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Final Year > Renal > Flashcards

Renal Flashcards

1
Q

Causes of pre-renal AKI

A

Low BP
Low cardiac output
Renal artery stenosis
Decreased intravascular volume

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2
Q

Causes of intrinsic AKI

A 
Acute tubular necrosis (can be causes by rhabdomyolysis)
Nephrotoxic drugs
Contrast dye
Interstitial nephritis
Glomerulonephritis
Vasculitis
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3
Q

Causes of post-renal AKI

A

BPH
Bladder cancer
Calculi
Obstruction

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4
Q

Which medication classes are nephrotoxic

A 
NSAIDs
ACEi
ARBs
Gentamycin
Contrast dye
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5
Q

Stage 1 AKI

A

Serum creatinine >26 or 1.5-2x baseline

Urine output <0.5ml/kg/hr for >6 hours

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6
Q

Stage 2 AKI

A

Serum creatinine 2-3x baseline

Urine output <0.5 ml/kg/hr for >12 hours

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7
Q

Stage 3 AKI

A

Serum creatinine >354 or >3x baseline or on RRT

Urine output <0.3 ml/kg/hr for >24 hours or anuric for >12 hours

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8
Q

Complications of AKI

A

High K
Pulmonary oedema/fluid overload if low urine output
Metabolic acidosis (kidney usually excretes H+)
Uraemic encaphalopathy
Uraemic pericarditis
Low Ca, high PO4

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9
Q

ECG changes in hyperkalaemia

A 
Small or no P waves
Prolonged PR interval
Wide QRS
Peaked T waves
Slurring into ST
VF
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10
Q

Treatment of hyperkalaemia

A 
IV Calcium gluconate or calcium chloride to stabilise the cardiac membranes
Beta-agonists to move K into cells
Bicarbonate to move K into cells
IV insulin to move K into cells
IV NaCl to increase renal K excretion
Diuretics to increase renal K excretion
Haemodialysis
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11
Q

Phases of AKI

A

Symptoms of underlying illness
Oliguric/anuric phase - low UO, high urea and creatinine, fluid retention, pulmonary oedema, hyperkalaemia, metabolic acidosis, lethargy, asterixis, uraemic encephalopathy/pericarditis. Lasts less than 2 weeks.
Polyuric/maintenance phase - filtration resumes but reabsorption still impaired, polyuria, low Na, low K. Lasts around 3 weeks
Recovery phase - renal function and urine production return to normal, can take up to 2 years

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12
Q

BUN:Creatinine ratio in pre-renal Vs intrinsic AKI

A

BUN:Cr basically tells you whether or not the tubules are still functioning
Creatinine is produced at a constant rate and all of it is excreted, non is reabsorbed, whereas urea is partially reabsorbed and affected by diet ect

In pre-renal AKI as normal all Cr is excreted, tubules are still working and reabsorbing urea so serum urea is higher. So BUN:Cr >20:1

In intrinsic AKI as normal all Cr is excreted, tubules aren’t working though so more urea being excreted than normal so less serum urea compared to pre-reanl. So BUN:Cr <20:1 (closer to 1)

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13
Q

Describe the urine Na concentration and urine osmolality in pre-renal AKI

A

Decreased renal blood flow but tubules still working
RAAS activated causing Na and H2O retention
Concentrated urine - high osmolality >500 but looking at just urine Na concentration this is low <20 because Na is being reabsorbed by the still-functioning tubules

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14
Q

Describe the urine Na concentration and urine osmolality in instrinsic AKI

A

Tubules damaged so cant function and cant reabsorb Na. So Na and H2O lost in urine - dilute urine with a high Na concentration. Low urine osmolality <350, high urinary Na concentration >40

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15
Q

What does low BP do to the afferent and efferent arterioles

A

Dilates the afferent, constricts the efferent

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16
Q

What does high BP do to the afferent and efferent arterioles

A

Constricts the afferent, dilates the efferent

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17
Q

Why are ACE inhibitors and NSAIDs nephrotoxic?

A

They interfere with compensatory mechanisms that maintain eGFR;
ACEi dilate the efferent arteriole
NSAIDs block prostaglandins that normally dilate the afferent arteriole (effectively constricting the afferent arteriole)

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18
Q

How do CKD affected kidneys appear on USS

A

Small with increased echogenicity

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19
Q

Why do you get polyuria/oedema/anaemia in CKD

A

Polyuria due to inability to concentrate urine (can’t reabsorb water, decreases urine osmolality)
Oedema due to proteinuria (can’t reabsorb protein) which decreases intravascular osmotic pressure so fluid leaks out of vessels
Normochromic normocytic anaemia due to decreased EPO production

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20
Q

Why do you get low Ca and high PO4 in CKD

A

Decreased renal function causes decreased activation of VitD so decreased production of calcitriol so decreased intestinal absorption of calcium
Decreased renal function results in less excretion of PO4

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21
Q

Stages of CKD (GFR)

A 
1 - >90 but with persistent albuminuria or hereditary renal disease
2 - 60-89
3a - 45-59
3b - 30-44
4 - 15-29
5 - <15 (end stage renal failure)
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22
Q

What are the 3 main things that can cause acute tubular necrosis? (ATN)

A

Prolonged/severe renal ischaemia
Nephrotoxins
Myoglobinuria/haemoglobinuria

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23
Q

What is the normal rate of urination for a healthy person?

A

0.5ml/kg/hr

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24
Q

Causes of CKD

A

Hypertension
Diabetes
Renal artery stenosis
Congenital/inherited - PCKD, Alports syndrome, medullary cystic disease
Glomerular disease - IgA nephropathy, Wegeners granulomatosis, amyloidosis, sickle cell
Interstitial disease - reflux nephropathy, TB, multiple myeloma

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25
Q

What are the signs and symptoms of CKD

A

Malaise, loss of appetite, insomnia, restless leg syndrome, nocturia, polyuria (inability to concentrate urine), itching, nausea, vomiting, diarrhoea, peripheral and pulmonary oedema, bruising, bone pain due to metabolic bone disease, anaemia (pallor)

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26
Q

What type of anaemia does CKD cause?

A

Normochromic, normocytic

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27
Q

Features of nephrotic syndrome and why they happen

A
  1. Proteinuria (due to loss of podocytes), >3g/24hrs or P:Cr >300, A:Cr >250
  2. Oedema (hypoalbuminuria due to urinary protein loss lowers intravascular oncotic pressure)
  3. Hypoalbuminaemia (<30g/L)

Hyperlipidaemia (hypoalbuminaemia causes liver to increase protein production to compensation and this causes lipid production to also increase)

Hypercoagulable state due to urinary loss of antithrombin 3

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28
Q

Features of nephritic syndrome

A 
Haematuria
Hypertension (due to low GFR causing fluid retention)
Oliguria (due to low GFR)
Azotaemia due to decreased excretion
RBC casts
Proteinuria
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29
Q

Difference in pathophysiology between nephrotic syndrome and nephritic syndrome

A

Nephrotic due to loss of podocytes so features are due to the resulting proteinuria
Nephritis due to immune complex deposition and inflammation in the glomeruli which damages the glomerulus and lowers GFR - resulting features are due to the low GFR

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30
Q

Causes of nephritic syndrome

A 
IgA nephropathy
HSP
Post-strep glomerulonephritis
Goodpasteurs syndrome 
Rapidly progressive GN (small vessel/ANCA vasculitis, SLE)
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31
Q

Causes of nephrotic syndrome

A 
Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy
Membranoproliferative glomerulonephritis 
DM
SLE
Myeloma
Amyloidosis
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32
Q

Two main causes of acute nephritic syndrome

A

Post-strep glomerulonephritis

IgA nephropathy

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33
Q

Management of nephrotic syndrome

A 
Salt restriction
Fluid restriction (1-1.5L/24hrs)
Loop diuretics 
Add ACEi/ARBs reduce proteinuria 
VTE prophylaxis
Renal biopsy
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34
Q

What are the 3 types of rapidly progressive/crescenteric glomerulonephritis

A 
Type 1 (Goodpasteurs) - linear immunofluorescence
Type 2 (immune complex mediated) - granular immunofluorescence
Type 3 (pauci-immune/vasculitic) - negative immunofluorescence
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35
Q

Which diseases are included in Type 2 RPGN

A

Post-strep GN
SLE
IgA nephropathy
HUS

36
Q

Which diseases are included in Type 3 RPGN

A

Granulomatosis with polyangitis (Wegeners)
Microscopic polyangitis
Eosinophilic granulomatosis with polyangitis (Churg-Strauss)

37
Q

cANCA positive vasculitis

A

GPA (granulomatosis with polyangitis/Wegeners)

38
Q

pANCA positive vasculitis

A

MP (microscopic polyangitis)

EGPA (eosinophilic granulomatosis with polyangitis/Churg-Strauss)

39
Q

Signs/symptoms of ANCA associated vasculitis

A

Fever, polymyalgia, polyarthralgia, headache, malaise, anorexia, weight loss
Nasal obstruction/ulcers/discharge/crusting, epistaxis, sinusitis
Cough, haemoptysis, pleuritis
Ulcers, papules, nodules, palpable purpura
Keratitis, conjuncitivitis, scleritis, episcleritis, uveitis, retinal vessel occlusion, optic neuritis
Mononeuritis multiplex
Nephritic syndrome

40
Q

Types of cystic renal disease

A 
ADPKD
ARPKD
Simple cysts
Acquired renal cystic disease
Von Hippel Lindau disease
41
Q

Extra-renal complications of ADPKD

A 
Berry aneurysms - SAH!!
Hepatic/pancreatic cysts
Spleen cysts
Mitral valve prolapse
Diverticuli
42
Q

Presentation of ADPKD

A

Early hypertension (around age 20)
Vague abdominal/loin discomfort with a palpable mass (often bilateral)
Acute pain or renal colic may be due to cyst rupture
Haematuria
UTI
CKD

43
Q

Causes of raised albumin/protein:creatinine ratio

A

Glomerulonephritis
Diabetes
Amyloidosis
Myeloma

44
Q

Causes of haematuria

A 
Malignancy (KUB)
Calculi
IgA nephropathy
Glomerulonephritis
Polycystic kidney disease
Alport syndrome
45
Q

What counts as a lower UTI

A

Cystitis

Prostatitis

46
Q

What counts as an upper UTI

A

Pyelonephritis

47
Q

What does a ‘complicated’ UTI mean

A

UTI in the presence of a structural/functional abnormality of the genitourinary tract e.g. obstruction, catheter, stones, neurogenic bladder, renal transplant

48
Q

Symptoms of cystitis

A 
Frequency
Dysuria
Urgency
Suprapubic pain
Polyuria
Haematuria
49
Q

Symptoms of acute pyelonephritis

A 
Fever
Rigor
Vomiting
Loin pain/tenderness
Costovertebral pain
Associated cystitis symptoms
Septic shock
50
Q

Symptoms of prostatitis

A 
Pain in the perineum/rectum/scrotum/penis/bladder/lower back
Fever
Malaise
Nausea
Urinary sx
Swollen/tender on PR exam
51
Q

Management of UTI in a non-pregnant woman

A

If 3+ symptoms/1 severe of cystitis and no vaginal discharge then treat empirically with 3 day course of trimethoprim/nitrofurantoin
If first line fails culture urine
If upper UTI do urine culture and start broad spec antibiotics

52
Q

Management of UTI in pregnant women

A

Can cause preterm delivery and IUGR
If asymptomatic bacteruria do a second sample
Treat with antibiotic
Avoid Ciprofloxacin/Trimethoprim in the first trimester
Avoid Nitrofurantoin in the third trimester

53
Q

Management of UTI in men

A

If lower UTI then 7 day course of trimethoprim/nitrofurantoin
If prostatitis then long (4wk) course Ciprofloxacin
If upper or recurrent UTI then urology referral

54
Q

Signs of hypovolaemia

A 
Low BP
Low UO
Non-visible JVP
Poor tissue turgor
Fast pulse
Daily weight loss
55
Q

Signs of fluid overload

A 
High BP
Raised JVP
Lung crepitations
Peripheral oedema
Gallop rhythm
56
Q

When do you treat hyperkalaemia

A

> 6.5 or with any ECG changes (do an ECG on anyone with K >6)

57
Q

How long does renal disease need to be present for to classify as CKD

A

> 3 months

58
Q

BP target for CKD patients; a) without DM b) with DM

A

a) <140/90

b) <130/80

59
Q

Three things that can go wrong with an AV fistula

A

Thrombosis
Stenosis
Steal syndrome

60
Q

When would you use haemofiltration rather than haemodialysis

A

When the patient is really haemodynamically unstable (low BP, critical care ect)

61
Q

Contraindications to renal transplant

A

Absolute: cancer with metastates
Temporary: active infection, HIV with viral replication, unstable CVD
Relative: congestive heart failure, CVD

62
Q

Factors contributing to renal transplant loss

A 
Donor factors - age, comorbidity, living/deceased, donor after brain death vs cardiac death
Rejection
Infection
BP/CVD
Recurrent renal disease in graft
63
Q

Presentation of IgA nephropathy

A

Asymptomatic microscopic haematuria or episodic visible haematuria, high BP, proteinuria

64
Q

Presentation of HSP

A

Purpuric rash on extensor surfaces typically on the legs, polyarthritis, abdominal pain (GI bleeding), nephritis

65
Q

Presentation of post-streptococcal glomerulonephritis

A

Around 2 weeks after throat infection or 3-6 weeks after skin infection
Haematuria, nephritis, oedema, high BP, oliguria

66
Q

Presentation of anti-GBM disease (Goodpasteurs)

A

Renal disease - oliguria/anuria, haematuria, AKI, renal failure
Lung disease - pulmonary haemorrhage, SOB, haemoptysis

67
Q

Signs and symptoms of hypernatraemia

A 
Lethargy
Thirst
Weakness
Irritability
Confusion
Signs of dehydration
Coma
Fits
68
Q

Causes of hypernatraemia

A

Usually due to loss of fluid > loss of Na
Diarrhoea/vomiting/burns
Diabetes insipidus
Primary hyperaldosteronism
Iatrogenic from fluids (excessive saline)

69
Q

Signs and symptoms of hyponatraemia

A

Anorexia, nausea, malaise
Headache, irritability, confusion, weakness, dropping GCS, seizures
Cardiac failure/oedema depending on cause
Low Na is an important cause of falls in the elderly

70
Q

Causes of hyponatraemia

A

Dehydrated;
Urinary Na >20 means sodium and fluid is being lost from the kidneys - Addisons disease, renal failure, too many diuretics, osmotic diuresis (high glucose or urea)
Urinary Na <20 means sodium and fluid is being lost elsewhere - diarrhoea, vomiting, fistulae, burns, small bowel obstruction, trauma, heat exposure, trauma

Not dehydrated;
Oedematous - nephrotic syndrome, cardiac failure, liver cirrhosis, renal failure
Not oedematous but urine osmolality >100 - SIADH
Not oedematous but urine osmolality <100 - water overload, severe hypothyroidism, glucocorticoid insufficiency

71
Q

Concerning signs and symptoms of hyperkalaemia

A 
Fast irregular pulse
Chest pain
Weakness
Palpitations
Light-headedness
72
Q

Causes of hyperkalaemia

A 
Oliguric renal failure
Addisons disease
K-sparing diuretics
Rhabdomyolysis
Metabolic acidosis (DM)
73
Q

Signs and symptoms of hypokalaemia

A

Muscle weakness, hypotonia, hyporeflexia, cramps, tetany, palpitations, arrythmias (can cause light-headedness), constipation

74
Q

ECG changes in hypokalaemia

A

Small or inverted T waves
Prominent U waves
Long PR interval
ST depression

75
Q

Causes of hypokalaemia

A 
Diuretics
Cushings syndrome/steroids/ACTH
Vomiting/diarrhoea
Pyloric stenosis
Conn's syndrome
76
Q

Signs and symptoms of hypercalcaemia

A 
'Bones, stones, groans and psychic moans'
Abdo pain, vomiting, constipation
Polyuria, polydipsia
Depression, anorexia, weight loss, tiredness, weakness
HTN
Confusion, pyrexia
Renal stones, renal failure
Low QT interval
77
Q

Causes of hypercalcaemia

A

Malignancy! (bone mets, PTHrP, myeloma)
Primary hyperparathyroidism
Sarcoidosis
Lithium

78
Q

Signs and symptoms of hypocalcaemia

A 
'SPASMODIC' pneumonic
Spasms (Trosseaus sign, Chvosteks sign)
Peri-oral paraesthesia
Anxious/irritable/irrational
Seizures
Muscle tone increased in smooth muscle causing colic, wheeze, dysphagia
Orientation impaired/confusion
Dermatitis
Impetigo herpetiformis
Cardiomyopathy (long QT interval)
79
Q

Causes of hypocalcaemia

A

CKD
Hypoparathyroidism
Low Mg
Low vitD

80
Q

What causes haemolytic uraemic syndrome?

A

It is a thrombotic microangiopathy
Usually 5-10 days after bloody diarrhoea in children - Usually caused by toxins from enterohaemorrhagic E.coli which damage endothelium (vessels and glomeruli) and cause microthrombi formation. Get haemolysis because of small vessel blockage by thrombi.

81
Q

What 2 extra blood tests can you do to assess for haemolysis and would they be high or low

A

High LDH

Low Haptoglobin

82
Q

What is the triad of haemolytic uraemic syndrome

A
  1. Low platelets - petechia, purpura, mucosal bleeding
  2. Microangiopathic haemolytic anaemia - fatigue, dyspnoea, pallor, jaundice
  3. Decreased renal function - haematuria, proteinuria, oliguria/anuria
83
Q

What is the pentad of thrombotic thrombocytopenic purpura

A
  1. Microangiopathic haemolytic anaemia - fatigue, pallor, jaundice
  2. Low platelets
  3. AKI
  4. Neurological symptoms - headache, palsies, seizure, confusion, coma
  5. Fever
84
Q

How does autosomal recessive PCKD present

A

Ante/perinatally with renal cysts (salt and pepper appearance on USS), congenital hepatic fibrosis and portal hypertension

85
Q

Features of Alport syndrome

A

Progressive renal insufficiency
High-tone sensorineural hearing loss
Visual changes - anterior lenticonus, bulging of lens seen on slit lamp examination

86
Q

Causes of cystic kidney disease

A 
Multicystic dysplastic kidneys (congenital)
ADPKD/ARPKD
Simple cysts
Acquired cysts
Tuberous sclerosis
Von Hippel Lindau
Medullary cystic kidney disease

Final Year (4 decks)

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