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YR6 Rotations > Medicine - Renal > Flashcards

Medicine - Renal Flashcards

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1
Q

What are the 2 main types of dialysis?

A

Haemodialysis
Peritoneal dialysis

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2
Q

What is required for haemodialysis?

A
  • Dialysis machine (patient’s blood is pumped OUTSIDE the body + through this machine)
  • Vascular access required via an AV fistula (longterm), or a temporary CVC
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3
Q

What happens inside a haemodialysis machine (broadly)?

A

Blood flows through tiny semi-permeable tubes surrounded by a dialysis solution (dialysate)
Filtration occurs via osmosis + diffusion - dialysis fluid contains solutes at a similar level to the level they would be in a healthy patient’s blood
Can add bicarbonate (to combat acidosis), EPO + drugs if needed
Heparin always added

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4
Q

How often should haemodialysis be performed?

A

4h treatment 3x per week

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5
Q

Give 5 complications of haemodialysis

A

Site infection
Stenosis at site
Bleeding
AV access steal syndrome
Dialysis disequilibrium syndrome

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6
Q

How many weeks does an AV fistula take to mature?

A

6-8w

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7
Q

What is Steal syndrome?

A

painful ischemia of the hand secondary to AV fistula or graft shunting blood away from the distal limb

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8
Q

How does peritoneal dialysis work?

A

Dialysis solution injected into abdo cavity through a permanent catheter.

High dextrose conc. of the solution draws waste products from blood into abdo cavity across the peritoneum.

After several hours of dwell time, the solution is drained, removing waste products from body, + exchanged for new dialysis solution.

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9
Q

What is Dialysis disequilibrium syndrome?

A

acute cerebral oedema secondary to rapid extraction of osmotically active substances (e.g., urea, NaCl) from the blood

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10
Q

What is continuous ambulatory peritoneal dialysis (CAPD)?

A

Patient operated- each exchange 30-40 mins + each dwell time 4-8h.
Patient can do normal activities with dialysis solution inside their abdomen

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11
Q

What is automated peritoneal dialysis (APD)?

A

dialysis machine fills + drains the abdomen while patient is sleeping, performing 3-5 exchanges over 8-10h each night

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12
Q

Give 3 advantages of PD

A
  • Offers more flexibility (can be done overnight)
  • Is better tolerated by patients
  • Less expensive
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13
Q

What is a tesio line?

A

Tunneled dual lumen central line
Used as a ‘bridge’ before an AV fistula can be put in
1 lumen enters the right atrium, the other sits outside the RA in the vena cava
Both lumens exit the body

(with a central line, only 1 lumen enters the skin)

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14
Q

Why is a normal vein unsuitable for haemodialysis, and why is an AV fistula used?

A

Normal vein would easily collapse/ thrombose with recurrent venepuncture
Vein in an AV fistula hypertrophies in response to turbulent flow of blood from artery + so can withstand repeated venepuncture

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15
Q

Recall some contra-indications to renal biopsy in acute renal failure

A
  • Obvious pre or post renal cause (these are contra-indications)
  • Significant coagulopathy
  • Infection at the site
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16
Q

What are the most common causes of AKI?

A

STOP:
- Sepsis/ dehydration
- Toxins (NSAIDs, nephrotoxic drugs),
- Obstruction in the urinary tract
- Parenchymal kidney disease

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17
Q

What are the most common causes of CKD?

A

Diabetic nephropathy
Hypertensive nephropathy
(PKD)

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18
Q

What are the primary functions of the kidney?

A

Salt + water balance

Acid base homeostasis

Endocrine function: vitamin D, EPO, renin-angiotensin system

Excrete waste

Electrolyte homeostasis

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19
Q

What symptoms might you expect from someone with CKD? (7)

A

Anaemia: SOB, fatigue, LoC, headache

Uraemia: encephalopathy, N+V, confusion, pruritis, pericarditis

Fluid overload: pedal oedema, pleural effusion, ascites, tiredness

Hyperkalaemia: palpitations, cardiac arrest, asymptomatic

Acidosis: N+V, tiredness

Increased drug action: opioid side effects

Reduced urine output

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20
Q

What diet should be followed in patients with very low creatinine clearance?

A

Low phosphate
(eg. avoid chocolate, shellfish, nuts)

Low K+ (avoid chocolate, bananas etc)

Fluid restricted (avoid alcohol + too much tea/ coffee)

Low salt (avoid processed foods)

Can take phosphate binders if diet restriction alone doesn’t succeed

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21
Q

Name one phosphate binder

A

Sevelamer

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22
Q

List 5 indications for emergency dialysis

A

A – Acidosis

E – Electrolyte imbalance (K+ >6.5, refractory to medical Mx)

I – Intoxication (certain drugs require dialysis to clear the blood)

O – Overload of fluid (refractory to diuretic Tx)

U – Uraemic encephalopathy + pericarditis

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23
Q

What mnemonic can be used for drugs that can be dialysed out?

A

BLAST
Barbiturates
Lithium
Alcohol
Salicylates
Theophylline

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24
Q

How does CKD affect phosphate and vitamin D?

A

1-alpha hydroxylation normally occurs in kidneys → leads to LOW vitamin D

kidneys normally excrete phosphate → leads to HIGH phosphate

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25
What problems arise from high phosphate and low vitamin D in CKD?
High phosphate level ‘drags’ calcium from bones→ osteomalacia Low calcium: due to lack of vitamin D + high phosphate Secondary hyperparathyroidism: due to low calcium, high phosphate + low vitamin D
26
Define acute kidney injury
Sudden decrease in GFR manifested by an increase in serum creatinine or oliguria over a period of hours/ weeks
27
What causes should be excluded first in AKI? Why?
Pre renal (hypovolaemia, sepsis) + post renal (stones, cancer) Renal causes require a biopsy
28
What can be used as an alternative to calcium gluconate in hyperkalaemia as a cardioprotective infusion?
Calcium chloride
29
How can AKI secondary to blood loss be differentiated into pre-renal and renal cause?
Pre: LOW urinary Na+ (hypovolaemia: kidneys hold on) Renal: HIGH urinary Na+ (ischaemia of tubules: loss)
30
How are intrinsic renal causes of AKI classified?
Glomerulonephritis: MCD, Membranous GN ATN: affects tubules AIN: affects surrounding tissue Vascular: small (microangiopathic- HUS, TTP) or large (obstructive- thrombosis/ emboli)
31
What is the cause of HUS? What triad os signs and symptoms does it present with?
E.coli toxin 0157 MAHA Thrombocytopenia AKI
32
What pentad of signs and symptoms characterises TTP?
MAHA Thrombocytopenia AKI Neurological impairment Fever
33
What characterises nephritic syndrome?
Haematuria Variable proteinuria Oliguria + red cell casts HTN
34
What is nephritic syndrome?
Subtype of intrinsic AKI with BLOOD + PROTEIN in urine indicative of glomerular disease
35
What is nephrotic syndrome?
1. Proteinuria (>3.5g/ 1.73m^2 body surface area/ 24h) 2. Hypoalbuminaemia (<30g/L) 3. Oedema (+ Hyperlipidaemia)
36
Name some proteins lost in nephrotic syndrome and the consequences of this
Loss of antithrombin-III, proteins C + S, + an associated rise in fibrinogen levels predispose to thrombosis. Loss of thyroxine-binding globulin lowers the total, but not free, thyroxine levels.
37
What causes the high level of proteinuria in nephrotic syndrome?
Injury of the podocyte (provides most of the protein filter barrier of the glomerulus)
38
Give 3 primary renal diseases presenting with nephrotic syndrome
Minimal change disease Membranous glomerulonephritis Focal Segmental Glomerular Sclerosis
39
Give 2 systemic causes presenting with nephrotic syndrome
Diabetes Amyloidosis
40
What is Chronic Kidney Disease?
Decrease in GFR present >3 months
41
Which 4 variables are used in the modification of diet in renal disease (MDRD) formula for eGFR?
Creatinine (serum) Age Gender Ethnicity
42
List 3 factors that will affect the MDRD estimation of GFR
Pregnancy Muscle mass (e.g. amputees (lower Cr), body-builders (higher Cr)) Eating red meat 12h prior to the sample being taken
43
What is Proliferative glomerulonephritis characterised by?
Increased no. cells in glomerulus Presents with NEPHRITIC syndrome
44
What is Non-proliferative glomerulonephritis characterised by?
Lack of glomerular cell proliferation Presents with NEPHROTIC syndrome
45
Give 6 causes of proliferative glomerulonephritis
IgA nephropathy Post-infectious glomerulonephritis Membranoproliferative glomerulonephritis Rapidly progressive glomerulonephritis (RPGN) Anti-GBM disease Vasculitic disorders (GPA + microscopic polyangitis)
46
What is IgA nephropathy aka? In which patient group is it usually seen?
Bergers disease Most common form of glomerulonephritis in adults Often young adults
47
How does IgA nephropathy usually present? What investigations are performed?
Haematuria 24-48h after URTI Urinalysis: haematuria Renal biopsy (definitive): increased no. mesangial cells
48
Describe management of mild, moderate and severe IgA nephropathy. What is the prognosis?
Mild: Self-limiting, F/U to check renal function Mod: ACEi Sev: High dose prednisolone 25% develop ESRF within 20-25y
49
What is Post-infectious glomerulonephritis most commonly associated with? What is the pathophysiology?
Group A beta-haemolytic Streptococcus infection (usually Strep. pyogenes) immune complex (IgG, IgM + C3) deposition in the glomeruli.
50
How does Post-infectious glomerulonephritis usually present?
Gross haematuria Proteinuria + Oedema Oliguria Headache + malaise 1-2w after strep infection
51
What investigations can be used for Post-streptococcal glomerulonephritis?
anti-streptolysin titre (ASOT). low C3 Biopsy Diffuse proliferative + exudative glomeronephritis EM: subepithelial humps- lumpy complex deposition
52
Mx and prognosis in post-streptococcal glomerulonephritis
Self limiting Good prognosis
53
What is Goodpasture’s syndrome?
small-vessel vasculitis a/w pulmonary haemorrhage + rapidly progressive glomerulonephritis. Caused by anti-GBM antibodies against type IV collagen.
54
Describe epidemiology of Goodpasture’s syndrome
M > F 2:1 Bimodal 20-30 + 60-70 HLA DR2 association
55
How does Goodpasture’s syndrome usually present?
Pulmonary haemorrhage: Haemoptysis RPGN: rapid onset AKI= nephritis → proteinuria + haematuria
56
What investigations can be used for Goodpasture’s syndrome?
Immunohistochemistry: Linear IgG deposits along basement membrane Antibodies: anti-GBM antibodies
57
Mx for Goodpasture’s syndrome
Prednisolone Plasmapheresis Cyclophosphamide
58
What is the likelihood of complete recovery of kidney function following an AKI if there is no pre-existing CKD?
80%
59
Recall 3 ECG changes in hyperkalaemia
Tented T waves Widening QRS complex Small p waves
60
What is the most common cause of nephrotic syndrome in adults?
Membranous glomerulonephritis
61
What are the components of the annual review for patients with type 2 diabetes?
``` Retinopathy screening Foot assessment for both sensation and doppler testing of vascular supply Albumin:creatinie ratio U+E Serum cholesterol HBa1c Review of any glucose monitoring Weight assessment Smoking status assessment ```
62
What are the indications for dialysis?
``` Refractory hyperkalaemia Refractory fluid overload Metabolic acidosis Uraemia symptoms CKD stage 5 ```
63
What will the urinary sodium be in pre-renal vs intrinsic renal ARF?
Pre-renal: urinary sodium low | Intrinsic renal: urinary sodium high
64
Recall the symptoms of HUS vs TTP
HUS: MAHA, thrombocytopaenia, AKI TTP: MAHA, thrombocytopaenia, AKI, neurological impairment and fever
65
Recall some key nephrotoxic drugs that should be stopped in AKI
``` stop the DAMN drugs Diuretics ACEi and ARBs Metformin NSAIDs ```
66
At what GFR would you do a routine nephrology referral?
Either at GFR <30 or a reduction in GFR over 12 months of >25% >15mL/min/1.73m^2
67
How can CKD be managed by diet?
1. Reduce dietary phosphate, sodium, potassium, fluids 2. Sevelamar (phosphate binder) - reduces uric acid and lipid levels 3. Vitamin D
68
Recall 4 features of adult polycystic kidney disease
Liver cysts Berry aneurysms Mitral valve prolapse Renal failure signs
69
What is the medical management of adult polycystic kidney disease?
Tolvaptan
70
Does IgA nephropathy cause nephrotic or nephritic syndrome?
Nephritic (rarely nephrotic)
71
Recall some signs and symptoms of IgA nephropathy
Purpuric rash (100%) Arthralgia (60-80%) Abdominal pain (60%) Glomerulonephritis (20-60%)
72
How should IgA nephropathy be managed?
Most cases will resolve spontaneously in 4w Joint pain --> NSAIDs Scrotal involvement/severe oedema/ severe abdominal pain --> oral prednisolone Renal involvement --> IV corticosteroids
73
What type of cancer is left varicocele most associated with?
Renal cell carcinoma
74
What is the most common form of renal tumour?
Clear cell carcinoma
75
Which urological cancer is most associated with painless haematuria?
Transistional cell carcinoma
76
In patients with CKD, what should be done before any scan that uses contrast?
Give IV saline --> volume expansion --> reduced chance of cast nephropathy
77
What are the variables in the Modification of Diet in Renal Disease equation, that affect eGFR?
``` CAGE: Creatinine Age Gender Ethnicity ```
78
What medication should be started in patients with CKD who have an ACR of >30?
ACE inhibitor
79
How does the size of kidneys differ in chronic diabetic nephropathy vs ckd of another cause?
Chronic diabetic nephropathy = large/normal kidneys | CKD = small kidneys
80
Give 4 causes of a normal anion gap metabolic acidosis
ABCD: Addison's Bicarb loss: prolonged diarrhoea, fistula Chloride Drugs e.g. acetazolamide
81
Give 4 causes of a raised anion gap.metabolic acidosis
Lactate: shock, sepsis, hypoxia Urate: renal failure Ketones: DKA, alcohol Acid poisoning: salicylates, methanol
82
What are the maintenance fluid requirements of an adult?
Water: 25-30 ml/kg/day K+, Na+, Cl: 1 mmol/kg/day Glucose: 50-100 g/day
83
What changes are acceptable in CKD after initiation of an ACEi?
Decrease in eGFR up to 25% Rise in creatinine up to 30% (Reduce filtration pressure, so small fall in glomerular filtration pressure (GFR) + rise in creatinine expected)
84
How does renal tubular acidosis present on ABG?
Normal anion gap metabolic acidosis, hyperchloraemia + low bicarbonate.

YR6 Rotations (22 decks)

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