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Finals > Renal > Flashcards

Renal Flashcards

1
Q

AKI

definition

A

an acute drop in kidney function

diagnosed by measuring the serum creatinine

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2
Q

AKI

NICE criteria for AKI

A
  • rise in Cr of ≥ 25 micromol/L in 48 hours
  • Rise in creatinine of ≥ 50% in 7 days
  • Urine output of < 0.5ml/kg/hour for > 6 hours
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3
Q

AKI

RFs

A
  • CKD
  • Heart failure
  • Diabetes
  • Liver disease
  • Older age (>65 years)
  • Cognitive impairment
  • Nephrotoxic meds: NSAIDS and ACEi
  • Use of a contrast medium: during CT scans
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4
Q

AKI

how can causes be split up

A

pre-renal
renal
post-renal

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5
Q

AKI

pre-renal causes

A

most common. Due to inadequate blood supply to kidneys reducing the filtration of blood

  • dehydration
  • hypotension (shock)
  • HF
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6
Q

AKI

renal causes

A

intrinsic disease in kidney leading to reduced filtration of blood:

  • glomerulonephritis
  • interstitial nephritis
  • acute tubular necrosis
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7
Q

AKI

post renal causes

A

obstruction to the outflow of urine from the kidney causing back pressure into the kidney

  • kidney stones
  • masses such as cancer in the abdo or pelvis
  • ureter or uretral strictures
  • enlarged prostate or prostate cancer
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8
Q

AKI

inx

A

urinalysis for protein, blood, leucocytes, nitrites and glucose

US: look for obstruction if suspected

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9
Q

AKI

what do leucocytes and nitrites suggest

A

infection

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10
Q

AKI

what does protein in the blood suggest

A

acute nephritis

but can be +ve in infection

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11
Q

AKI

what does glucose suggest in the urinalysis

A

diabetes

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12
Q

AKI

mnx

A

correct underlying cause:

  • fluid rehydration with IV fluids in pre-renal AKI
  • stop nephrotoxic medications
  • relieve obstruction in post renal AKI: e.g. insert catheter for a pt in retention from an enlarged prostate
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13
Q

AKI

complications (4)

A
  • hyperkalaemia
  • fluid overloads, HF, pulmonary oedema
  • metabolic acidosis
  • uraemia (high urea)
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14
Q

AKI

what can uraemia lead to

A

encephalopathy or pericarditis

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15
Q

CKD

what is it

A

a chronic reduction in kidney function

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16
Q

CKD

causes

A
  • Diabetes
  • Hypertension
  • Age-related decline
  • Glomerulonephritis
  • Polycystic kidney disease
  • Medications: NSAIDS, PPIs and lithium
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17
Q

CKD

RFs

A
  • Older age
  • Hypertension
  • Diabetes
  • Smoking
  • Use of medications that affect the kidneys
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18
Q

CKD

presentation

A

usually asymptomatic

  • Pruritus (itching)
  • Loss of appetite
  • Nausea
  • Oedema
  • Muscle cramps
  • Peripheral neuropathy
  • Pallor
  • Hypertension
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19
Q

CKD

how to test eGFR

A

using a U&E blood test

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20
Q

CKD

how many eGFR tests are required to confirm dx

A

2

3m apart

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21
Q

CKD

inx

A
  • eGFR
  • urine albumin:creatinine ratio shows proteinuria (≥ 3mg/mmol is significant)
  • urine dipstick: haematuria (1+ of blood)
  • renal US
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22
Q

CKD

what is the G score

A

based on the eGFR

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23
Q

CKD

G1

A

eGFR >90

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24
Q

CKD

G2

A

eGFR 60-89

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25
Q

CKD

G3a

A

eGFR 45-59

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26
Q

CKD

G3b

A

eGFR 30-44

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27
Q

CKD

G4

A

eGFR 15-29

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28
Q

CKD

G5

A

eGFR <15 (known as “end-stage renal failure”)

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29
Q

CKD

what is the A score

A

based on the albumin : creatinine ratio

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30
Q

CKD

A1

A

< 3mg/mmol

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31
Q

CKD

A2

A

3 – 30mg/mmol

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32
Q

CKD

A3

A

> 30mg/mmol

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33
Q

CKD

what is needed for a dx of CKD

A

eGFR of <60 or proteinuria (≥ 3mg/mmol)

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34
Q

CKD

complications (5)

A
  • Anaemia
  • Renal bone disease
  • Cardiovascular disease
  • Peripheral neuropathy
  • Dialysis related problems
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35
Q

CKD

when does NICE suggest referral to a specialist

A
  • eGFR < 30
  • ACR ≥ 70 mg/mmol
  • Accelerated progression: decrease in eGFR of 25% or 15 ml/min in 1 year
  • Uncontrolled hypertension despite ≥ 4 antihypertensives
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36
Q

CKD

what are the aims of mnx

A
  • Slow the progression of the disease
  • Reduce the risk of cardiovascular disease
  • Reduce the risk of complications
  • Treating complications
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37
Q

CKD

how would you slow the progression of the disease

A
  • optimise diabetic control
  • optimise hypertensive control
  • treat glomerulonephritis
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38
Q

CKD

how would you reduce the risk of complications

A
  • exercise, maintain a healthy weight, stop smoking
  • dietary advice about phosphate, Na, K + water intake
  • offer atorvastatin 20mg for primary prevention of CVD
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39
Q

CKD

how would you treat complications

A
  • Metabolic acidosis: PO sodium bicarb
  • Anaemia: iron + EPO
  • renal bone disease: vit D
  • end stage renal failure: dialysis, renal transplant
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40
Q

CKD

which pts are offered ACEi to treat HTN

A
  • Diabetes plus ACR > 3mg/mmol
  • Hypertension plus ACR > 30mg/mmol
  • All patients with ACR > 70mg/mmol
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41
Q

CKD

what is the aim BP

A

<140/90

(or < 130/80 if ACR > 70mg/mmol).

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42
Q

CKD

what needs to be monitored

A

serum K because CKD and ACEi both cause hyperkalaemia

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43
Q

CKD

why is there anaemia of CKD

A
  • healthy kidney cells produce EPO (hormone that stimulates production of RBCs)
  • damaged kidney cells produce less EPO
  • therefore drop in RBCs and subsequent anaemia
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44
Q

CKD

how can anaemia of CKD be treated

A

with erythropoiesis stimulating agents such as exogenous erythropoietin

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45
Q

CKD

why are blood transfusions limited in anaemia of CKD

A

they can sensitise the immune system (allosensitisation)

so that transplanted organs are more likely to be rejected

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46
Q

CKD

what should be treated before offering erythropoetin

A

iron deficiency

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47
Q

CKD

what is renal bone disease aka?

A

CKD mineral bone disorder (CKD-MBD)

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48
Q

CKD

what are 3 features of renal bone disease

A
  • osteomalacia (softening)
  • osteoporosis (brittle bones)
  • osteosclerosis (hardening)
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49
Q

CKD

what are the spinal x-ray changes in someone with renal bone disease

A

‘rugger jersey’ spine (stripes found on a rugby shirt)

sclerosis of both ends of the vertebra (denser white)

osteomalacia in the centre of the vertebra (less white)

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50
Q

CKD

renal bone disease: why is there high serum phosphate

A

reduced phosphate excretion

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51
Q

CKD

renal bone disease: why is there low active vit D

A

because the kidney cannot metabolise vit D to its active form as effectively

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52
Q

CKD

renal bone disease: what is Active vit D essential in

A
  • calcium absorption from the intestines and kidneys

- bone turnover

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53
Q

CKD

renal bone disease: why does secondary hyperparathyroidism occur

A

because the parathyroid glands react to low serum Ca and high serum phosphate by excreting more PTH

this leads to increased osteoclast activity which leads to the absorption of Ca from bone

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54
Q

CKD

renal bone disease: why does osteomalacia occur

A

due to increased turnover of bones without adequate Ca supply

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55
Q

CKD

renal bone disease: why does osteosclerosis occur

A

occurs when the osteoblasts respond by increasing their activity to match the osteoclasts

by creating new tissue in the bone. But due to low Ca level, this new tissue is not properly mineralised

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56
Q

CKD

renal bone disease: why does osteoporosis occur

A

due to other RFs such as ages and use of steroids

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57
Q

CKD

mnx of renal bone disease

A
  • active forms of vit D (alfacalcidol + calcitriol)
  • low phosphate diet
  • bisphosphonates to treat osteoporosis
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58
Q

Acute Tubular Necrosis

what is it

A

damage and death (necrosis) of the epithelial cells of the renal tubules

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59
Q

what is the most common cause of AKI

A

acute tubular necrosis

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60
Q

Acute Tubular Necrosis

why does damage to the kidney cells occur

A

due to ischaemia or toxins

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61
Q

Acute Tubular Necrosis

is it reversible

A

yes because epithelial cells have the ability to regenerate

usually takes 7-21d to recover

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62
Q

Acute Tubular Necrosis

causes from ischaemia (3)

A
  • shock
  • sepsis
  • dehydration
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63
Q

Acute Tubular Necrosis

causes from toxins (3)

A
  • radiology contrast dye
  • gentamycin
  • NSAIDs
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64
Q

Acute Tubular Necrosis

pathognomonic finding specific to it

A

‘muddy brown casts’ found on urinalysis

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65
Q

Acute Tubular Necrosis

urinalysis findings

A
  • muddy brown casts

- renal tubular epithelial cells in the urine

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66
Q

Acute Tubular Necrosis

trx

A

the same as with other causes of an AKI

  • supportive mnx
  • IV fluids
  • stop nephrotoxic medications
  • treat complications
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67
Q

Renal Transplant

how many years of life is added compared with just using dialysis in end stage kidney failure

A

10 years

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68
Q

Renal Transplant

how are patients and donor kidneys matched

A

based on the HLA type A, B and C on Ch6

they don’t have to fully match but the less they match, the more likely the transplant is to fail

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69
Q

Renal Transplant

procedure

A

pt’s own kidneys are left in place

the donor kidney’s blood vessels are connected (anastomosed) with the patient’s pelvic vessels, usually the external iliac vessles

the donor kidney’s ureter is anastomosed directly with the pt’s bladder

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70
Q

Renal Transplant

where is the donor kidneyplaced

A

anterior in the abdomen and can be palpated in the iliac fossa

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71
Q

Renal Transplant

what incision is used

A

hockey stick incision

there will be a hockey stick scar

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72
Q

Renal Transplant

how to reduce the risk of transplant rejection

A

life long immunosuppression regime:

  • Tacrolimus
  • Mycophenolate
  • Prednisolone

other possible immunosuppressants:

  • Cyclosporine
  • Sirolimus
  • Azathioprine
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73
Q

Renal Transplant

complications relating to the transplant (3)

A
  • transplant rejection (hyperacute, acute, chronic)
  • transplant failure
  • electrolyte imbalances
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74
Q

Renal Transplant

complications related to immunosuppressants

A
  • IHD
  • T2DM (steroids)
  • infections more likely
  • inidal infections (PCP. CMV, PJP, TB)
  • non-Hodgkin’s lymphoma
  • skin cancer (SCC)
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75
Q

Glomerulonephritis

define nephritis

A

inflammation of the kidneys

not a syndrome or diagnosis

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76
Q

Glomerulonephritis

define nephritic syndrome or acute nephritic syndrome

A

a group of symptoms. not a diagnosis. Has no set criteria

  • haematuria
  • oliguria
  • proteinuria
  • fluid retention
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77
Q

Glomerulonephritis

what amount of protein in the urine points towards nephritic syndrome

A

<3g/24hrs

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78
Q

Glomerulonephritis

define nephrotic syndrome

A

a group of symptoms without specifying the underlying cause

they must fulfil this criteria:

  • peripheral oedema
  • proteinuria (>3g/24hrs)
  • serum albumin <25g/L
  • hypercholesterolaemia
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79
Q

Glomerulonephritis

what is Glomerulonephritis

A

an umbrella term applied to conditions that cause inflammation of or around the glomerulus and nephron

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80
Q

Glomerulonephritis

define interstitial nephritis

A

inflammation of the space between cells and the tubules (interstitium) within the kidney

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81
Q

Glomerulonephritis

what are the 2 types of interstitial nephritis

A

acute interstitial nephritis

chronic tubulointerstitial nephritis

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82
Q

Glomerulonephritis

define glomerulosclerosis

A

the pathological process of scarring of the tissue in the glomerulus

not a diagnosis

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83
Q

Glomerulonephritis

what can glomerulosclerosis be caused by (3)

A
  • any type of glomerulonephritis
  • obstructive uropathy (blockage of urine outflow)
  • focal segmental glomerulosclerosis
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84
Q

Glomerulonephritis

name some specific types

A
  • Minimal change disease
  • Focal segmental glomerulosclerosis
  • Membranous glomerulonephritis
  • IgA nephropathy (AKA mesangioproliferative glomerulonephritis or Berger’s disease)
  • Post streptococcal glomerulonephritis (AKA diffuse proliferative glomerulonephritis)
  • Mesangiocapillary glomerulonephritis
  • Rapidly progressive glomerulonephritis
  • Goodpasture Syndrome
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85
Q

glomerulonephritis

what are most types treated with

A
  • immunosuppression (e.g. steroids)

- BP control by blocking the renin-angiotensin system (ACEi or ARB)

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86
Q

glomerulonephritis

what might frothy urine suggest

A

proteinuria –> nephrotic syndrome

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87
Q

glomerulonephritis

what may nephrotic syndrome predispose pts to

A
  • thrombosis
  • HTN
  • high cholesterol
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88
Q

glomerulonephritis

what is the most common cause of nephrotic syndrome in children

cause and trx

A

minimal change disease

idiopathic
steroids

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89
Q

glomerulonephritis

what is the most common cause of nephrotic syndrome in adults

A

focal segmental glomerulosclerosis

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90
Q

glomerulonephritis

what is IgA nephropathy aka

A

Berger’s disease

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91
Q

glomerulonephritis

what is the most common cause of primary glomerulonephritis (not caused by another disease)

A

IgA nephropathy (Berger’s disease)

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92
Q

glomerulonephritis

what is the peak age of presentation of IgA nephropathy (Berger’s disease)

A

20s

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93
Q

glomerulonephritis

what does histology show in IgA nephropathy (Berger’s disease)

A

IgA deposits and glomerular mesangial proliferation

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94
Q

glomerulonephritis

what is the most common glomerulonephritis overall

A

membranous glomerulonephritis

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95
Q

glomerulonephritis

what is the peak age in Membranous glomerulonephritis

A

bimodal peak in age in the 20s and 60s

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96
Q

what does histology show in Membranous glomerulonephritis

A

IgG and complement deposits on the basement membrane

97
Q

what are the causes of Membranous glomerulonephritis

A

70% are idiopathic

can be secondary to malignancy, rheumatoid disorders and drugs (NSAIDs)

98
Q

what is Post streptococcal glomerulonephritis aka

A

diffuse proliferative glomerulonephritis

99
Q

how old are patients usually in Post streptococcal glomerulonephritis

100
Q

how does Post streptococcal glomerulonephritis present

A
  • 1-3w after streptococcal infection (e.g. tonsillitis or impetigo)
  • nephritic syndrome
  • usually a full recovery
101
Q

Ddx for a patient with acute renal failure and haemoptysis

A
  • Goodpasture syndrome

- Wegener’s granulomatosis

102
Q

pathophysiology of Goodpasture syndrome

A

Anti-GBM antibodies attack glomerulus and pulmonary basement membranes

this causes glomerulonephritis and pulmonary haemorrhage

103
Q

what antibody is Goodpasture syndrome associated with

A

anti-GBM antibodies

104
Q

what antibody is Wegener’s granulomatosis associated with

105
Q

how may a pt with Wegener’s granulomatosis present

A
  • haemoptysis
  • acute renal failure
  • wheeze
  • sinusitis
  • saddle-shaped nose
106
Q

what does histology show in rapidly progressive glomerulonephritis

A

crescentic glomerulonephritis

107
Q

how does rapidly progressive glomerulonephritis present

A

a very acute illness with sick pts

but responds well to trx

108
Q

cause of rapidly progressive glomerulonephritis

A

often secondary to Goodpasture’s syndrome

109
Q

Haemolytic Uraemic Syndrome

classic triad

A
  1. haemolytic anaemia
  2. AKI
  3. low platelet count
110
Q

Haemolytic Uraemic Syndrome

what is it

A

when there is thrombosis in small blood vessels throughout the body

usually triggered by the shiga toxin

111
Q

Haemolytic Uraemic Syndrome

how does thrombocytopenia happen

A

the formation of blood clots consumes platelets

112
Q

Haemolytic Uraemic Syndrome

how does anaemia happen

A

the blood clots within the small vessels chop up the RBCs as they pass by (haemolysis) causing anaemia

113
Q

Haemolytic Uraemic Syndrome

how does AKI occur

A

the blood flow through the kidney is affected by the clots and damaged RBCs leading to AKI

114
Q

Haemolytic Uraemic Syndrome

what produces the shiga toxin

A

e.coli 0157 (most common)

Shigella

115
Q

Haemolytic Uraemic Syndrome

what increases the risk of developing HUS

A

use of abx and anti-motility medications such as loperamide to treat gastroenteritis

116
Q

Haemolytic Uraemic Syndrome

presentation

A

e.coli 0157 causes brief gastroenteritis with bloody diarrhoea

5d after:

  • reduced urine output
  • haematuria or dark brown urine
  • abdo pain
  • lethargy + irritability
  • confusion
  • HTN
  • bruising
117
Q

Haemolytic Uraemic Syndrome

mnx

A

medical emergency

supportive mnx:

  • antihypertensives
  • blood transfusions
  • dialysis
118
Q

Hyperkalaemia

main complication

A

cardiac arrhythmias such as ventricular fibrillation

119
Q

Hyperkalaemia

causes (5) (from conditions)

A
  • AKI
  • CKD
  • Rhabdomyolysis
  • adrenal insufficiency
  • tumour lysis syndrome
120
Q

Hyperkalaemia

causes (5) (from medications)

A
  • aldosterone antagonists (spironolactone + eplerenone)
  • ACEi
  • Angiotensin II receptor blockers
  • NSAIDs
  • potassium supplements
121
Q

Hyperkalaemia

diagnosis

A

U&E blood test

but pay attention to Cr, urea, eGFR for kidney failure

122
Q

Hyperkalaemia

what may lead to a falsely elevated potassium

A

haemolysis (breakdown of RBCs) during sampling

123
Q

Hyperkalaemia

what inx is required with a K >6mmol/L

124
Q

Hyperkalaemia

what are the ECG changes

A
  • tall peaked T waves
  • flattening or absence of P waves
  • broad QRS complexes
125
Q

Hyperkalaemia

mnx for K ≤ 6 mmol/L with otherwise stable renal function

A
  • don’t need urgent trx

- change in diet + meds

126
Q

Hyperkalaemia

mnx for pts with potassium ≥ 6 mmol/L and ECG changes

A

urgent treatment

127
Q

Hyperkalaemia

mnx for pts with potassium ≥ 6.5 mmol/L regardless of the ECG

A

urgent trx

128
Q

Hyperkalaemia

what is the mainstay of trx

A

insulin (actrapid 10U) + dextrose infusion (50ml of 50%)

IV calcium gluconate

129
Q

Hyperkalaemia

what does the insulin and dextrose infusion do

A

drives carbohydrates into cells and takes K with it, reducing the blood K

130
Q

Hyperkalaemia

what does calcium gluconate do

A

stabilise the cardiac muscle cells and reduces the risk of arrhythmias

131
Q

Hyperkalaemia

what other options lower the K (apart from insulin, dextrose + calcium gluconate)

A
  • neb salbutamol
  • IV fluids
  • PO calcium resonium
  • sodium bicarb
  • dialysis
132
Q

Hyperkalaemia

how does neb salbutamol work

A

temporarily drives K into cells

133
Q

Hyperkalaemia

how do IV fluids help

A
  • increases urine output

which encourages K loss from the kidneys

134
Q

Hyperkalaemia

how does PO calcium resonium work

A

draws K out the gut and into the stools

works slowly and suitable for milder cases

135
Q

Hyperkalaemia

how does sodium bicarb work

A

for acidotic patients with renal failure

it drives K into cells as the acidosis is corrected

136
Q

Hyperkalaemia

when would dialysis be required

A

in severe or persistent cases associated with renal failure

137
Q

what trx do you give before a CT scan with IV contrast to someone with CKD

A

IV 0.9% NaCl

volume expansion reduces risk of contrast nephropathy

138
Q

Renal Tubular Acidosis

what is it

A

metabolic acidosis due to pathology in the tubules of the kidney

there are 4 types

139
Q

Renal Tubular Acidosis

what are the tubules responsible for

A

balancing H+ and HCO3- between the blood and urine

and maintaining a normal pH

140
Q

Renal Tubular Acidosis

which types are most relevant in clinical practice and may come up in exams

A

type 1 and 4

141
Q

Renal Tubular Acidosis

what is type 1

A

the distal tubule is unable to excrete H+

142
Q

Renal Tubular Acidosis

causes of type 1

A
  • genetic: autosomal + recessive
  • SLE
  • Sjogren’s syndrome
  • PBC
  • hyperthyroidism
  • sickle cell anaemia
  • Marfan’s syndrome
143
Q

Renal Tubular Acidosis

type 1 presentation

A
  • failure to thrive in children
  • hyperventilation to compensate for the metabolic acidosis
  • CKD
  • bone disease (osteomalacia)
144
Q

Renal Tubular Acidosis

inx findings in type 1

A
  • hypokalaemia
  • metabolic acidosis
  • high urinary pH>6
145
Q

Renal Tubular Acidosis

trx in type 1

A

PO bicarbonate

146
Q

Renal Tubular Acidosis

what is type 2

A

the proximal tubule is unable to reabsorb HCO3- from the urine into the blood

XS HCO3- is excreted in the urine

147
Q

Renal Tubular Acidosis

what is the main cause of type 2

A

Fanconi’s syndrome

148
Q

Renal Tubular Acidosis

inx findings in type 2

A
  • hypokalaemia
  • metabolic acidosis
  • high urinary pH>6
149
Q

Renal Tubular Acidosis

trx of type 2

A

PO bicarbonate

150
Q

Renal Tubular Acidosis

what is type 3

A

a combination of type 1 and 2 with pathology in the proximal and distal tubule

rare

151
Q

Renal Tubular Acidosis

what is type 4 caused by

A

reduced aldosterone:

  • adrenal insufficiency
  • ACEi + spironolactone
  • SLE, diabetes, HIV affect the kidneys
152
Q

Renal Tubular Acidosis

what is the most common type

153
Q

Renal Tubular Acidosis

Type 4 inx findings

A
  • hyperkalaemia
  • high chloride
  • metabolic acidosis
  • low urinary pH
154
Q

Renal Tubular Acidosis

mnx of type 4

A
  • fludrocortisone
  • sodium bicarb
  • trx of the hyperkalaemia may be required
155
Q

pt presents with haematuria following a URTI. What is it

A

IgA nephropathy

156
Q

classic presentation of a pt with acute interstitial nephritis

A
  • non-oliguric acute renal failure
  • hypersensitivity triad: rash, fever, eosinophilia
  • triggered by medication
157
Q

presentation of a pt with acute glomerulonephritis

A
  • haematuria
  • oligouria
  • HTN
  • mil/mod proteinuria
158
Q

peritoneal dialysis fluid is cloudy. pt presents with fever and abdo pain. What is the most likely organism

A

staph epidermidis from translocated skin flora

159
Q

what antibodies will be raised in post-strep glomerulonephritis

A

anti-streptolysin O antibodies

160
Q

what are contraindications for a renal transplant

A
  • cancer
  • active infections
  • severe co-morbidity
161
Q

PKD

what is it

A

a genetic condition where the kidneys develop multiple fluid filled cysts

162
Q

PKD

what findings outside the kidneys is PKD associated with

A
  • hepatic cysts

- cerebral aneurysms (SAH!)

163
Q

PKD

what may be felt on examination

A

palpable enlarged kidneys

164
Q

PKD

what are the types

A

autosomal dominant

autosomal recessive

165
Q

PKD

dx

A

US and genetic testing

166
Q

PKD

what genes are affected in the autosomal dominant type

A

PKD-1: Ch16 (85% cases)

PKD-2: Ch4

167
Q

PKD

autosomal dominant type extra-renal manifestations

A
  • cerebral aneurysms
  • hepatic, splenic, pancreatic, ovarian + prostatic cysts
  • cardiac valve disease (mitral regurg)
  • colonic diverticula
  • aortic root dilatation
168
Q

PKD

autosomal dominant type complications

A
  • chronic loin pain
  • HTN
  • CVD
  • gross haematuria (cyst ruptures)
  • renal stones
  • end-stage renal failure
169
Q

PKD

what is the autosomal recessive type caused by

A

a gene on Ch6 (rarer and more severe)

170
Q

PKD

how does autosomal recessive type often present as

A

in pregnancy with oligohydramnios as the fetus does not produce enough urine

171
Q

PKD

why do neonates present with resp failure shortly after birth in the autosomal recessive type

A

oligohydramnios leads to underdevelopment of the lungs

172
Q

PKD

what dysmorphic features are present in the autosomal recessive type

A
  • underdeveloped ear cartilage
  • low set ears
  • flat nasal bridge
173
Q

PKD

what may pts have before reaching adulthood in autosomal recessive type

A

end stage renal failure

174
Q

PKD

medication mnx in autosomal dominant PKD

A

Tolvaptan (vasopressin receptor antagonist)

can slow the development of cysts and progression of renal failure

175
Q

PKD

supportive mnx for complications

A
  • antihypertensives
  • analgesia (renal colic)
  • abx
  • drainage of infected cysts
  • dialysis
  • renal transplant
176
Q

PKD

monitor

A
  • US
  • bloods for renal function
  • BP
  • MR angiogram to dx intracranial aneurysms
177
Q

PKD

why avoid contact sport

A

risk of cyst rupture

178
Q

what is fibromuscular dysplasia

A

a group of non-atherosclerotic, non-inflammatory arterial diseases that most commonly involve the renal and carotid arteries

179
Q

‘string of beads’ appearance on MRI angiography

what is it

A

fibromuscular dysplasia

180
Q

Dialysis

what is it

A

a method for performing the filtration tasks of the kidneys artificially in patients with end stage renal failure or complications of renal failure

removes excess fluid, solutes and waste products

181
Q

Dialysis

indications for acute dialysis in pt with a severe AKI

A

AEIOU

  • acidosis
  • electrolyte abnormalities
  • intoxication of certain meds
  • Oedema
  • uraemia sx e.g. seizures, reduced consciousness
182
Q

Dialysis

indications for long term dialysis

A
  • end stage renal failure (CKD stage 5)

- any of the acute indications continuing long term (AEIOU)

183
Q

Dialysis

what are the 3 main options for dialysis in pts requiring it long term

A
  • continuous ambulatory peritoneal dialysis
  • automated peritoneal dialysis
  • haemodialysis
184
Q

Dialysis

what is peritoneal dialysis

A

uses the peritoneal membrane as the filtration membrane

a special dialysis solution containing dextrose is added to peritoneal cavity

Ultrafiltration occurs from the blood, across the peritoneal membrane, in to the dialysis solution

dialysis solution is then replaced, taking away the waste products that have filtered out of the blood into the solution

185
Q

Dialysis

what is used for inserting and removing dialysis solution in peritoneal dialysis

A

Tenckhoff catheter

186
Q

Dialysis

what is continuous ambulatory peritoneal dialysis

A

the dialysis solution is in the peritoneum at all times.

187
Q

Dialysis

what is automated dialysis

A

A machine continuously replaces dialysis fluid in the abdomen overnight to optimise ultrafiltration

188
Q

Dialysis

complications of peritoneal dialysis

A
  • bacterial peritonitis
  • peritoneal sclerosis
  • ultrafiltration failure
  • weight gain
  • psychosocial effects
189
Q

Dialysis

what is ultrafiltration failure (in peritoneal dialysis)

A

pt absorbs dextrose in the filtration solution

which reduces the filtration gR aking ultrafilrtation less effective

190
Q

Dialysis

how can weight gain occur? (in peritoneal dialysis)

A

as they absorb carbs in the dextrose solution

191
Q

Dialysis

what is haemodialysis

A

their blood is filtered by a haemodialysis machine

192
Q

Dialysis

options for haemodialysis

A

They need good access to an abundant blood supply:

  • tunnelled cuffed catheter
  • arterio-venous fistula
193
Q

Dialysis

what is a tunnelled cuffed catheter (haemolysis)

A

a tube inserted into the subclavian or jugular vein with a tip that sits in the superior vena cava or right atrium

194
Q

Dialysis

what does the Dacron cuff on the tunnelled cuffed catheter do

A

promotes healing and adhesion of tissue to the cuff, making the catheter more permanent

provides a barrier to bacterial infection.

195
Q

Dialysis

what is the main complication of tunnelled cuffed catheters

A

infection and blood clots within the catheter

196
Q

Dialysis

what is an AV fistula

A

an artificial connection between an artery to a vein

bypasses the capillary system and allows blood to flow under high pressure from the artery directly into the vein

197
Q

Dialysis

name some options of AV fistulas

A
  • Radio-cephalic
  • Brachio-cephalic
  • Brachio-basilic (less common and more complex operation)
198
Q

Dialysis

how would you examine an AV fistula

A
  • skin integrity
  • aneurysms
  • palpable thrill (a fine vibration felt over the anastomosis)
  • machinery murmur on auscultation
199
Q

Dialysis

AV fistula complications

A
  • Aneurysm
  • Infection
  • Thrombosis
  • Stenosis
  • STEAL syndrome
  • High output heart failure
200
Q

Dialysis

AV fistula complications: what is STEAL syndrome

A

inadequate blood flow to the limb distal to the AV fistula.

The AV fistula “steals” blood from the distal limb

201
Q

Dialysis

AV fistula complications: how does STEAL syndrome cause distal ischaemia

A

the blood is diverted away from where is was supposed to supply and flows straight into the venous system

202
Q

Dialysis

AV fistula complications: why is there high output heart failure

A
  • rapid return of blood to the heart
  • increased pre-load in the heart (how full the heart is before it pumps). - This leads to hypertrophy of the heart muscle and heart failure.
203
Q

Dialysis

can you take blood from a fistula

A

NO

This is a lifeline for the patient to allow them access to dialysis. If it gets damaged it will set them back and you will be in big trouble.

204
Q

what is the most common cause of glomerular pathology and CKD in the UK

A

diabetic nephropathy

205
Q

Diabetic Nephropathy

what is glomerulosclerosis

A

The chronic high level of glucose passing through the glomerulus causes scarring

206
Q

Diabetic Nephropathy

why is there proteinuria

A

damage to the glomerulus allows protein to be filtered from blood to urine

207
Q

Diabetic Nephropathy

diabetics should have regular screening for diabetic nephropathy by testing what?

A

albumin:creatinine ratio and U&Es.

208
Q

Diabetic Nephropathy

what is the trx of choice in diabetics for BP control

209
Q

Diabetic Nephropathy

pt has diabetic nephropathy but a normal BP, should you start ACEi

210
Q

Interstitial Kidney Disease

what is interstitial nephritis

A

inflammation of the space between cells and tubules (the interstitium) within the kidney

211
Q

Interstitial Kidney Disease

what is glomerulonephritis

A

inflammation around the glomerulus

212
Q

Interstitial Kidney Disease

what are the 2 types of interstitial nephritis

A
  • acute interstitial nephritis

- chronic tubulointerstitial nephritis

213
Q

Interstitial Kidney Disease

presentation of acute interstitial nephritis

A
  • AKI
  • hypertension
    generalised hypersensitivity reaction:
  • rash
  • fever
  • eosinophilia
214
Q

Interstitial Kidney Disease

what is acute interstitial nephritis

A

acute inflammation of the tubules and interstitium

usually caused by a hypersensitivity reaction

215
Q

Interstitial Kidney Disease

cause of acute interstitial nephritis

A

a hypersensitivity reaction to:

  • Drugs (e.g. NSAIDS or abx)
  • Infection
216
Q

Interstitial Kidney Disease

mnx of interstitial nephritis

A
  • treat underlying cause

- steroids

217
Q

Interstitial Kidney Disease

what is chronic tubulointerstitial nephritis

A

chronic inflammation of the tubules and interstitium.

218
Q

Interstitial Kidney Disease

presentation of chronic tubulointerstitial nephritis

219
Q

Interstitial Kidney Disease

cause of chronic tubulointerstitial nephritis

A

large number of underlying autoimmune, infectious, iatrogenic and granulomatous disease causes

220
Q

Interstitial Kidney Disease

mnx of chronic tubulointerstitial nephritis

A
  • treat underlying cause

- steroids

221
Q

Rhabdomyolysis

what is it

A

skeletal muscle tissue breaks down and releases breakdown products into the blood

222
Q

Rhabdomyolysis

triggers

A

extreme underuse or overuse or a traumatic injury

223
Q

Rhabdomyolysis

what does muscles cell death (apoptosis) release

A
  • myoglobin (causing myoglobinurea)
  • potassium
  • phosphate
  • creatine kinase
224
Q

Rhabdomyolysis

what is the most immediately dangerous breakdown product and why

A

Potassium

hyperkalaemia can cause cardiac arrhythmias that can potentially result in a cardiac arrest

225
Q

Rhabdomyolysis

why does AKI occur

A

the breakdown products are filtered by the kidney and cause injury to the kidney

Myoglobin is particular toxic to the kidney in high concs

226
Q

Rhabdomyolysis

causes

A
  • prolonged immobility
  • extremely rigorous exercise
  • crush injuries
  • seizures
227
Q

Rhabdomyolysis

signs + sx

A
  • muscle aches + pain
  • oedema
  • fatigue
  • confusion
  • red-brown urine
228
Q

Rhabdomyolysis

what is the key inx in establishing dx

A

Creatine kinase (CK)

229
Q

Rhabdomyolysis

what causes the urine to be a red-brown colour

A

myoglobinurea (myoglobin in the urine)

230
Q

Rhabdomyolysis

inx

A
  • CK
  • urine dipstick (+ve for blood)
  • U&E: AKI, hyperkalaemia
  • ECG: hyperkalaemia
231
Q

Rhabdomyolysis

mnx

A
  • IV fluids
  • consider IV sodium bicarb (to make urine more alkaline)
  • consider IV mannitol
  • treat complications esp hyperkalaemia
232
Q

Rhabdomyolysis

why would you consider IV mannitol as trx

A
  • to increase GFR to help flush the breakdown products

- reduce oedema surrounding muscles + nerves

233
Q

Rhabdomyolysis

what arrhythmia can hyperkalaemia cause

A

ventricular fibrillation

234
Q

what is a common side effect of tacrolimus

235
Q

difference in presentation between IgA nephropathy and post-streptococcal glomerulonephritis

A

igA: 1-2 days after a URTI

post-strep: 1-2 weeks

236
Q

lady trying to conceive and has G6PD deficiency

she has a UTI. what do you prescribe

A

Cefalexin

nitrofurantoin is CI’d with G6PD deficiency

237
Q

drug which causes acute interstitial nephritis

238
Q

sudden headache. PMH: autosomal dominant kidney disease

what is it

A

subarachnoid haemorrhage

APKD is associated with subarachnoid haemorrhage

Finals (47 decks)

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