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4 CSIM2 > Renal medicine > Flashcards

Renal medicine Flashcards

1
Q

where in the nephron does Type 2 renal tubule acidosis affect and what are the biochemical signs?

A

PCT - glycosuria, aminoaciduria, acidosis

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2
Q

where in the nephron do loop diuretics act on?

A

ascending loop

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3
Q

where in the nephron do thiazide diuretics act on

A

distal tubule

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4
Q

where in the nephron do drugs like spironolactone act on?

A

collecting ducts

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5
Q

how and why does trimethoprim affect creatinine results

A

it raises serum creatinine without affecting GFR because it inhibits the secretion of creatinine in the tubules.

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6
Q

how do NSAIDs and ACEi affect renal perfusion

A

NSAIDs vasoconstrict afferent arterioles while ACEi dilate efferent arterioles.

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7
Q

what happens if someone takes both an NSAID and an ACEi?

A

reduce blood going in and increased blood leaving, would severely starve the nephron of blood causing kidney failure or exacerbating one.

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8
Q

how do drugs like metformin and sulphonylurea affect the kidney?

A

they are not nephrotoxic, but they are both renally excreted. metformin has an increased risk of lactic acidosis and sulphonylurea has a risk of hypoglcyaemia, in renal impairment, these risks are elevated.

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9
Q

describe the anatomy of the kidney

A

fibrous capsule surrounding cortex whith the medulla in the centre. renal artery goes in and supplies afferetn arterioles and leaves via the efferent arterioles to continue to surround the nephrons and transport blood back out through the renal vein.

filtrate goes through nephron, into CD, into renal papilla, minor calyx and into major calyx finally into renal pelvis and to the ureter

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10
Q

describe the anatomy of the glomerulus

A

nest of capillaries surrounding by fenestrated epithelium and podocytes to ensure large and charged particles don’t get throught. PCT -> loop of henle -> DCT -> CD

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11
Q

what happens at the PCT

A

most solutes reabsorbed

60-80% water
60-70% sodium
80-90% calcium
90% potassium
90% bicarb
90% glucose
100% amino acids

secretion of creatinine and uric acid

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12
Q

what happens in the loop of henle

A

one-way membranes cause the solute to concentrate as the interstitium is higher in concentration than the loop

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13
Q

what happens in the DCT

A

5% sodium reabsorbed, potassium reabsorbed

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14
Q

what happens in the collecting duct

A

action of ADH inserting aquaporins
secretion of acid
absorption of remaining sodium

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15
Q

describe the endocrine function of the kidney

A

EPO

vitamin D

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16
Q

how does kidney failure affect bone metabolism

A

cannot activate vit D, so gut doesn’t absorb calcium, kidney doesn’t absorb calcium, result in hypocalcemia and 2ndary hyperparathyroidism

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17
Q

most common cause of ckd

A

diabetes

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18
Q

what to ask about in renal history

A

diabetes, cdvs (incl. hypertension), urinary changes, pain, systemic symptoms, signs of infection

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19
Q

what can be assessed in observation of someone with suspected kidney impairment

A

fluid status - dehydration or fluid overload?

(pulmonary)edema? or dry/mottled skin?

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20
Q

what does a raised JVP tell you ?

A

fluid overload

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21
Q

what does urinalysis tell you

A

assessment of filtration ability, by seeing things that aren’t supposed to be in the urine like lecocytes, glucose, portein, blood, ketones, ph, specific gravity, nitrites

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22
Q

what is creatinine and how is it affected

A

byproduct of muscle respiration. affected by age and muscle mass. but also in renal impairment due to decreased ability to filter it caused by reduced GFR

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23
Q

what is urea and how can it be interpreted in renal impairment

A

metabolite of ammonia metabolism. raised in illness, but not specific to renal causes.

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24
Q

how are electrolyte levels changed in renal impairment - potassium sodium calcium pH?

A

hyperkalaemia, hyponatraemia, hypocalcaemia, and acidaemia usually.

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25
Q

what other investigations can be done in renal impairment

A

immunology, cultures, microscopy, imaging, biopsy.

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26
Q

what is postobstructive diuresis?

A

complication that happens after relieve of post-renal obstruction where kidney starts to loose more fluid and sodium than it should causing hypovolaemia

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27
Q

what 5 things are required for a functioning kidney

A 
adequate perfusion
intact glomerular vasculature
patent tubules
functioning tubular cells
patent outflow
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28
Q

causes of pre-renal AKI

A

hypovolaemia
low cardiac output
distributive hypovolaemia
vasoconstrictive drugs

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29
Q

risk factors of AKI

A

preexisting CKD
older age
diabetes, atherosclerosis, liver disease, hypertension. heart failure

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30
Q

what can trigger AKI in a vulnerable patient?

A

hypovolaemia, antihypertensives, nsaids, imaging contrast

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31
Q

most common intrinsic cause of AKI?

A

acute tubular necrosis

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32
Q

what is ATN ?

A

vascoconstriction and ischaemia of intrarenal micro vessels causing cell injury and necrosis/apoptosis

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33
Q

what can cause ATN?

A

renal ischaemia, toxins like aminoglycosides, platinum, lithium

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34
Q

what can trigger ATN

A

sepsis, infection, cholestatic jaundice, hypotension, rhabdomyolysis

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35
Q

what are the biochemical signs of ATN

A 
hyperkalaemia
hyperphosphataemia
hypocalcaemia
hyponatraemia
uraemia
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36
Q

other signs of ATN

A 
fluid overload
purritis
anorexia, nausea, vomiting
reduced GCS
haemorrhagic events - GI bleeding, epistaxis
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37
Q

what other causes of intrinsic AKI are there

A

tubular interstitial disease
tubular obstruction by casts
glomerulonephritis
microvascular injury

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38
Q

what can cause post renal AKIs?

A

BPH or prostate cancer causing obstruction
kidney stones
retroperitoneal masses
constipation

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39
Q

complications of AKI?

A

hyperkalaemia causing cardiac instability
salt and water accumulation causing fluid overload
uraemia and toxin accumulation
metabolic acidosis

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40
Q

what are features of uraemia and toxin accumulation?

A

nausea vomiting anorexia
pericarditis, pleurisy, ECG changes
fitting, coma
bleeding risk

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41
Q

why is there bleeding risk in uraemia?

A

because of toxicity to platelets

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42
Q

what are features of metabolic acidosis

A

haemodynamic instability
circulatory collapse
reduces GCS
arrhythmias

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43
Q

what investigations to do for AKI?

A 
urinalysis, ECG
bloods - FBC, LFTs, U&Es, creatinine, CRP, ESR, calcium
cultures, blood film, microscopy
antibody testing 
imaging, biopsy
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44
Q

when should urine microscopy be done?

A

if urinalysis shows protein and blood

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45
Q

what might be seen on urine microscopy in haematuria and proteinuria?

A

red cell casts, or myoglobin casts in rhabdomyolysis

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46
Q

how to tell the difference between an AKI and a CKD?

A

previous bloods, trend of creatinine
USS kidneys to see if atrophied
duration of symptoms
if discrete cause can be identified

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47
Q

what is the criteria for stage 1 AKI?

A

1.5-2x increase in creatinine in 7 days, or increase of 26 mmol/L within 48 hours.

or less than 0.5ml/kg/hr in 6 hours urine outpue

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48
Q

what is the criteria for stage 2 AKI?

A

2-3x increase in creatinine in 7 days

or less than 0.5ml/kg/hr in 12 hours urine outpue

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49
Q

what is the criteria for stage 3 AKI?

A

> 3x increase in creatinine over 7 days OR higher than 354 mmol/L

or urine output less than 0.3ml/kg/hr for 24 hours or anuria for 12 hours

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50
Q

what drugs should be modified or stopped in AKI?

A

NSAIDs, ACEi/ARBs, opioid analgesics, some antibiotics, metformin, insulin, benzos, diuretics,

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51
Q

What is the definition of CKD

A

Abnormal urinary sediments (haematuria and/or proteinuria)
Fall in gfr
Anatomical abnormality in kidney

For longer than 3 months

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52
Q

What anatomical changes account for the physiological changes in CKD?

A

Glomerular filtration damage which causes sedimentation abnormality

Reduced number of functional nephrons and reduced function of remaining nephrons - account for fall in GFR

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53
Q

What are the most some causes of CKD

A

Diabetes
Hypertension
Intrinsic glomerular or tubular disease
Urinary tract obstruction

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54
Q

How does CKD present usually?

A

Early CKD is usually asymptomatic, features would usually only include hypertension, some microalbuminuria. Usually found incidentally or in screening.

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55
Q

What are some features of late CKD (when is late CKD defined as?)

A

<30 GFR

Reduced concentration, poor sleep, fatigue, nausea and vomiting, anorexia

Bruising, itching, skin pigmentation

Fluid retention (Edema)

Bone pain

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56
Q

What are features of severe CKD

A

Uraemic encephalopathy

Pericarditis - chest pain

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57
Q

What are some complications of late stage CKD

A 
Anaemia
Cardiovascular risk
GI complications
Bone disease
Neurological abnormalities
Endocrine dysfunction
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58
Q

What is renal osteodystrophy?

A

A host of bone dysfunction caused by CKD, due to calcium and phosphate levels leading to PTH changes and vitamin D abnormalities.

Results in brittle bones

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59
Q

How is CKD diagnosed

A

Urinary sample for ACR measurement and eGFR calculation

For more than 3 months.

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60
Q

How is hypertension and ckd related

A

One may cause the other. Always screen for the other if presenting if one.

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61
Q

What can be done to diagnose CKD, if someone with hypertension develops CKD?

A

Biopsy

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62
Q

What are the downsides of using creatinine to estimate GFR?

A

Varys according to patient factors, non-linear relationship with GFR, some secretion in tubules.

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63
Q

What is required to stage CKD as G4A2

A

EGFR or 15-29

ACR if 3-30

64
Q

What is a better biochemical marker than creatinine to estimate GFR?

A

Cystatin C

65
Q

What is the clinical course of CKD like

A

Most symptoms come at stage 3 CKD. Most will die of cardiovascular compliations, few will progress to stage 5 CKD.

66
Q

What factors in CKD are most useful in managing to increase life span

A

Blood pressure - ACEi
Proteinuria - ACEi
Glycaemic control - SGLT2 inhibitor

67
Q

Explain why cardiovascular risk increases in CKD

A

Increased risk of MI, strokes, heart failure due to calcification of vessels causing increased BP and increased afterload.

68
Q

What are some associated risk factors of cardiovascular risk in CKD

A

Calcium and phosphate levels
Hyperparathyroidism
Uraemia
Inflammation

69
Q

Describe pathophysiology of diabetic nephropathy

A

Increased blood glucose leads to

Haemodynamic changes, overactive RAAS, and hypoxia and inflammation of kidneys

This progresses to albuminuria and intrinsic kidney damage in the form of glomerulosclerosis and tubulointerstitial fibrosis

These lead to loss of filtration function

70
Q

How long does diabetic nephropathy usually take to progress to end stage kidney disease?

A

25 years

71
Q

How does GFR change in the early stages of Diabetic nephropathy?

A

Increased GFR due to GBM thickening and mesangial expansion

72
Q

How should diabetics be screened for diabetic nephropathy>

A

Annual screening includes urinary testing for ACR and serum testing for eGFR

73
Q

What test results is required for CKD to be diagnosed?

A

EGFR <60 and/or ACR more than 3mg/mmol for mnore than 3 months

74
Q

what are the indications for starting dialysis in AKI?

A 
Acidosis
Electrolytes (esp potassium)
Ingestions (poisoning e.g. ethylene glycol)
Ooverload (pulmn edema)
Uraemic encephalopathy/pericarditis
75
Q

how does haemodialysis work?

A

moving blood through semipermeable membrane to remove toxins and let water back in through osmosis.

76
Q

complications of haemodialysis?

A

rapid shift in electrolyte balance results in nausea, vomiting, cramps, cardiac arrythmias, headaches.

77
Q

how does peritoneal dialysis work?

A

dialysate is pumped into peritoneal cavity, using peritoneum as membrane for dialysis

78
Q

disadvantages of peritoneal dialysis?

A

weight gain, hyperglycaemia, peritonitis

79
Q

possible iatrogenic complications of haemodialysis?

A

infection
thrombosis
bleeding
bleeding

80
Q

what must be considered in a patient before renal transplant

A

no contraindicated comorbidities, no malignancy, no chronic infections.

where the kidney is coming from

matching of donor - HLA and blood type

81
Q

what are the complications of organ transplant

A

organ dysfunction, rejection, GvHD, immunosuppresion leading to infection, malignancy

82
Q

what are the 5 characteristics of nephrotic syndrome?

A 
>3.5g/day proteinuria
hypertension
edema due to salt and water retention
lipiduria
hyperlipidaemia
83
Q

what are 2 classifications of nephritic syndromes

A

acute or rapidly progressing

84
Q

features of acute nephritis

A 
haematuria
<3.5g/day proteinuria
edema
AKI
hypertension
85
Q

difference between acute nephritis and rapidly progressing nephritis

A

rapidly progresing nephritis has features of focal necrosis, +/- crescents and rapid renal failure over weeks

86
Q

what syndrome would mainly podocyte damage cause?

A

nephrotic

87
Q

what structures are mainly damage in nephritic syndrome

A

endothelial and mesangial cells

88
Q

what happens if there is damage in podocytes, endothelial cells and mesangial cells

A

mixed nephrotic/nephritic syndrome

89
Q

hypertension is a feature of nephrotic syndrome, T or F?

A

F

90
Q

what immunological features are present in FSGS

A

C3 and IgM

91
Q

how do amyloid deposits stain?

A

they stain pink with green bifringence under polarised light with congo red

92
Q

what are 4 features of nephrotic syndrome?

A

heavy proteinuria (>3.5g/day)
edema
hypoalbuminaemia
hyperlipidaemia

93
Q

what causes hypoalbuminaemia in nephrotic syndrome?

A

increased catabolism of albumin resorbed in the tubules

94
Q

what causes hyperlipidaemia in nephrotic syndrome?

A

increased lipoprotein production in hypoalbumin state

95
Q

what causes edema in nephrotic syndrome?

A

increased sodium and water retention

96
Q

what causes proteinuria in nephrotic syndrome?

A

damage to glomerular filtration barrier

97
Q

describe the causes of physiological proteinuria

A

PU without HU
PU <1g/day
asymptomatic
normal renal function

can be caused by postural PU or post infection PU

98
Q

what are 3 non systemic causes of nephrotic syndrome

A

minimal change disease
membranous glomerulopathy
focal segmental glomerulosclerosis

99
Q

what are some features of minimal change disease

A

facial edema, proteinuria. no immune complexes found.

100
Q

minimal change disease often leads to CKD, T or F

A

F

101
Q

what can trigger minimal change disease

A

atopy
drugs (NSAIDs, antibiotics, etc)
infections

102
Q

C3 and IgM are a common feature of minimal change disease, T or F

A

F, usually no immune complexes found

103
Q

describe FSGS

A

sclerosis of some glomeruli, not all, and some sections of each tuft.

104
Q

what are the types of FSGS

A

primary and secondary

105
Q

describe the clinical course of primary FSGS

A

progressive destruction of glomeruli, tubules and interstitium.

106
Q

what immunological features are present in FSGS

A

C3 and IgM

107
Q

what are some clinical signs of FSGS

A

massive PU

HU, H/T and renal impairment

108
Q

what can cause secondary FSGS

A

drugs
infection
genetics

109
Q

who usually gets membranous glomerulopathy

A

mostly male

110
Q

clinical features of membranous glomerulopathy

A

asymptomatic PU, nephrotic SD, +/- microscopic HU, H/T or renal impairment

111
Q

what is the prognosis for membranous glomerulopathy

A

1/3 get better
1/3 get partial recovery
1/3 progress to CKD

112
Q

what are some good prognostic factors in membranous glomerulopathy

A

female
younger
asymptomatic at presentation

113
Q

what immune features are present in membranous glomerulopathy

A

IgG4 and C3

114
Q

how does amyloid deposits stain?

A

they stain pink, and exhibit green birefringence under polarised light in red congo stain.

115
Q

macroglossia, racoon eyes, and shoulder pad sign; these are pathognomonic for what disease?

A

amyloidosis

116
Q

what immunologic criteria are associated with SLE?

A 
ANA
anti dsDNA antibodies
anti smooth muscle antibodies
anti-phospholipid antibodies
low complement C3, C4
positive direct coomb's test
117
Q

what disease exhibits effacement of foot processes

A

minimal change disease

118
Q

what forms the the ‘crescent’ seen in rapidly progressing glomerulonephritis?

A

macrophages and epithelial cells in bowman’s space.

119
Q

what investigation is done to identify ANCA proteins

A

immunofluorescence

120
Q

how does ANCA vasculitis cause damage?

A

the ANCA antibodies bind to neutrophils, activating them to bind to endothelium, causing degranulation of neutrophils, promoting inflammation and causing damage.

121
Q

what are 5 complications of nephrotic syndrome and how to manage them

A 
hyperlipidaemia - statins
thromboembolism - anticoagulation
infections - vaccinations
protein malnutrition
AKI - CKD
122
Q

difference between nephrotic and nephritic syndrome

A

nephrotic - insidious onset, edematous, no hypertension, no raised jvp, high PU, minimal HU and red cell casts, low serum albumin

nephritic - acute/rapidly progressing, edematous, hypertnsive, raised jvp, minimal PU, HU with red cell casts, +/- low serum albumin

123
Q

most common cause of nephrotic syndrome?

A

diabetes

124
Q

what investigations to do in proteinuria?

A

urinaysis, then quantification with 24 hour collection OR urine albumin/creatinine ratio (ACR)

125
Q

what is the ACR diagnostic of microproteinuria? and frank proteinuria

A

> 2,5 in men, >3 in women,

> 30 in both for frank PU

126
Q

what are the features of nephritic syndrome

A 
hypertension
edema
haematuria
non-nephrotic proteinuira
redufction in eGFR
127
Q

list some causes of nephritic syndrome

A 
post streptococcal nephritis
IgA nephropathy
anti-GBM GN
alport's syndrome
ANCA +ve vasculitis
128
Q

what are some mixed nephritic nephrotic causes

A

SLE
HSP
mesangiocapillary glomerulonephritis

129
Q

what are some causes of haematuria

A

non-glomerular - stones, cancer, infection, sickle cell, pckd, BPH, exercise induced, renal vein thrombosis, trauma,

glomerular- glomerulonephritis, IgA nephropathy, alport’s sd

130
Q

what are some painful causes of visible haematuria

A 
trauma
stones
renal vein trhombosis
infection
pckd
131
Q

what are some painless causes of frank haematuria

A

bladder cancer
exercise induced
post streptococcal glomerulonephritis

132
Q

what can cause a false +ve haematuria dipstick

A

myoglobinuria after rhabdo
semen
drugs
menses

133
Q

what are features of glomerular disease

A

symmetrical kidney involvement
dysfunctional filtration
injury to filtration structure

134
Q

what comprises the filtration structure of the nephron

A

endothelial cells
basement membrane
podocytes
mesangial cells

135
Q

damage to what structures cause nephrotic syndrome, nephritic syndrome and mixed?

A

damage to podocytes cause nephrotic syndrome
damage to endothelium and mesangial cells cause nephritic syndrome
damage to both cause mixed

136
Q

2 classifications of nephritic syndrome

A

acute and rapidly progressing

137
Q

how to differentiate acute and rapidly progressing nephritis

A

acute has - HU, edema, AKI, hypertension, proteinuria (<3.5g/day)

RPGN - includes necrotic features and +/- crescentic features, renal failure occurs over weeks

138
Q

how to investigate proteinuria or haematuria?

A 
ask about UTI symptoms
urinalysis
urine microscopy
blood tests - U&amp;Es, ACR, eGFR
biopsy
imaging
139
Q

for someone with newly diagnosed renal anaemia, what should be prescribed?

A

iron supplement, then EPO

140
Q

how to treat mineral bone disease in diabetic nephropathy?

A

check PTH
low phosphate diet, phosphate binders
vitamin D

141
Q

in an intrinsic AKI where are 3 possible sites of damage?

A

tubular
glomerulonephritis
interstitial

142
Q

what happens in acute tubular necrosis?

A

acute ischaemia to tubules cause necrosis and sloughing off of epithelial cells, creating casts. these casts obstruct the tubules causing back pressure, resulting in reduced GFR.

143
Q

what are the effects of acute tubular necrosis?

A

reduced GFR causes more toxins to be left in the blood, resulting in azotemia, metabolic acidosis and an increased BUN

144
Q

what can cause acute tubular necrosis?

A

from a prerenal AKI or toxins

145
Q

what kind of toxins cause ATN?

A 
aminoglycosides antibiotics
lead
myoglobin in rhabdo
ethylene glycol
radiocontrast
uric acid (TL sd)
146
Q

what kind of AKI would tumour lysis syndrome cause?

A

ATN

147
Q

what kind of casts would be seen on microscopy in ATN?

A

epithelial casts

148
Q

pathophysiology of acute glomerulonephritis?

A

inflammation in glomerulus characterised by AgAb complexes with complement activation. this causes damage to podocytes, resulting in PU and HU. increased membrane permeability then also causes reduced GFR because of reduced pressure, thus causing azotemia, oliguria, edema and hypertension

149
Q

why does GFR go down in acute glomerulonephritis?

A

damage to podocytes cause increased permeability, reduced Glomrular filtration pressure, reducing GFR.

150
Q

what characterises acute interstitial necrosis?

A

eosinophils and neutrophil infiltration of interstitium

151
Q

clinical features of acute interstitial necrosis?

A

eosinophiluria, oliguria, rash, fever

152
Q

what can acute interstitial necrosis lad to?

A

renal papillary necrosis, causing haematuria and flank pain

153
Q

what is the BUN:Creatinine ratio, FENa, and urine osmolality in acute interstitial necrosis?

A

BUN:creatinine ratio goes below 15:1 because tubules cannot resorb stuff

FENa increases to >2%

urine osmolalitiy increases because of impaired resorption

154
Q

what is the BUN:Creatinine ratio, FENa, and urine osmolality in prerenal AKI?

A

BUN:creatinine ratio >20:1 (RAAS activation, more Na reabsorption, urea follows)
FENa <1%
urine osmolality will be low

155
Q

what is the normal BUN:creatinine ratio?

A

5-20:1

156
Q

what happens in postrenal AKI?

A

blockage or compression causes pressure to build up in tubules, this reduces pressure gradient, causing reduced GFR, causing azotemia, oliguria.

increased pressure in tubules will then increased reabsorption of whatever was filtered out, causing increased BUN:crt ratio, reduced FENa, reduced Urine Na+ concentration.

157
Q

what happens in prolonged postrenal AKI

A

tubules get damaged, reduced ability to reabsorption things, causing FENa to rise, BUN:Crt to fall

4 CSIM2 (11 decks)

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