic syndrome classed as?

A

proteinuria

196
Q

what are the 5 main types of primary/idiopathic GN?

A
  • minimal change
  • focal segmental glomerulosclerosis (FSGS)
  • membranous GN
  • membranoproliferative GN
  • IgA nephropathy
197
Q

what is the commonest cause of GN in children?

A

minimal change nephropathy

198
Q

what does minimal change nephropathy look like on LM, IF and EM?

A

normal renal biopsy on LM and IF with foot process fusion on EM

199
Q

what percent of patients go into complete remission with oral steroids in minimal change nephopathy?

A

94%

200
Q

what is a second line drug for minimal change nephropathy?

A

cyclophosphamide/CSA

201
Q

what has been identified as a possibly cause of minimal change nephropathy?

A

IL-13

202
Q

does minimal change nephropathy cause progressive renal failure?

A

no

203
Q

what is the commonest cause of nephrotic syndrome in adults?

A

focal segmental glomerulosclerosis

204
Q

what can focal segmental glomerulosclerosis be secondary to?

A
  • HIV
  • Heroin use
  • Obesity
  • Reflux nephropathy
205
Q

appearance of focal segmental glomerulosclerosis on immunofluresence?

A

minimal Ig and complement deposition

206
Q

what percentage of patients with focal segmental glomerulosclerosis go into remission with prolonged steroids?

A

60%

207
Q

what do 50% of patients focal segmental glomerulosclerosis progress to?

A

end stage renal failure after 10 years

208
Q

what do 67% of patients with focal segmental glomerulosclerosis have increased levels of?

A

soluble urokinase plasminogen activator receptor (suPAR)

209
Q

what is the second most common cause of nephrotic syndrome in adults worldwide?

A

membranous nephropathy

210
Q

what are the important secondary causes of membranous nephropathy?

A
  • infections
  • connective tissue diease
  • malignancies
  • drugs
211
Q

what infections can cause membranous nephropathy?

A

hep B, parasites

212
Q

what drugs can can membranous nephropathy?

A

gold/penicillamine

213
Q

treatment options for membranous nephropathy?

A
  • steroids
  • alkylating agents
  • B cell monoclonal Ab
214
Q

what % of patients with membranous nephropathy progress to end stage renal failure in 10 years?

A

30%

215
Q

in other 65s, what % of patients with membranous nephropathy have an underlying malignancy?

A

25%

216
Q

what has been identified as the case of primary membranous nephropathy in about 70% of cases?

A

Anti PLA2r antibody

217
Q

where is Anti PLA2r antibody deposited in membranous nephropathy?

A

between glomerular BM and podocytes

218
Q

what is the commonest GN in the world?

A

IgA nephropathy

219
Q

what does a renal biopsy show in IgA nephropathy?

A

mesangial cell proliferation and expansion on light microscopy with IgA deposits in mesangium on immunofluoresence

220
Q

when is macroscopic haematuria usually present in IgA nephropathy?

A

after resp/GI infection

221
Q

what other systemic feature is IgA nephropathy assocaited with?

A

Henoch-Schonlein Purpura (HSP)

222
Q

what type of rash is Henoch-Schonlein Purpura ?

A

purpuric, non-blaunching rash

223
Q

managment of IgA nephropathy?

A

BP control with ACEi and ARBS. Fish oil

224
Q

what ANCA -positive causes are there for rapidly progressive GN?

A

GPA

MPA

225
Q

what ANCA-negative causes are there for rapidly progressive GN?

A
  • Goodpastures
  • Henoch scholein purpura/IgA
  • SLE
226
Q

how can a crescent lead to necrotic glomerulus?

A
  • glomerulus becomes compressed and ischemic then necrotic
227
Q

what are the anti-GBM antibodies acting against in Goodpastures diseae?

A

the BM of glomeruli and BM of alveoli

228
Q

treatment for rapidly progressive GN?

A
  • treatment should be prompt

- strong immunosuppression with supportive care including dialysis if needed

229
Q

what is overt diabetic nephropathy is chaacterized by?

A

persistent albuminuria ie 300mg/24h on at least 2 occasions spearated by 3-6 months

230
Q

what affect does diabetic nephropathy have on the afferent arteriole?

A

it causes vasodilation

231
Q

what does dilation of the afferent arteriole in diabetic nephropathy cause?

A

hyperfilatration at the glomeruli, increased GFR initially, increased pressure

232
Q

pathogenesis of diabetic nephropathy?

A
  • renal hypertrophy
  • mesangial expansion
  • nodule formation
  • inflammation
  • proteinuria
  • tubulo-interstitial fibrosis
233
Q

what are the lesions called in nodular diabetic glomerulosclerosis?

A

Kimmelsteil-Wilson lesion

234
Q

what is renovascular hypertension?

A

a secondary form of hypertension usually caused by renal artery stenosis

235
Q

what conditions come under renovascular disease?

A
  • fibromuscular dysplasia

- atherosclerotic renovascular disease

236
Q

what is ischaemic nephropathy?

A
  • refers to the reduced GFR associated with reduced renal blood flow beyond the level of autoregulatory compensation
237
Q

what can ischaemic nephropathy lead to over time?

A

renal atrophy and progressive CKD

238
Q

what sex is fibromuscular dysplasia more likely to affect and what age group?

A

females, 15-50 years

239
Q

what % of fibromuscular dysaplasia is familial?

A

10%

240
Q

what other conditions is fibromuscular dysplasia associated with?

A

other heriditary condition eg Ehlers-Danlos and Marfans

241
Q

what other arteries other than the renal arteries can fibromuscular dysplasia involve?

A

cerebral arteries eg carotid artery

242
Q

what is multiple myeloma?

A

cancer of plasma cells

243
Q

what can cause kidney problems in multiple myeloma?

A

multiple myelomas feature the production of a paraprotein - an abnormal antibody which can cause kidney problems

244
Q

signs of multiple myeloma?

A
  • anaemia
  • hypercalcaemia
  • renal failure
  • amyloidosis
  • recurrent infection
245
Q

symptoms of multiple myeloma?

A
  • bone pain
  • weakness
  • fatigue
  • weight loss
246
Q

what can cause bone pain in a multiple myeloma?

A
  • from the lytic bone lesions

- or from the hypercalcaemia

247
Q

why is a dipstick test in multiple myeloma often negative for protein?

A
  • dipstick looks for albumin

- in multiple myeloma, abnormal proteins are lost in MM

248
Q

what urine test is used to investigate multiple myeloma?

A

Bence-Jones protein in urine

249
Q

average age for myeloma in males?

A

80

250
Q

average age for myeloma in females?

A

70

251
Q

what is amyloidosis characterised by?

A

the deposition in extracellular spaces of a proteinaceous material

252
Q

what are the 2 types of renal amyloidosis?

A

primary (AL) amyloid and secondary (AA) amyloid

253
Q

what is the classic histology of amyloidosis?

A

positive Congo red staining showing apple-green birifringence under polarised light

254
Q

what things can cause secondary amyloidosis?

A

a chronic inflammatory condition eg RA, myeloma, IBD etc

255
Q

when does small vessel vasculitits associated with ANCA usually present?

A

in 5th, 6th and 7th decade

256
Q

how can GPA (Wegners) affect the nose?

A

nasal crusting, sinusitis, persistent rhinorrhea, otitis media, oral/nasal ulcers, bloody nasal discharge

257
Q

what is eGPA (churg-strauss) classically characterised by?

A

late-onset asthma and eosinophilia

258
Q

what % of patients with lupus have renal involvement at presentation?

A

up to 50%

259
Q

what is a type A drug reaction?

A

-augmented pharmacologic effects which is dose dependent and predictable

260
Q

type B drug reaction?

A

bizarre effects - dose independent and unpredictable

261
Q

type C drug reaction?

A

chronic effects

262
Q

type D drug reaction?

A

delayed effects

263
Q

type E drug reactions?

A

end-of-treatment effects

264
Q

type F drug reaction?

A

failure of therapy

265
Q

what can long term use of NSAIDS cause?

A

hypertension

266
Q

what causes the adverse reaction in type E?

A
  • end of treatment

- abrupt withdrawal of drug and rebound effect

267
Q

what type of adverse reaction is a drug-drug interaction?

A

type A

268
Q

why should patients stop taking their statin when they are on antibiotics?

A

taking them together increases the risk of muscle aches and pains largely

269
Q

why must you be careful when prescribing an ACEi and sulphonylurea at the same time?

A

ACEi increase hypoglycemic effect of SU

270
Q

what do patients with Parkinsons have an increased risk of when you prescribe them a drug?

A

increased risk of drug induced confusion

271
Q

what drugs can cause urinary retention in BPH?

A
  • decongestants

- anticholinergics eg tiotropium bromide

272
Q

what drugs lower seizure threshold?

A
  • neuroleptics, tramadol, quinolones
273
Q

what drug does food high in Vit E&K interact with?

A

warfarin

274
Q

what foods are rich in potassium?

A

bananas, oranges, green leafy vegetables

275
Q

what drugs interact with potassium rich foods?

A
  • ACEi
  • ARBs
  • K-sparing diuretics
276
Q

why is there an adverse reaction if beta blockers are stopped abruptly?

A

there is a loss of physiological “coping”

277
Q

examples of a type D drug reaction?

A
  • secondary malignancy post chemotherapy

- craniofacial abnormalilties in children of women taking isotretinoin

278
Q

prelonged therapy on what drug can cause Cushings disease?

A

steroid therapy

279
Q

what disease can prolonged treatment of beta-blocker cause?

A

diabetes

280
Q

if a drug in the BNF has a black triangle next to it?

A

a new drug, to caution prescriber to be extra vigilent when prescribing it as everything is not known about it

281
Q

what is the most frequent life-threatening hereditary disease?

A

ADPKD

282
Q

does type 1 or type 2 ADPKD progress to end stage renal failure at an earlier stage?

A

type 1 develops ESRF at earlier stage

283
Q

in ADPKD, how long after the presentation of renal cysts do liver cysts present?

A

about 10 years later

284
Q

in patiens with ADPKD, when should they be screened for berry aneurysms?

A

family history

285
Q

what cardiac problems can someone with ADPKD get?

A

mitral/aortic prolapse

286
Q

what GI disease do patients with ADPKD have an increased prevelance of?

A

diverticular disease

287
Q

what will be seen on US in ADPKD?

A

mutiple bilateral cysts, renal enlargement

288
Q

how early can early onset ADPKD present?

A

in utero or first year of life

289
Q

managment of ADPKD before dialysis?

A
  • rigorous control of hypertension
  • hydration
  • proteinuria reduction
  • control cyst haemorrhage and/or infection
290
Q

in ARPKD, where are cysts seen arrising from?

A

the collecting duct system

291
Q

how is 85% of alports syndrome cases inherited?

A

X-linked inheritance

292
Q

what is there a disorder of in alprorts syndrome?

A

type IV collagen matrix

293
Q

what is the mutation in alports syndrome?

A

COL4A5 gene

294
Q

how does alports usually present?

A

haematuria

295
Q

when is proteinuria seen in alports?

A

later in disease

296
Q

what are the extra renal manifestations of alports?

A
  • sensorineural deafness
  • ocular defects - anterior lentoconus
  • leiomyomatosis of oesophagus/genitalia - rare
297
Q

what is seen on renal biopsy of alports?

A

variable thickness of GBM, with splitting of the lamina densa

298
Q

what is anderson fabrys disease? what is the deficiency?

A

inborn error of Glycosphingolipid metabolism. deficiency of alpha-galactosidase A

299
Q

how is anderson fabry disease inherited?

A

X linked

300
Q

what organs/cells does anderson fabry disease affect?

A

kidneys, liver, lungs, erythrocytes

301
Q

how is anderson fabrys disease diagnosed?

A
  • plasma/leuocyte a-GAL activity
  • skin biopsy
  • renal biopsy
302
Q

clinical features of anderson fabry disease?

A
  • renal failure
  • cutaneous- angiokeratomas
  • cardiomyopathy, valvular disease
  • stroke, acroparaesthsia
  • psychiatric
303
Q

what can be seen in renal biopsy of anderson fabry disease?

A

concentric lamellar inclusions within lysosomes

304
Q

what is the treatment of anderson fabrys disease?

A

enzyme replacement - Fabryzyme

305
Q

inheritance pattern of medullary cystic kidney?

A

autosomal dominant

306
Q

what is the morphology of medullary cystic kidney?

A

abnormal renal tubules leading to fibrosis

307
Q

where are the cysts located in medullary cystic kidney?

A

in the corticomedullary junction/medulla

308
Q

what is the average presentation age of medullary cystic kidney?

A

28 years

309
Q

what is the best choice of treatment in medullary cystic kidney?

A

renal transplantation

310
Q

what happens to the collecting ducts in medullary sponge kidney?

A

they dilate

311
Q

what do they cysts contain in medullary sponge kidney?

A

they have calculi

312
Q

how is the diagnosis of medullary sponge kidney diagnosed?

A

by excretion urography - to demarcate calculi

313
Q

what is the first pharmacological option fr arresting the disease process in ADPKD?

A

tolvaptan

Renal (10 decks)

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