Brainscape's Knowledge GenomeTM

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


See full index

Phase 3b > Renal > Flashcards

Renal Flashcards

1
Q

Name the causes of End-Stage Renal Failure

A

Pyelonephritis
Diabetic nephropathy
Glomerulonephritis
Polycystic Kidney Disease

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

Define Acute Kidney Injury

A

Rapid reduction in kidney function over hours to days, as measured by serum urea and creatinine

Common, occurs in up to 18% of hospital patients

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

What is the NICE criteria for an AKI?

A

Rise in creatinine >25 umol/L in 48 hours
Rise in creatinine of >50% in 7 days
Urine output of <0.5ml/kg/hour for >6 hours

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

What are the risk factors for AKI?

A 
Age >75
Chronic kidney disease
Heart failure
Diabetes
Liver disease
Drugs (nephrotoxic - NSAIDs, ACE-inhibitors etc...)
Sepsis
Cognitive impairment
Contrast medium - CT scans
Poor fluid intake
Previous AKI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the Pre-Renal causes of an AKI?

A 
Hypotension (hypovolaemia, sepsis)
Renal artery stenosis
Heart failure/MI
Dehydration
Drugs e.g. ACE-inhibitors, NSAIDs
GI bleeding
Vomiting and diarrhoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the Intrinsic causes of an AKI?

A

Acute tubular necrosis (most common)
Glomerulonephritis (SLE, HSP, infections, drugs, anti-GBM disease, ANCA vasculitis)
Interstitial nephritis (drugs, lymphoma)
Vascular disease (thrombosis, HUS/TTP, scleroderma)
Rhabdomyolysis
Radiocontrast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the Post-Renal causes of an AKI?

A

Kidney stones
Malignancy (ureteric, bladder, prostate)
Ureter or urethral strictures
Enlarged prostate or prostate cancer (BPH) (high PSA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the nephrotoxic drugs?

A

CANT DAMAG

Contrast
ACE-inhibitors
NSAIDs
Therapeutic index (narrow)
Diuretics
Antibiotics (Penicillin, cephalosporin)
Metformin
ARB
Gentamicin/gold
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why are changes in creatinine assessed and not total amount when calculating AKI staging?

A

Because the total amount is affected by muscle mass, gender, age and ethnicity. Will be higher in those with a larger muscle mass etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is stage 1 on the KDIGO staging system?

A

Creatinine increase 1.5-1.9 x baseline

Urine output <0.5 mL/kg/hour for >6 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is stage 2 on the KDIGO staging system?

A

Creatinine increase 2.0-2.9 x baseline

Urine output <0.5 mL/kg/hour for >12 hours

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

What is stage 3 on the KDIGO staging system?

A

Creatinine increase >3 x baseline OR >354umol/L

Urine output <0.3 mL/kg/hour for >24 hours OR anuria for 12 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What the symptoms of AKI

A 
Decreased urine
Vomiting
Dizziness (orthostatic suggests pre-renal)
Orthopnoea (fluid overload)
Altered mental state
Signs of uraemia
Peripheral oedema
Hyper/hypotension
Muscle tenderness (rhabdomyolysis)
Ascites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Investigations in an AKI

A

U&E’s - elevated creatinine, high serum potassium (most important) -> hyperkalaemia >5.5, metabolic acidosis
Urinalysis - leucocytes & nitrites = infection, proteinuria and haematuria = glomerular disease (Acute nephritis), glucose = diabetes
FBC - Anaemia (CKD, blood loss), thrombocytopenia (HUS, TTP)
Imaging - Renal/urinary tract USS (KUB) -> obstruction, cysts, mass
ECG -> hyperkalaemic signs = tall tented T waves, absent P waves, broad QRS complex, sinusoidal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Management for an AKI

A

Stop nephrotoxic drugs - NSAIDs. ACE-inhibitors
Fluid rehydration with IV fluids in pre-renal
CTKUB for obstruction
Uraemic/acidaemia => dialysis
Treat hyperkalaemia -> Insulin + glucose, calcium gluconate
Odema = Oxygen, CPAP, Diamorphine, furosemide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Complications of an AKI

A

Hyperkalaemia
Pulmonary oedema
Metabolic acidosis
Uraemia (high urea) -> can lead to encephalopathy/pericarditis

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

Define Chronic Kidney Disease

A

Impaired renal function for >3 months based on abnormal structure or function (proteinuria or haematuria), or GFR <60 ml/min/1.73m/m for >3 months with or without evidence of kidney damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Causes of CKD

A 
Diabetes - 40%
Hypertension
Glomerulonephritis (IgA nephropathy, FSG, lupus, amyloidosis)
Polycystic kidney disease
Mediciations - lithium, PPI's, NSAID's
Pyelonephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the clinical exam picture of a patient with CKD?

A

Hypertensive diabetic over the age of 50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Risk factors for CKD

A 
Old age
Hypertension
Smoking
Obesity
Diabetes
Medications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Symptoms for CKD

A 
Usually asymptomatic
Nausea and vomiting
Fatigue (anaemia - lack of EPO)
Muscle cramps
Anorexia
Pruritus (itching)
Oedema (salt and water retention)
Bone pain
Pallor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Stages of CKD

A

Stage 1 = GFR >90 with evidence of kidney damage
Stage 2 = GFR 60-89 with evidence of kidney damage

Stage 3a = GFR 45-59 with or without kidney damage
Stage 3b = GFR 30-44 with or without kidney damage
Stage 4 = GFR 15-29 with or without kidney damage

Stage 5 = GFR <15 - End-Stage Renal Failure

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

Investigations for CKD

A

Urinalysis - haematuria, proteinuria, leucocytes or nitrites = infection
U&E’s - eGFR - two tests 3 months apart, serum creatinine is elevated
FBC - normochromic, normocytic anaemia
Glucose
Renal USS -> small kidney <9cm = obstruction, large kidney = amyloidosis, myeloma
Renal biopsy - if unexplained CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Name the complications of CKD

A 
Anaemia
Renal bone disease (CKD-mineral and bone disorder)
CV disease
Peripheral neuropathy
Hyperkalaemia
Dialysis related problems
Pulomonary oedema
Metabolic acidosis
Protein malnutrition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Explain the pathophysiology behind anaemia in CKD

A

Anaemia is as a result of EPO deficiency (also blood loss, ACE-inhibitors, chronic disease). EPO stimulates RBC production

Treatment: Erythropoeitin

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

Explain the pathophysiology behind CKD mineral and bone disorder

A

Vitamin D deficiency causes low Calcium (hypocalcaemia) which causes PTH elevation (hyperparathyroidism)

Results in osteoporosis, osteomalacia, osteosclerosis

Treatment: Vitamin D (alfacalcidol and calcitriol), Calcium supplements, Bisphosphonates

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

Treatment for CKD

A

Stop nephrotoxic drugs
Relieve obstruction
Reduce risk of CV disease: stop smoking, lose weight
Glycaemic control
Treat BP -> ACE-inhibitors, ARB, CCB
Manage complications: Anaemia, renal bone disease
Oedema: loop diuretics (furosemide) + fluid restriction

Dialysis and renal transplant in end stage renal failure

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

Define nephritic syndrome including symptoms

A

Refers to a group of symptoms, not a diagnosis

Haematuria
Oliguria (reduced urine output)
Fluid retention
Proliferative

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

What are the causes of nephritic syndrome?

A

IgA nephropathy
Post-streptococcal
Rapidly progressive GN
SLE

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

Define IgA nephropathy

A

Most common cause of primary glomerulonephritis
Peak is 20 years old
Visible haematuria
Renal biopsy - IgA deposits and mesangial proliferation
Treatment: ACE-inhibitors or immunosuppression (steroids)

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

Define post-streptococcal nephritic syndrome

A

Occurs 1-12 weeks after a sore throat (tonsilitis)
Causative organism = Strep pyogenes
Supportive treatment -> resolves over 2-4 weeks

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

Define rapidly progressive GN

A

Histology shows crescentic glomerulonephritis
Fever, myalgia, weight loss

Goodpasture’s syndrome: Kidney failure + haemoptysis. Anti-GBM antibodies. Treatment = High dose IV steroids, cyclophosphamide, plasma exchange.

Wegener’s granulomatosis - c-ANCA
Microscopic polyangiitis - p-ANCA

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

Define SLE related to glomerulonephritis

A

More common in African’s
Vascular, glomerular and tubulointerstitial damage
Class I-IV (increasing severity), class V (membranous)
Anti DS DNA/ANA antibodies
Treatment: IV methylprednisolone + cyclophosphamide

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

What is the triad of nephrotic syndrome?

A

Oedema
Proteinuria (>3.5g/24 hours)
Hypoalbuminaemia

(Hyperlipidaemia as a fourth)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Causes of nephrotic syndrome?

A

Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy
Mesangiocapillary GN

Diabetic nephropathy
Hepatitis B/C
SLE
Amyloidosis
Drugs (NSAIDs, gold, penicillamine, anti-TNF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Complications of nephrotic syndrome

A 
Susceptibility to infections
DVT/PE
Hyperlipidaemia (Cholesterol >10mmol/L)
AKI
Hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Define minimal change disease

A

Commonest cause of nephrotic syndrome in children
Caused by: NSAIDs, Hodgkin’s lymphoma
Abnormal podocytes - under electron microscope
Treatment: Prednisolone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Define focal segmental glomerulosclerosis

A

Most common in adults
Focal scars on glomeruli
Idiopathic causes or secondary to HIV
Responds to corticosteroids in 30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Define membranous nephropathy

A

Autoimmune
Can be associated with malignancy, NSAID’s, RA
Thickened glomerular basement membrane
Spike and dome appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Investigations for glomerulonephritis

A 
Renal biopsy
FBC's
U&amp;E's
ESR
Urinalysis
ANCA
Hep B/C/HIV
Anti-DSDNA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Treatment for glomerulonephritis

A

Reduce oedema -> loop diuretics (furosemide)
Diet - fluid and salt restriction
Reduce proteinuria -> ACE-inhibitors/ARB to control BP
Treat complications: Statins for hyperlipidaemia, anticoagulation for thrombosis (DVT/PE)
Stop causative drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Define polycystic kidney disease

A

Genetic condition where the kidneys develop multiple fluid filled cysts
Commonest inherited disease causing ESRF

Two types: Autosomal dominant (ADPKD) - more common
Autosomal recessive (ARPKD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What genes are affected in autosomal dominant PKD

A

PKD-1 chromosome 16 (85%) - reach ESRF in 50s

PKD-2 chromosome 4 (15%) - slower reach ESRF in 70s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Signs of ADPKD

A 
Renal enlargement with cysts
Abdominal pain + haematuria (haemorrhage into a cyst)
Cyst infection
Renal calculi
Hypertension
Progressive renal failure
CV disease (hypertension)
Palpable, enlarged kidneys
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Extra-renal manifestations of ADPKD

A

Cerebral aneurysms -> SAH: headaches
Hepatic, splenic, pancreatic, ovarian and prostate cysts
Cardiac valve disease (mitral regurgitation)
Colonic diverticula
Aortic root dilatation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What gene is affected in autosomal recessive PKD

A

Gene on chromosome 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How does ARPKD present?

A

Enlarged kidneys, renal cysts and congenital hepatic fibrosis
Usually ESRF before adulthood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Investigations for PKD

A 
Genetic testing - PKD1 or PKD2
Renal USS - Age 18-39 = >3 unilateral or bilateral cysts
Age 40-59 >2 cysts in each kidney
Age >60 >4 cysts in each kidney
U&amp;E's - creatinine
Screen for SAH - MR angiography
Urinalysis - protein, bacteria
ECG - LVH
Echo - aortic root dilatation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Management for PKD

A

Hypertension = ACE-i/ARB/CCB
ESRD = Dialysis/renal transplant
Renal stones = analgesia
Infection = Antibiotics e.g. ciprofloxacin
Tolvaptan (vasopressin receptor antagonist) -> slows development of cysts

50
Q

Define Alport syndrome

A

2nd most common inherited cause of kidney failure
Most commonly X-linked dominant
Affects young males
Mutations in COL4A5 gene - mutation in basement membrane collagen (type IV collagen)

51
Q

Signs of Alport syndrome

A

Haematuria
Proteinuria
Renal failure
Deafness

52
Q

Treatment for Alport syndrome

A

Possibly ACE-inhibitors

53
Q

Define the stages of diabetic nephropathy

A

GFR increases
Glomerular hyperfiltration
Microalbuminuria
Nephropathy -> proteinuria increase

54
Q

What lesions do you see in diabetic nephropathy?

A

Kimmelstiel-Wilson lesions -> nodular glomerulosclerosis

55
Q

Treatment for diabetic nephropathy

A

ACE-inhibitors/ARB - to reduce intra-glomerular pressure and proteinuria/treat blood pressure

56
Q

Define renal tubular acidosis

A

Is metabolic acidosis due to impaired acid secretion by the kidney
There is hyperchloraemic, metabolic acidosis + normal anion gap

57
Q

Define type 1 renal tubular acidosis

A

Distal tubule pathology

Distal tubule unable to excrete hydrogen ions

58
Q

Causes of type 1 renal tubular acidosis

A 
Genetic
SLE
Sjogren's syndrome
Marfan's syndrome
Sickle cell
Hyperthyroidism
59
Q

Symptoms of type 1 renal tubular acidosis

A

Failure to thrive in children/rickets
Osteomalacia
Renal calculi

60
Q

Investigations for type 1 renal tubular acidosis

A

Urine pH >5.5
Metabolic acidosis
Hypokalaemia

61
Q

Treatment for type 1 renal tubular acidosis

A

Oral sodium bicarbonate

62
Q

Define type 2 renal tubular acidosis

A

Proximal tubule pathology
Inability of the proximal tubule to reabsorb bicarbonate from the urine. Results in excess bicarbonate in the urine -> metabolic acidosis

63
Q

Causes of type 2 renal tubular acidosis

A

Fanconi’s syndrome
Drugs (lead, acetazolamide)
Interstitial nephritis/myeloma

64
Q

Investigations for type 2 renal tubular acidosis

A

Hypokalaemia

High excretion of bicarbonate

65
Q

Treatment for type 2 renal tubular acidosis

A

Oral bicarbonate

66
Q

Define type 4 renal tubular acidosis

A

Most common cause of renal tubular acidosis

Reduced aldosterone secretion -> hyperkalaemia

67
Q

Causes of type 4 renal tubular acidosis

A 
Addison's disease
Diabetic nephropathy
SLE
HIV
Drugs: ACE-inhibitors, spironolactone, NSAIDs, ciclosporin, beta-blockers
68
Q

Investigations for type 4 renal tubular acidosis

A

Hyperkalaemia
High chloride
Metabolic acidosis
Low urinary pH <5.5

69
Q

Treatment for type 4 renal tubular acidosis

A

Fludrocortisone - replaces aldosterone

Hyperkalaemia treatment = Calcium resonium, furosemide

70
Q

Define type 3 renal tubular acidosis

A

Combination of type 1 and 2

Pathology in the proximal and distal tubule

71
Q

Define Fanconi syndrome

A

Proximal tubular dysfunction leading to loss of amino acids, glucose, phosphate and bicarbonate in urine.

72
Q

Complications of Fanconi syndrome

A

Dehydration
Metabolic acidosis
Oesteomalacia/rickets
Electrolyte abnormalities

73
Q

Causes of Fanconi syndrome

A 
Wilson's disease
Lead
Mercury
Gentamicin
Cisplatin
Myeloma
Amyloidosis
74
Q

Treatment for Fanconi syndrome

A

Sodium bicarbonate

Potassium, phosphate, vitamin D supplements

75
Q

Define pyelonephritis

A

Infection/inflammatory disease of renal parenchyma, calyces and pelvis that may be acute, recurrent or chronic

76
Q

Causes of pyelonephritis

A

E.coli (ascending infection from lower urinary tract or due to bloodstream spread of infection (sepsis))

In diabetes -> klebsiella/candida
In HIV/Malignancy/transplant -> candida

77
Q

Risk factors for pyelonephritis

A

Infants and old age
Structural abnormalities - PKD, horseshoe kidney, VUR
Foreign body - stone, catheterisation
Impaired renal function
Immunocompromised - DM, transplant, malignancy, radio/chemotherapy, HIV
Pregnancy
Obstruction - BPH, stone, bladder neck obstruction, foreign body

78
Q

Symptoms of pyelonephritis

A

Loin pain
Fever/rigors
Renal tenderness
Vomiting/nausea

79
Q

Investigations for pyelonephritis

A 
MC&amp;S of midstream urine
Urine dipstick - blood, protein, nitrites, leukocytes
Urinalysis
Gram stains
FBC
ESR/CRP raised
Blood cultures - sepsis
Renal USS - stones, abscess
Contrast CT
DMSA - renal scarring
80
Q

Treatment for pyelonephritis

A 
Mild/moderate = ciprofloxacin or cefixime
Severe = Admit to hospital
IV ceftriaxone or IV ciprofloxacin
IV fluids
IV paracetamol (pain and fever)
Catheterisation
81
Q

Complications of pyelonephritis

A

Renal failure
Abscess formation
Parenchymal renal scarring
Recurrent UTI’s

82
Q

Define renal cell carcinoma

A

Renal malignancy arising from proximal renal tubular epithelium

It accounts for 85% of renal cancer

83
Q

Types of renal cell carcinomas

A 
Clear cell (80%) - due to cholesterol and glycogen
Papillary tumour (15%)
84
Q

Risk factors for renal cell carcinoma

A

Smoking
Middle aged man - 55 years old
Renal transplant and dialysis
Von Hippel-Lindau syndrome

85
Q

Symptoms of renal cell carcinoma

A

Classic triad = Haematuria
Loin pain
Abdominal mass

Anorexia
Malaise
Weight loss
Left sided varicocele (due to left testicular vein compression)
Stauffer’s syndrome = cholestasis/hepatosplenomegaly

86
Q

Investigations for renal cell carcinoma

A 
FBC - polycythaemia from EPO secretion
Creatinine - elevated
Urinalysis - haematuria +/- proteinuria
LFTs - raised ALT/AST
Abdominal/pelvis USS = cysts, mass, metastases
CT abdo/pelvis
MRI
Chest X-ray
87
Q

Treatment for renal cell carcinoma

A

Radical nephrectomy (partial for T1, laparoscopic for T2)
Radio and chemo resistant
Sunitinib, bevacizumab, sorafenib - tyrosine kinase inhibitors

88
Q

Staging for renal cell carcinoma

A 
T1 = Confined to kidney <7cm
T2 = Confined to kidney >7cm
T3 = To major veins or adrenals (e.g. vena cava)
T4 = Beyond gerota fascia
LNs = para-aortic and hilar
89
Q

Define Wilm’s tumour (nephroblastoma)

A

Childhood tumour of primitive renal tubules and mesenchymal cells. (commonest in children)

90
Q

Symptoms of Wilm’s tumour

A

Abdominal mass

Haematuria

91
Q

Define interstitial nephritis

A

Inflammation of the space between cells and tubules (the interstitium)

92
Q

What does acute interstitial nephritis present with?

A

AKI and hypertension

93
Q

Causes of acute interstitial nephritis

A 
NSAIDs
Antibiotics
Infection - staphs/streps
Autoimmune - SLE, sarcoidosis
Diuretics
Allopurinol
Omeprazole
94
Q

Symptoms of acute interstitial nephritis

A

Mild renal impairment
Rash
Fever
Eosinophilia

95
Q

Treatment for acute interstitial nephritis

A

Stop underlying cause

Prednisolone -> reduces inflammation

96
Q

What does chronic interstitial nephritis present with?

A

CKD

97
Q

Causes of chronic interstitial nephritis

A 
Analgesic nephropathy
Autoimmune - RA, SLE, Sjogren's
Myeloma
Sickle cell
Drugs
98
Q

Treatment for chronic interstitial nephritis

A

Manage underlying cause

Steroids

99
Q

Define acute tubular necrosis

A

Damage and death (necrosis) of the epithelial cells of the renal tubules -> epithelial cells have ability to regenerate, takes 7-21 days.

Most common cause of AKI

100
Q

Causes of acute tubular necrosis

A

Shock
Sepsis
Dehydration
Radiology contrast dye

Gentamicin
NSAIDs
Lithium
Heroin

101
Q

Investigations for acute tubular necrosis

A

Urinalysis - “muddy brown casts”

102
Q

Treatment for acute tubular necrosis

A

IV fluids
Stops nephrotoxic medications
Treat complications

103
Q

Define haemolytic uraemic syndrome (HUS)

A

Medical emergency
Occurs when there is thrombosis in small blood vessels
Triggered by a bacterial toxin called shiga toxin -> caused by e.coli 0157 and shigella

104
Q

Symptoms of haemolytic uraemic syndrome

A 
Anorexia
Diarrhoea
Abdominal pain
AKI
Haematuria/dark brown urine
Confusion
Hypertension
Bruising
Nausea/vomiting
105
Q

Investigations for haemolytic uraemic syndrome

A

Blood film - decreased platelets (thrombocytopenia)

Proteinuria/haematuria

106
Q

Treatment for haemolytic uraemic syndrome

A

Dialysis for AKI
Plasma exchange
Antihypertensives

107
Q

Define rhabdomyolysis

A

Skeletal muscle tissue breaks down and releases contents into blood.
The muscle cells (myocytes) undergo cell death (apoptosis) and release: Myoglobin (toxic to kidney = AKI), Potassium (hyperkalaemia), Phosphate, Creatine kinase

108
Q

Causes of rhabdomyolysis

A

Prolonged immobility (elderly, frail and falling on the floor)
Rigorous exercise (ultramarathon/triathlon)
Crush injury
Seizures
Alcohol
Statins
Neuroleptic malignant syndrome

109
Q

Symptoms of rhabdomyolysis

A 
Muscle aches and pain
Oedema
Fatigue
Red-brown urine
Confusion
110
Q

Investigations for rhabdomyolysis

A

Creatine kinase >1,000-100,000 units/L
Myoglobinuria - myoglobin in the urine “red-brown” colour
U&E’s - increased K and PO, decreased Ca, = hyperkalaemia
ECG = hyperkalaemia - tall tented t waves, absent p waves, broad QRS complex, ventricular fibrillation

111
Q

Treatment for rhabdomyolysis

A

IV fluids for rehydration and filtration
IV sodium bicarbonate to alkalinize urine ph >6.5
IV mannitol
Treat complications: Hyperkalaemia -> insulin and dextrose, IV calcium gluconate

112
Q

What are the indications for dialysis in an AKI patient?

A 
Acidosis
Electrolyte abnormalities
Intoxication
Oedema
Uraemia symptoms
113
Q

How does haemodialysis work?

A

Blood is passed over a semi-permeable membrane against dialysis fluid flowing through in the opposite direction.
Blood is always meeting a less-concentrated solution and diffusion of small solutes occurs down the concentration gradient
Regime: Hospital 3x per week (4 hours)

114
Q

Complications of haemodialysis

A 
Access - infection, thrombosis, aneurysms, stenosis
Hypotension
Time-consuming
Nausea/vomiting
Headache
Fatigue
115
Q

How does peritoneal dialysis work?

A

The peritoneum is used a semi-permeable membrane. A special dialysis solution containing dextrose is added to the peritoneal cavity. Involves a Tenckhoff catheter used for inserting and removing dialysis solution
Regime: Continuous ambulatory peritoneal dialysis = 4 exchanges of 20 mins. Automated dialysis = occurs overnight.

116
Q

Complication of peritoneal dialysis

A 
Bacterial peritonitis
Peritoneal stenosis
Weight gain
Hernia
Hyperglycaemia
117
Q

Absolute contraindications for renal transplantation

A

Active infection
Cancer
Severe comorbidity

118
Q

What needs to be matched for a renal transplant?

A

ABO blood group
HLA tissue match (A, B, C on chromosome 6)
Antibody screening

119
Q

What drug is used for immunosuppresson induction in renal transplant?

A

Basiliximab

120
Q

What drugs are used for immunosuppression maintenance in renal transplant?

A

Triple therapy:
Calcineurin inhibitor (Tacrolimus or ciclosporin)
Antimetabolite (Azathioprine or mycophenolate)
Prednisolone

121
Q

Complications of renal transplant

A 
Transplant rejection (hyperacute, acute or chronic)
CV disease (hypertension)
Infection (HSV, CMV)
Malignancy (skin, lymphoma)
Drug toxicity
Delayed graft function

Phase 3b (18 decks)

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