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3b General care > Nephrology > Flashcards

Nephrology Flashcards

1
Q

List examples of loop diuretics

A

furosemide, bumetanide

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2
Q

How do loop diuretics work?

A

inhibit the Na/K/Cl co transporter in the loop of henle so reduce the absorption of NaCl

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3
Q

What are the adverse effects of loop diuretics?

A

hypokalaemia, hypomagnesaemia, hypocalcaemia, hyponatraemia
hypotension
gout

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4
Q

List examples of thiazide diuretics

A

indapamide , bendroflumethiazide

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5
Q

How do thiazide diuretics work?

A

inhibit the sodium reabsorption in the distal convoluted tubule by blocked Na/Cl symporter

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6
Q

What are the adverse effects of thiazide diuretics?

A 
dehydration
hyponatraemia, hypokalaemia
gout
postural hypotension 
impaired glucose tolerance
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7
Q

List examples of potassium sparing diuretics and how they work

A

sodium channel blockers -> amiloride

aldosterone antagonists at the mineralocorticoid receptor at the DCT -> spironolactone

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8
Q

What are the adverse effects of potassium sparing diuretics?

A

dizziness
malaise
AKI
hyperkalaemia *

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9
Q

What is creatinine?

A

product of muscle metabolism and measure of kidney function

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10
Q

Where does sodium reabsorption occur?

A

70% - proximal tubule
25% - loop of henle
5% - DCT

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11
Q

Describe how blood pressure is controlled by the kidney?

A
  1. low blood pressure detected by the afferent arteriole in the kidney
  2. juxtaglomerular apparatus activated
  3. kidney secretes renin
  4. renin converts angiotensinogen to angiotensin 1
  5. ACE converts angiotensin 1 to angiotensin 2
  6. activates aldosterone in the adrenal glands to stimulate reabsorption of salt and water
  7. acts directly on blood vessels to cause vasoconstriction
  8. results in rise in blood pressure
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12
Q

List the 5 functions of the kidney

A
  1. remove waste products in the urine (e.g. drugs, toxins, products of metabolism)
  2. regulates water in body and blood pressure
  3. produces EPO for RBC production
  4. activates vitamin D into 1- hydroxy- vitamin D
  5. acid base balance (removes H+ and absorbs HCO3)
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13
Q

Define AKI?

A

acute insult in GFR from baseline, increase in creatinine +/- oliguria (<0.5 ml/kg/hr)

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14
Q

List the pre renal causes of AKI

A

= problems in other major organs causing impaired renal perfusion

renal artery stenosis
heart failure
sepsis
ischaemia
hypovolaemia e.g. vomiting, diarrhoea
hypotension 
hepatorenal syndrome
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15
Q

List the intrinsic causes of AKI

A

= damage to the glomeruli, renal tubules or interstitium of the kidneys

glomerulonephritis
acute tubular necrosis 
toxins and drugs 
interstitial nephritis
IgA nephropathy
tumour lysis syndrome 
rhabdomyolysis
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16
Q

List the post renal causes of AKI

A

= problems after the kidneys e.g. obstruction to urine coming from kidneys

INTRINSIC - stones, tumour, pyelonephritis

EXTRINSIC - BPH, tumour, retroperitoneal fibrosis

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17
Q

Which drugs are nephrotoxic and can cause an AKI

A 
NSAIDS
ACE-I
ARBs
gentamicin
diuretics
omeprazole
anti fungals
rifampicin 
radio iodine contrast
lithium
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18
Q

List the risk factors for an AKI

A 
elderly
drugs and toxins 
IV contrast 
organ dysfunction e.g. liver disease, CKD, heart failure, diabetes
multiple myeloma
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19
Q

How does AKI present?

A

often asymptomatic and found on bloods but can cause…

reduced urine output (<0.5 ml/kg/hr) **
nausea and vomiting
peripheral oedema
uraemia signs

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20
Q

What is the criteria for an AKI?

A

** rise in creatinine >26mmol/l in 48 hrs **

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21
Q

How is an AKI staged?

A

stage 1 =
1.5- 1.9 X baseline creatinine OR
UO <0.5 ml/kg/hr for 6-12 hours

stage 2 =
2-2.9 x baseline creatinine
UO <0.5 ml/lg/hr for >12 hours

stage 3 = 3 x baseline creatinine
UO <0.3 ml/kg/hr for >24 hrs

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22
Q

How is AKI diagnosed and investigated?

A

U&E
Creatinine elevated (normal 0.7 -1.2 mg/dL) - not best early indicator as wont change until next day so measure UO
high serum potassium
metabolic acidosis

** renal ultrasound **
do 24 hrs after AKI if dont know cause

find the cause…
urine dip and urinanalysis, FBC, ECG, blood cultures, vasculitis screen, renal biopsy

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23
Q

How is AKI managed?

A
  1. ABCDE - fluids
  2. review medication
    stop nephrotoxic drugs or renally excreted drugs
  3. monitor urine output - catheterise
  4. treat hyperkalaemia
  5. if not responding, RRT
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24
Q

When is RRT indicated in AKI?

A 
uraemia 
no urine output and fluid overload
severe resistent hyperkalaemia 
severe metabolic acidosis
overdose of lithium
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25
Q

Which drugs are renally excreted and should be stopped in AKI to prevent toxicity?

A

metformin
lithium
digoxin
opioids e.g. codeine, tramadol

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26
Q

Define CKD

A

> 3 months of proteinuria or haematuria +/- reduction in GFR to <60ml/min/1.73m^2

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27
Q

What are the causes of CKD?

A

Diabetic nephropathy **
hypertension *
renal vascular disease*

+
glomerulonephritis (nephrotic/ nephritic) - focal segmental glomerulosclerosis, membranous nephropathy, lupus nephritis, amyloidosis
PKD
obstructive uropathy e.g. myeloma, renal tumour

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28
Q

what are the symptoms of CKD?

A 
extreme fatigue **
weakness * 
peripheral oedema **
pruritus 
anorexia / weight gain / poor appetite
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29
Q

What are the complications of CKD?

A

anaemia ** (reduced EPO and iron deficiency)
renal osteodystrophy (due to decreased phosphate excretion)
CV disease
hyperkalaemia
pulmonary oedema
metabolic acidosis
secondary hyperparathyroidism

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30
Q

Why do pts get anaemia in CKD?

A

Lack of EPO produced by kidneys + iron deficiency

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31
Q

What are the stages of CKD?

A

STAGE 1 - eGFR >90

STAGE 2 - eGFR 60-89

STAGE 3a - eGFR 45-59

STAGE 3b - eGFR 30-44

STAGE 4- eGFR 15-29

STAGE 5 - eGFR <15 (start RRT)

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32
Q

How is the eGFR calculated?

A

estimate of renal function using a formula that calculates it by:

  • creatinine
  • age
  • ethnicity
  • gender
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33
Q

How is CKD investigated?

A
  1. serum creatinine
  2. renal USS
  3. eGFR <60
  4. urine albumin creatinine ratio (proteinuria) HIGH
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34
Q

How is CKD managed?

A
  1. find the cause -> control diabetes, statins, weight loss, smoking cessation
  2. manage HTN -> ACE-I with target <130/90
  3. manage anaemia -> epoitin alfa + ferrous sulphate (side effects of EPO = urticaria, HTN, bone aches)
  4. manage oedema -> loop diuretic, restrict salt
  5. manage renal bone disease -> vit D, calcium rich diet
  6. RRT if stage 5 (5-7 eGFR) or palliative care
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35
Q

What are the options in renal replacement therapy?

A
  1. haemodialysis
  2. peritoneal dialysis
  3. renal transplant
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36
Q

Who is haemodialysis most suitable for?

A

elderly, frail, if unsuitable for surgery or at home dialysis (most common for)

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37
Q

How can you maximise your kidney function before starting haemodialysis?

A 
smoking cessation
manage HTN
good glycemic control in diabetics 
salt restriction 
activated VIT D supplement 
weight loss
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38
Q

how does haemodialysis work?

A
  1. blood removed from AV fistula on the arterial side
  2. blood enters dialyzser
  3. dalteparin added to prevent clots
  4. blood passed over semi permeable membrane against dialysis fluid - small solutes diffuse across along conc gradient and waste products diffuse out
  5. blood travels through venous pressure monitor and air detector
  6. waste products in dialysis fluid removed
  7. clean purified blood returned to vein in AV fistula
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39
Q

Where do they get access for haemodialysis?

A

via arterio-venous fistula **

created 8 weeks before start dialysis

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40
Q

What are the adverse effects of an AV fistula?

A

bulging veins
cold hands
gangrene
heart failure

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41
Q

What is the regimen for haemodialysis?

A

3 x a week at the hospital for 4 hours at a time

OR 5 x per week for 2-3 hours at home

42
Q

How do patients feel after haemodialsysi?

A

tired, hypotensive, dizzy, unwell, sweaty

43
Q

What are the short and long term complications of haemodialysis?

A

access complications e.g. infection, thrombus, endocarditis
no urine output
fluid restrictions e.g. 500ml-1L a day
feel unwell: nausea, vomiting, headache, tired
pyschosocial impact and lifestyle change
hyperparathyroidism
cardiac arrhythmias

44
Q

Who is peritoneal dialysis suitable for?

A

young, independent, lack of access to healthcare, eGFR 11-12

45
Q

How does peritoneal dialysis work?

A
  1. dialysate fluid infused into peritoneal cavity via catheter
  2. high dextrose conc solutions draws water via osmosis and waste products via diffusion from the blood into the abdo cavity via peritoneum
  3. after several hours of dwell time, dialysis solution drained and remove waste products from body
  4. exchange for new dialysis solution
46
Q

What is the regimen for peritoneal dialysis?

A
  1. CONTINUOUS AMBULATORY PERITONEAL DIALYSIS - each exchange 30 mins and dwell time 4-8 hours, pt can go about normal activities during that time
  2. AUTOMATED PERITONEAL DIALYSIS
    3-5 exchanges over 8-10 hours overnight when pt asleep
47
Q

What are the contraindications for peritoneal dialysis?

A 
abdo adhesions
previous mutliple abdo surgery
stoma
obesity 
intestinal disease
48
Q

What are the complications of peritoneal dialysis?

A
  1. peritonitis **
  2. catheter problems e.g. infection, leak, blockages
  3. constipation
  4. weight gain, fluid retention
  5. hernia
49
Q

When would you suspect peritonitis in PD?

A

cloudy PD effluent
abdo pain
fever
tenderness

50
Q

How is peritonitis in PD pts treated?

A

gentamicin or vancomycin

51
Q

What are the advantages of kidney transplants?

A

increased survival
enable pregnancy
reverse SE e.g. anaemia, renal bone disease
increased quality of life

52
Q

Who are kidney transplants suitable for?

A

young, fit patients that still have 5 years of good quality of life after transplant

53
Q

What are the 2 types of kidney transplant?

A
  1. cadaveric ** - 10-12 years lifespan

2. living donor- 12-15 years lifespan

54
Q

What are the disadvantages of kidney transplant?

A

long waiting time (>3 years wait)
technical - difficulty storing and retrieving
rejection
disease recurrence
operation complications e.g. infection, pain, DVT
side effects of immunosuppression: skin cancer, infection

55
Q

What do the pts need to match to receive a kidney transplant?

A
  1. ABO blood group
  2. HLA tissue match
  3. antibody screening
56
Q

Describe the procedure for a kidney transplant?

A
  1. induction with basiliximab and IV methylpred
  2. surgery - donor kidney transplanted into the groin connecting to the external iliac veins
  3. long term immunosuppression - increases risk of skin cancer and CMV
57
Q

Which medication for immunosupression are pts on after a kidney transplant?

A
  1. prednisolone
  2. calcineurin inhibitors e.g. tacrolimus, ciclosporin
  3. azathioprine
58
Q

What are the 4 types of rejection after a kidney transplant?

A
  1. HYPERACUTE (mins)
  2. ACCELERATED (days) -> fever, swollen kidney, rising creatinine
  3. ACUTE CELLULAR (weeks) -> fluid retention, rising BP, rising creatinine
  4. CHRONIC (years) -> graft biopsy shows fibrosis, atrophy and vascular changes

acute <6 months
chronic >6 months

59
Q

What type of cancer is common in Renal cell carcinoma?

A

adenocarcinoma from the proximal tubule epithelium (COMMONLY CLEAR CELL)

60
Q

What are the possible risk factors for RCC?

A 
smoking *
hypertension *
irradiation
FH
Von Hippel Lindau disease
obesity
renal transplant and dialysis
61
Q

How does RCC present?

A

TRIAD OF:

  1. haematuria
  2. loin pain
  3. abdominal mass

+ weight loss, malaise, anorexia, L varicocele (compresses the L testicular vein)

62
Q

How can RCC spread?

A

25% have mets at presentation
LOCAL -> Renal vein
LYMPH -> to para aortic and hilar lymph nodes (cause CANON BALL LUNG METS)
BLOOD -> bone, liver, lung

63
Q

How is RCC diagnosed?

A
  1. BP rise (renin secretion from tumour)
  2. urine microscopy and culture - haematuria
  3. FBC, ESR, U&E - polycythaemia (EPO secretion from tumour), raised ESR
  4. ULtrasound or CT
64
Q

How is RCC managed?

A
  1. radical nephrectomy

2. biological therapies e.g. sunitib (tyrosine kinase inhibitors)

65
Q

How is RCC staged using TNM?

A

T1 - confined to kidney and <7 cm
T2 - confined to kidney and >7cm
T3 - major veins or adrenals
T4 - beyond gerota fascia

66
Q

Which bacteria causes pyelonephritis?

A

E.coli **
klebsiella
proteus

(bacteria ascends from lower urinary tract or spreads haematogenously)

67
Q

What are the risk factors for pyelonephritis?

A
  1. age - elderly, young
  2. foreign bodies - catheter, cystoscopy, stones
  3. anatomical variants - PKD, horseshoe kidney, double ureter
  4. obstruction- BPH, stones, neurogenic bladder, bladder neck obstruction
  5. immunocompromised - diabetes, transplant pts, HIV, alcohol
  6. male sex
  7. pregnancy
68
Q

How does pyelonephritis present?

A
  1. loin pain
  2. fever
  3. renal tenderness

+ malaise, UTI symptoms (dysuria, increased urgency and frequency), rigors, nausea and vomiting

69
Q

What are the complications of pyelonephritis?

A 
urosepsis 
renal failure 
abscess formation
parenchymal renal scarring (look for hydronephrosis on USS)
recurrent UTIs
70
Q

How is pyelonephritis investigated?

A
  1. urine dipstick + midstream urinanalysis and MC&S - +ve WBC, RBC, gram stain
  2. septic screen - FBC, U&E, LFT, blood culture, ESR/CRP, ABG
  3. renal ultrasound and contrast CT
71
Q

How is pyelonephritis managed?

A
  1. IV ciprofloxacin 500mg (amoxicillin/ cefalexin for pregnancy)
  2. IV fluids
  3. IV paracetemol
72
Q

List the causes of hyperkalaemia

A

renal - AKI, CKD, renal tubular acidosis
drugs - potassium sparing diuretics, ACE-I, ARBs, NSAIDS, ciclosporin, beta blockers
metabolic acidosis
rhabdomyolysis
blood transfusion
Addisons
diet - banana, kiwi, orange, avocado

73
Q

How does hyperkalaemia present?

A

weakness and fatigue
flaccid paralysis
arrhythmias and chest pain
depressed tendon reflexes

74
Q

How would you investigate hyperkalaemia?

A
  1. 12 lead ECG
  2. ABG - metabolic acidosis
  3. U&E - high serum K
  4. review medication
75
Q

What changes would you see on ECG in hyperkalaemia?

A

tall tented T waves
loss of p waves
wide QRS
VF!!!

76
Q

How is hyperkalaemia managed?

A
  1. ABCDE and 12 lead ECG
  2. IV 10ml of 10% calcium gluconate - stabilises cardiac membrane (give up to 4 doses)
  3. insulin / 10% dextrose infusion of 250ml over 15 mins (shifts K to intracellular compartment)
  4. nebulised salbutamol
77
Q

How can polycystic kidney disease be inherited?

A
  1. AUTOSOMAL DOMINANT - more common

2. autosomal recessive - less common

78
Q

What happens in autosomal recessive PKD and how does it present?

A

defect in chromosome 6 encoding fibrocystin (needed fro renal tubule development)

detected on prenatal USS or early infancy
presents as potter syndrome or end stage renal failure

79
Q

What are the 2 types of autosomal dominant PKD?

A

ADPKD 1 -> chromosome 16 encoding polycystin 1 **

ADPKD 2 -> chromsome 4 encoding polycystin 2

80
Q

What does polycystin (the defect in ADPKD) do and how does it cause pathology?

A

polycystin 1 and 2 combine to make a protein complex in calcium regulation at actin and intermediate filaments

  • > disruption of polycystin causes imapired cell signalling and causes proliferation
  • > there is cyst expansion by fluid secretion
  • > cysts compress normal architecture and intrarenal vasculature
  • > leads to interstitial fibrosis and tubular atrophy
81
Q

How does AD PKD present?

A

abdo discomfort **
haematuria
hypertension **

+ palpable kidneys, hepatomegaly, UTI

82
Q

What are the possible complications of AD PKD?

A 
CKD
end stage renal failure
SAH
hypertension
hepatomegaly* (due to liver cysts)
mitral valve prolapse
83
Q

How is AD PKD diagnosed?

A

abdominal ultrasound and need:

  1. 2 cysts unilateral or bilateral if <30 y/o
  2. 2 cysts in both kidneys if 30-60 y/o
  3. 4 cysts in both kidneys if >60 y/o

+ genetic testing

84
Q

What is important to do in PKD?

A

family testing !! screen for SAH and HTN

85
Q

HOW is PKD managed?

A
  1. HTN -> ACE-I / ARB for life
  2. for ESRF -> RRT
  3. to slow progression -> tolvaptan (vasopressin receptor 2 antagonist)
86
Q

What are the causes of nephrotic syndrome?

A

Minimal change disease (children *)
focal segmental glomerulosclerosis (younger adults)
membranous glomerulonephritis (older adults)
amyloidosis
diabetic nephropathy

87
Q

What is the triad for nephrotic syndrome?

A
  1. peripheral oedema
  2. proteinuria
  3. hypoalbuminaemia
88
Q

what are the complications of nephrotic?

A

hyperlipidaemia
increased risk of thrombosis (renal vein thrombosis) -> loss of anti thrombin, protein C/S
increased risk of infection -> loss of IgG
hypocalcaemia -> vit D and albumin lost in urine
AKI

89
Q

How is nephrotic syndrome managed?

A
  1. find cause (renal biopsy = definitive **) and treat
  2. anti coagulant
  3. steroids
  4. penicillin prophylaxis and pneumococcal vaccination
  5. fluid restrict, restrict salt
  6. statin
90
Q

How is nephritic syndrome caused?

A

IgA nephropathy (Bergers disease) - post URTI
Alport syndrome
Goodpastures syndrome
vasculitis - wegeners, polyangitis

91
Q

What are the clinical features of nephritic syndrome?

A
  1. haematuria
  2. hypertension
  3. AKI

+ proteinuria, malaise, weight loss, fever, skin rash, abdo pain

92
Q

How is nephritic syndrome managed?

A

IV prednisolone

93
Q

What are the signs of uraemia?

A

altered mental state
pericarditis
arrhythmias
itch

94
Q

List the signs of rhabdomyolysis

A

tea coloured urine (myoglobin in urine)

confused

95
Q

List the signs O/E of CKD?

A 
pallor
peripheral oedema
hypertension
brusing
uraemia tinge
excoration
96
Q

list the side effects of ACE-I

A 
dry cough
nephrotoxic - cause AKI
hypotension
hyperkalaemia
urticaria
97
Q

How does rhabdomyolysis cause AKI?

A

breakdown of skeletal muscle causes release of creatinine kinase - causes acute tubular necrosis and creatinine obstructs tubercles

98
Q

List the causes of rhabdomyolysis?

A 
fall/ prolonged lying 
excessive exercise
crush injuries
burn 
drugs e.g. statin 
neuroleptic malignant syndrome 
seizures
99
Q

what is found in the urine in rhabdomyolysis?

A

urinary myoglobin

100
Q

what is the microscopy of the urine in rhabdomyolysis?

A

muddy brown granular casts

101
Q

what is found on histology of IgA nephropathy?

A

mesangial proliferation
IgA deposits
C3 deposits

3b General care (4 decks)

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