Brainscape's Knowledge GenomeTM

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


See full index

YR6 Rotations > Medicine - Renal > Flashcards

Medicine - Renal Flashcards

1
Q

What are the 2 main types of dialysis?

A

Haemodialysis
Peritoneal dialysis

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

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

How often should haemodialysis be performed?

A

4h treatment 3x per week

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

Give 5 complications of haemodialysis

A

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

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

How many weeks does an AV fistula take to mature?

A

6-8w

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

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

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

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

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

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

Give 3 advantages of PD

A
  • Offers more flexibility (can be done overnight)
  • Is better tolerated by patients
  • Less expensive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

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

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

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

What are the most common causes of CKD?

A

Diabetic nephropathy
Hypertensive nephropathy
(PKD)

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

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

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

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

Name one phosphate binder

A

Sevelamer

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

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

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

A

BLAST
Barbiturates
Lithium
Alcohol
Salicylates
Theophylline

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What problems arise from high phosphate and low vitamin D in CKD?

A

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

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

Define acute kidney injury

A

Sudden decrease in GFR manifested by an increase in serum creatinine or oliguria over a period of hours/ weeks

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

What causes should be excluded first in AKI? Why?

A

Pre renal (hypovolaemia, sepsis) + post renal (stones, cancer)
Renal causes require a biopsy

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

What can be used as an alternative to calcium gluconate in hyperkalaemia as a cardioprotective infusion?

A

Calcium chloride

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

How can AKI secondary to blood loss be differentiated into pre-renal and renal cause?

A

Pre: LOW urinary Na+ (hypovolaemia: kidneys hold on)

Renal: HIGH urinary Na+ (ischaemia of tubules: loss)

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

How are intrinsic renal causes of AKI classified?

A

Glomerulonephritis: MCD, Membranous GN

ATN: affects tubules

AIN: affects surrounding tissue

Vascular: small (microangiopathic- HUS, TTP) or large (obstructive- thrombosis/ emboli)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the cause of HUS? What triad os signs and symptoms does it present with?

A

E.coli toxin 0157

MAHA
Thrombocytopenia
AKI

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

What pentad of signs and symptoms characterises TTP?

A

MAHA
Thrombocytopenia
AKI
Neurological impairment
Fever

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

What characterises nephritic syndrome?

A

Haematuria
Variable proteinuria
Oliguria + red cell casts
HTN

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

What is nephritic syndrome?

A

Subtype of intrinsic AKI with BLOOD + PROTEIN in urine indicative of glomerular disease

35
Q

What is nephrotic syndrome?

A
  1. Proteinuria (>3.5g/ 1.73m^2 body surface area/ 24h)
  2. Hypoalbuminaemia (<30g/L)
  3. Oedema

(+ Hyperlipidaemia)

36
Q

Name some proteins lost in nephrotic syndrome and the consequences of this

A

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
Q

What causes the high level of proteinuria in nephrotic syndrome?

A

Injury of the podocyte
(provides most of the protein filter barrier of the glomerulus)

38
Q

Give 3 primary renal diseases presenting with nephrotic syndrome

A

Minimal change disease
Membranous glomerulonephritis
Focal Segmental Glomerular Sclerosis

39
Q

Give 2 systemic causes presenting with nephrotic syndrome

A

Diabetes
Amyloidosis

40
Q

What is Chronic Kidney Disease?

A

Decrease in GFR present >3 months

41
Q

Which 4 variables are used in the modification of diet in renal disease (MDRD) formula for eGFR?

A

Creatinine (serum)
Age
Gender
Ethnicity

42
Q

List 3 factors that will affect the MDRD estimation of GFR

A

Pregnancy
Muscle mass (e.g. amputees (lower Cr), body-builders (higher Cr))
Eating red meat 12h prior to the sample being taken

43
Q

What is Proliferative glomerulonephritis characterised by?

A

Increased no. cells in glomerulus
Presents with NEPHRITIC syndrome

44
Q

What is Non-proliferative glomerulonephritis characterised by?

A

Lack of glomerular cell proliferation
Presents with NEPHROTIC syndrome

45
Q

Give 6 causes of proliferative glomerulonephritis

A

IgA nephropathy

Post-infectious glomerulonephritis

Membranoproliferative glomerulonephritis

Rapidly progressive glomerulonephritis (RPGN)

Anti-GBM disease

Vasculitic disorders (GPA + microscopic polyangitis)

46
Q

What is IgA nephropathy aka? In which patient group is it usually seen?

A

Bergers disease
Most common form of glomerulonephritis in adults
Often young adults

47
Q

How does IgA nephropathy usually present? What investigations are performed?

A

Haematuria
24-48h after URTI

Urinalysis: haematuria
Renal biopsy (definitive): increased no. mesangial cells

48
Q

Describe management of mild, moderate and severe IgA nephropathy. What is the prognosis?

A

Mild: Self-limiting, F/U to check renal function

Mod: ACEi

Sev: High dose prednisolone

25% develop ESRF within 20-25y

49
Q

What is Post-infectious glomerulonephritis most commonly associated with? What is the pathophysiology?

A

Group A beta-haemolytic Streptococcus infection (usually Strep. pyogenes)

immune complex (IgG, IgM + C3) deposition in the glomeruli.

50
Q

How does Post-infectious glomerulonephritis usually present?

A

Gross haematuria
Proteinuria + Oedema
Oliguria
Headache + malaise
1-2w after strep infection

51
Q

What investigations can be used for Post-streptococcal glomerulonephritis?

A

anti-streptolysin titre (ASOT).
low C3

Biopsy
Diffuse proliferative + exudative glomeronephritis
EM: subepithelial humps- lumpy complex deposition

52
Q

Mx and prognosis in post-streptococcal glomerulonephritis

A

Self limiting

Good prognosis

53
Q

What is Goodpasture’s syndrome?

A

small-vessel vasculitis a/w pulmonary haemorrhage + rapidly progressive glomerulonephritis.

Caused by anti-GBM antibodies against type IV collagen.

54
Q

Describe epidemiology of Goodpasture’s syndrome

A

M > F 2:1
Bimodal 20-30 + 60-70
HLA DR2 association

55
Q

How does Goodpasture’s syndrome usually present?

A

Pulmonary haemorrhage: Haemoptysis

RPGN: rapid onset AKI=
nephritis → proteinuria + haematuria

56
Q

What investigations can be used for Goodpasture’s syndrome?

A

Immunohistochemistry: Linear IgG deposits along basement membrane

Antibodies: anti-GBM antibodies

57
Q

Mx for Goodpasture’s syndrome

A

Prednisolone
Plasmapheresis
Cyclophosphamide

58
Q

What is the likelihood of complete recovery of kidney function following an AKI if there is no pre-existing CKD?

A

80%

59
Q

Recall 3 ECG changes in hyperkalaemia

A

Tented T waves
Widening QRS complex
Small p waves

60
Q

What is the most common cause of nephrotic syndrome in adults?

A

Membranous glomerulonephritis

61
Q

What are the components of the annual review for patients with type 2 diabetes?

A 
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
Q

What are the indications for dialysis?

A 
Refractory hyperkalaemia 
Refractory fluid overload 
Metabolic acidosis 
Uraemia symptoms 
CKD stage 5
63
Q

What will the urinary sodium be in pre-renal vs intrinsic renal ARF?

A

Pre-renal: urinary sodium low

Intrinsic renal: urinary sodium high

64
Q

Recall the symptoms of HUS vs TTP

A

HUS: MAHA, thrombocytopaenia, AKI

TTP: MAHA, thrombocytopaenia, AKI, neurological impairment and fever

65
Q

Recall some key nephrotoxic drugs that should be stopped in AKI

A 
stop the DAMN drugs 
Diuretics 
ACEi and ARBs 
Metformin 
NSAIDs
66
Q

At what GFR would you do a routine nephrology referral?

A

Either at GFR <30 or a reduction in GFR over 12 months of >25% >15mL/min/1.73m^2

67
Q

How can CKD be managed by diet?

A
  1. Reduce dietary phosphate, sodium, potassium, fluids
  2. Sevelamar (phosphate binder) - reduces uric acid and lipid levels
  3. Vitamin D
68
Q

Recall 4 features of adult polycystic kidney disease

A

Liver cysts
Berry aneurysms
Mitral valve prolapse
Renal failure signs

69
Q

What is the medical management of adult polycystic kidney disease?

A

Tolvaptan

70
Q

Does IgA nephropathy cause nephrotic or nephritic syndrome?

A

Nephritic (rarely nephrotic)

71
Q

Recall some signs and symptoms of IgA nephropathy

A

Purpuric rash (100%)
Arthralgia (60-80%)
Abdominal pain (60%)
Glomerulonephritis (20-60%)

72
Q

How should IgA nephropathy be managed?

A

Most cases will resolve spontaneously in 4w
Joint pain –> NSAIDs

Scrotal involvement/severe oedema/ severe abdominal pain –> oral prednisolone

Renal involvement –> IV corticosteroids

73
Q

What type of cancer is left varicocele most associated with?

A

Renal cell carcinoma

74
Q

What is the most common form of renal tumour?

A

Clear cell carcinoma

75
Q

Which urological cancer is most associated with painless haematuria?

A

Transistional cell carcinoma

76
Q

In patients with CKD, what should be done before any scan that uses contrast?

A

Give IV saline –> volume expansion –> reduced chance of cast nephropathy

77
Q

What are the variables in the Modification of Diet in Renal Disease equation, that affect eGFR?

A 
CAGE: 
Creatinine 
Age 
Gender 
Ethnicity
78
Q

What medication should be started in patients with CKD who have an ACR of >30?

A

ACE inhibitor

79
Q

How does the size of kidneys differ in chronic diabetic nephropathy vs ckd of another cause?

A

Chronic diabetic nephropathy = large/normal kidneys

CKD = small kidneys

80
Q

Give 4 causes of a normal anion gap metabolic acidosis

A

ABCD:
Addison’s
Bicarb loss: prolonged diarrhoea, fistula
Chloride
Drugs e.g. acetazolamide

81
Q

Give 4 causes of a raised anion gap.metabolic acidosis

A

Lactate: shock, sepsis, hypoxia
Urate: renal failure
Ketones: DKA, alcohol
Acid poisoning: salicylates, methanol

82
Q

What are the maintenance fluid requirements of an adult?

A

Water: 25-30 ml/kg/day
K+, Na+, Cl: 1 mmol/kg/day
Glucose: 50-100 g/day

83
Q

What changes are acceptable in CKD after initiation of an ACEi?

A

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
Q

How does renal tubular acidosis present on ABG?

A

Normal anion gap metabolic acidosis,
hyperchloraemia + low bicarbonate.

YR6 Rotations (22 decks)

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