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Phase II > Renal > Flashcards

Renal Flashcards

1
Q

What is nephritic syndrome

A 
Hypertension
Blood- Haematuria occurs due to podocytes developing large pores which allows blood and protein to escape into the urine.
Some protein
Fast onset
Low urine volume due to poor function
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2
Q

What is nephrotic syndrome

A

Proteinuria >3.5g in 24hrs
Oedema
Hypoalbuminaemia
Hyperlipidaemia (by product of increased albumin production)

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3
Q

Causes of nephritic syndrome

A

Post strep glomerulo nephitis

IgA Nephropathy

DM/ Vasculitis

Rapidly progressive glomerular nephritis

  • Goodpastures
  • Vasculitis - Wegner’s/ Churg strauss/ microscopic polyangitis
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4
Q

Causes of nephrotic syndrome

A

Primary:
Minimal change
FSGS
Membranous glomerulonephitis

Secondary:
SLE

Hep B and C

HIV

Diabetes mellitus

Malignancy
Amyloidosis

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5
Q

What is haemolytic uraemic syndrome

A

Triad of

Thrombocytopenia
Haemolytic Anaemia
AKI

Children
Emergency

Often after food poisoning/ gastroenteritis e.g. E coli, Shigella, Campylobacter

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6
Q

What is minimal change glomerulonephritis

A

Nephrotic
• Childhood/ adolescence (commonest cause in children)
• Responds to steroids
• May recur
• Usually no progression to renal failure
• Loss of podocytes due to unknown circulating factor (not immune complex)

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7
Q

What is FSGS

A

• Commonest in adults?
Other end of spectrum from minimal change
• Less responsive to steroids (need ciclosporin etc)
• Fibrosis/ scarring/ glomerulosclerosis
• Circulating factor causes – transplants often it recurs
• Progressive to renal failure
High recurrence in transplants

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8
Q

What is Membranous glomerulonephritis?

A
  • Causes kidney failure in a third of patients
  • Immune complex deposits
  • Autoimmune (likely) or secondary e.g. lymphoma, lupus or malaria.
  • IgG
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9
Q

What happens to kidneys in DM in context of nephrotic?

A
  • Thickening of the basement membrane/ collagen
  • Microvascular damage
  • Mesangialsclerosis
  • Progressive renal failure
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10
Q

Describe IgA nephropathy

A
  • Commonest GN
  • Any age
  • Haematuria can be invisible
  • Mucosal infections relationship
  • Variable histology and course
  • Possible proteinuria
  • Often renal failure
  • Mesangial damage and scarring
  • Immune complex deposition
  • appears within a day or two after a URTI
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11
Q

Describe hereditary nephropathies

A 
•	Thin GBM nephropathy
•	Benign familial nephropathy
•	Isolated haematuria (blood is normal)
•	Alport:
X linked
Abormal collagen IV
Associated with deafness
Abnormal GBM
Progressive to renal failure
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12
Q

What is Goodpastures?

A

• Uncommon
• Rapidly progressive
• Acute onset of severe nephritic syndrome
• Association with pulmonary haemorrhage (smokers)
• Autoantibody to collagen IV in BM
• Treatable by immune suppression and plasmaphoresis if caught early
(steroids and cyclophosphamide)
• IgG deposition with no Em deposit and inflam cells
Anti GBM

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13
Q

Renin and aldosterone levels in Cushings Conns and Renal artery stenosis. Results?

A

Cushing’s and Conn’s would be associated with a high aldosterone and a low renin, renal artery stenosis would be associated with a high renin and aldosterone, Liddle’s (genetic) is associated with a low renin and aldosterone.

Hypertension and hypokalaemia

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14
Q

Treatment hyperglycaemia

A

Manage precipitating factors, stop drugs e,g, ACEi

Stabilisation of the cardiac membrane
intravenous calcium gluconate by slow IV injection titrated to ECG response

Short-term shift in potassium from extracellular to intracellular fluid compartment
combined insulin/dextrose infusion
nebulised salbutamol
Consider NaHCo3 if acidotic

Removal of potassium from the body
calcium resonium (orally or enema)
loop diuretics
dialysis

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15
Q

Cause and treatment of most common solid organ transplant recipiants

A

Cytomegalovirus

Ganciclovir

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16
Q

Post-op complications of renal transplant

A 
Post-op problems
ATN of graft
vascular thrombosis
urine leakage
UTI

Hyperacute acute rejection (minutes to hours)
due to pre-existent antibodies against donor HLA type 1 antigens (a type II hypersensitivity reaction)
rarely seen due to HLA matching

Acute graft failure (< 6 months)
usually due to mismatched HLA. Cell-mediated (cytotoxic T cells)
other causes include cytomegalovirus infection
may be reversible with steroids and immunosuppressants

Causes of chronic graft failure (> 6 months)
both antibody and cell mediated mechanisms cause fibrosis to the transplanted kidney (chronic allograft nephropathy)
recurrence of original renal disease (MCGN > IgA > FSGS)

Long term cancer - 25% have cancer after 20 years (often skin)

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17
Q

ABG in sepsis

A

Patients who have sepsis often have a raised serum lactate due to the hypoperfusion of their peripheries. This gives them a metabolic acidosis with a raised anion gap.

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18
Q

Raised anion gap vs normal?

A

If the anion gap is raised, this suggests that there is increased production, or reduced excretion, of fixed/ organic acids e.g.
Lactic acid (sepsis, tissue ischaemia)
Urate (renal failure)
Ketones (diabetic ketoacidosis)
Drugs/ toxins (salicylates, methanol, ethylene glycol)

If there is a metabolic acidosis with a normal anion gap, then this is either due to loss of bicarbonate, or accumulation of H+ ions. Causes include:
Renal tubular acidosis
Diarrhoea
Addison's disease
Pancreatic fistula
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19
Q

Management of acute renal colic

A

IM or oral Diclofenac
Alpha-adrenergic blockers to aid ureteric stone passage

US - 45% sensitivity
Non-contast CT if not

Lithotripsy or nephrolithotomy for severe cases. most pass within 4 weeks

<0.5cm then conservative

If assocaited infection then urgent need for decompression so percutaneous nephrostomy (in loin)

If large proximal stone (e.g. 2.3cm staghorn calculi) then pecutaneous nephrolithotomy as lipotrypsy has low clearence rate

Complex stone disease of CI of lithotripsy (preggers) then ureteroscopy

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20
Q

Prevention of stones

A

Calcium stones may be due to hypercalciuria, which is found in up to 5-10% of the general population.
high fluid intake
low animal protein, low salt diet (a low calcium diet has not been shown to be superior to a normocalcaemic diet)
thiazides diuretics (increase distal tubular calcium resorption)

Oxalate stones
cholestyramine reduces urinary oxalate secretion
pyridoxine reduces urinary oxalate secretion

Uric acid stones
allopurinol
urinary alkalinization e.g. oral bicarbonate

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21
Q

factors which effect eGFR

A

pregnancy
muscle mass (e.g. amputees, body-builders)
eating red meat 12 hours prior to the sample being take

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22
Q

eGRF variables

A

CAGE - Creatinine, Age, Gender, Ethnicity

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23
Q

Complications in peritoneal dialysis

A

peritonitis: coagulase-negative staphylococci such as Staphylococcus epidermidis is the most common cause. Staphylococcus aureus is another common cause
sclerosing peritonitis

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24
Q

Way of diagnosing ATN

A

ATN rest the kidney, no fluid - one litre restriction. If you get brown cell card, fraction of Na in urine - More than 1% in urine = ATN.

Damage to tubular cells due to prolonged ischaemia or toxins
Kidneys can no longer concentrate urine or retain sodium - urine osmolality low, urine sodium high

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25
Q

Staging of AKI

A

Stage Creatinine Urine production
1 Increase 1.5-1.9x baseline < 0.5ml/kg/h for >6 consecutive hours
2 Increase 2.0-2.9x baseline < 0.5ml/kg/h for >12 consecutive hours
3 Increase > 3x baseline or >354 µmol/L < 0.3ml/kg/h for > 24h or anuric for 12h
3 also is renal replacement therapy

Only one thing needed

26
Q

Causes of transient or spurious non-visible haematuria

A

urinary tract infection
menstruation
vigorous exercise (this normally settles after around 3 days)
sexual intercourse

27
Q

Causes of persistent non-visible haematuria

A 
cancer (bladder, renal, prostate)
stones
benign prostatic hyperplasia
prostatitis
urethritis e.g. Chlamydia
renal causes: IgA nephropathy, thin basement membrane disease
28
Q

Testing of haematuria

A

urine dipstick is the test of choice for detecting haematuria
persistent non-visible haematuria is often defined as blood being present in 2 out of 3 samples tested 2-3 weeks apart
renal function, albumin:creatinine (ACR) or protein:creatinine ratio (PCR) and blood pressure should also be checked
urine microscopy may be used but time to analysis significantly affects the number of red blood cells detected

29
Q

When to refer for haematuria for cancer screening

A

Urgent
>45 and unexplain visible haematuria (no UTI
Non-urgent
Aged >60 with recurrent or persistent unexplained UTI

30
Q

What is Henoch- Schonlein purpura

A

palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
abdominal pain
polyarthritis
features of IgA nephropathy may occur e.g. haematuria, renal failure

analgesia for arthralgia
treatment of nephropathy is generally supportive. There is inconsistent evidence for the use of steroids and immunosuppressants

Self limiting

31
Q

Causes of hypokalaemia

A

1.) Increased potassium loss:
Drugs: thiazides, loop diuretics, laxatives, glucocorticoids, antibiotics
GI losses: diarrhoea, vomiting, ileostomy
Renal causes: dialysis
Endocrine disorders: hyperaldosteronism, Cushing’s syndrome (OBVIOUSLY spirono is aldosterone antagonist)

2.) Trans-cellular shift
Insulin/glucose therapy
Salbutamol
Theophylline
Metabolic alkalosis
  1. ) Decreased potassium intake
  2. ) Magnesium depletion (associated with increased potassium loss)
32
Q

Treatment hypokalaemia

A

Mild to mod 2.5-3.4 = oral KI if asymptomatic and no ECG changed

Severe hypokalaemia <2.5 or symptomatic = IV replacement, ITU/ cardiac monitoring. If no CI to fluiod therapy e.g. HF, then dilute to low concs to avoid plebitis. Don’t exceed 20mmol/hr

33
Q

What is ADPKD

A

Aut dom polycystic kidney disease
1/1000 Caucasians
Two loci PKD1 and 2 polycystin-1 and 2
Type 1 presents earlier

US diagnosed based on age and number of cysts 2 or more and <60. 4 in both aged >60

Enlarged kidney

34
Q

How to tell DI?

A

Water suppression test -
Stage 1 - no drink for 8 hours, measure weight and urine osmolality
Stage 2 - Give Desmopressin (like ADH) if nephrogenic there will be no response

35
Q

Treatment of DI

A 
Nephrogenic = Chlorothiazide
Cranial = desmopressin (synthetic vasopressin)
36
Q

Features of chlamydia

A

asymptomatic in around 70% of women and 50% of men

women: cervicitis (discharge, bleeding), dysuria
men: urethral discharge, dysuria

37
Q

Symptoms of anaemia in CKD

A

Tachy
Pale
Aoritc flow murmur
Predispsosition to LVH

38
Q

Causes of anaemia in renal failure

A

reduced erythropoietin levels - the most significant factor
reduced erythropoiesis due to toxic effects of uraemia on bone marrow
reduced absorption of iron
anorexia/nausea due to uraemia
reduced red cell survival (especially in haemodialysis)
blood loss due to capillary fragility and poor platelet function
stress ulceration leading to chronic blood loss

39
Q

How to calculate anion gap?

A

([Na+] + [K+]) - ([Cl] + [HCO3]) (how many anions extra)

The anion gap is used to classify metabolic acidosis into either;
Raised anion gap seen in e.g. diabetic ketoacidosis or,
Normal anion gap seen in patients with diarrhoea due to gastrointestinal bicarbonate loss.

40
Q

Side effects of EPO

A

accelerated hypertension potentially leading to encephalopathy and seizures (blood pressure increases in 25% of patients)
bone aches
flu-like symptoms
skin rashes, urticaria
pure red cell aplasia* (due to antibodies against erythropoietin)
raised PCV increases risk of thrombosis (e.g. Fistula)
iron deficiency 2nd to increased erythropoiesis

41
Q

Diabetes inspidius is characterised by what biochem?

A

Diabetes insipidus is characterised by a high plasma osmolality and a low urine osmolality

42
Q

Signs of hypovolaemia

A

Low BP, tachy, poor tissue turgor (hand pinch), sunken eyes, dry mucous membranes, daily weight loss, low urine output, cap refil.

Cap refil, BP, skin turgor are late chanes

43
Q

Signs of hypervolaemia

A

High BP, High JVP, weight gain, high urine output, lung crepitaions, periopheral oedema, gallop rhythm

44
Q

When to use colloid?

A

Blood for haemorrhage. HAS in speciallist use for hepatorenal syndrome

45
Q

Controversy regarding HCO3 in acidosis

A

Generate CO2 - adequate ventilation needed to prevent resp acidosis worsening
NaHCO3 given so NA load and volume load which can cause fluid overload.

Treat cause and in AKI may need RRT

46
Q

Possible indications for RRT in AKI

A

INdividual but suggestions:

Persistent acidosis or hyperkalaemia
Uraemia
Fluid overload unresponsive

47
Q

Complications of RRT

A 
Bleeding from anti coag
Damage from catheter 
Drug accumulation/ clearence
Altered nutrition
Procedural hypotension
48
Q

Symptoms/ complications of AKI

A 
Hyperkalaemia
	Hypertension
	Uraemia
		Pericarditis
		Acidosis
		Confusion
		Coma
Fluid overload
49
Q

Pre renal causes AKI

A 
Hypotension/ dehydration
		Vascular volume decrease e.g. haemorrhage
		CO decrease e.g. cardiogenicshocl, MI
		Peripheral vasodilation e.g. sepsis, drugs
	Renal artery stenosis
	Renal vasoconstriction
		NSAIDS, ACEi
HRS
50
Q

Renal causes AKI

A

INterstitial
Gentamicin, Cephalosporin, Lithium, Diuretics, pyelonephritis, infiltration e.g. sarcoid
Glomerular disease e.g. FSGS Goodpastures, Glomerulonephritis, ATN (prolonged hypoperfusion)
Vessels e.g. Vasculitis, Haemolytic uraemic syndrome, Thrombotic thrombocytopenic papura (autosomal recessive), DIC (due to cancers, trauma, sepsis, infection, allergy, aortic aneurisms)

51
Q

Post renal causes AKI

A 
Ureteric stricture
	Renal calculi
	Transition cell Carcinoma
	Pelvic mass
Iatrogenic ureter damage
52
Q

RFs AKI

A 
CKD
	CVD
	Maligancy
	Age
	Male
	CliverD
Complex surgery
53
Q

Initial management of AKI

A 
NEWS >7 consider ITUK+
			ECG - potassium
			Treat if >6.5 or ECG change
		Examine
BP - fluid trial 500ml in 15min x 4
54
Q

Monitoring of AKI

A

Catheter
K+Obs every 4 hrs
Lactate if signs of sepsis
Daily creatine (24hr behind response)

55
Q

Investigations AKI

A

Urine dip

		USS kidney
		LFTs (HRH)
		Thombocytopenia (if yes then bloodfilm for HUS)
		Intrinsic renal disease
			Igs
			Complement
			ANA
			ANCE
Anti-GBM
56
Q

Supportative treatment AKI

A

Sepsis
Stop nephrotoxic meds
Stop drugs that may cause comps e.g. diuretics (K) metformin (acidosis), antihypertensives
Check drug doses
Gastroprotection and nutritional support
Avoid contrast
Consider referral e.g. stage 3

57
Q

More defiinitve treatment AKI

A 
Refer to renal team if comps or stage 3 AKI
		Depends on cause
		Renal - biopsy and refer
		Post renal 
			Catheter
			Nephrostomy
			Urological interventio
		Mange fluid balance, acidosis, hyperkalaemia
58
Q

Complications of nephrotic syndrome

A

Loss of AT3, C and S - rise in fibrogen predispose to thrombosis

Los of Thyroxine binding globulin but not free thyroxine

59
Q

Signs and nsymptoms of polycystic kidney disease

A 
HTY - RAAS overactivity
Headache
Haematuria
Polyuria
Back pain
Cyst infections
60
Q

Treatment polycystic

A

Dietary restrictions

RRT

61
Q

What is diffuse proliferative glomerulonephritis?

A

classical post-streptococcal glomerulonephritis in child
presents as nephritic syndrome / acute kidney injury
most common form of renal disease in SLE

62
Q

What is clot retention??

A

Clot retention occurs as a sequal to bleeding in the urological tract. Large clots can become wedged in the urethra and cause acute urinary retention.

It can be seen under any circumstance where there is macroscopic haematuria, but patients are most susceptible post operatively if bladder irrigation is not sufficient; they suffer from clot retention within the catheter.

Treatment of the non operated patient is catheterisation with a three way catheter, with irrigation. In the post operative patient attempts should be made to mechanically free the clot.

Phase II (18 decks)

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