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Renal disease Flashcards

1
Q

Painful pins and needles + unable to distinguish hot and cold when bathing feet =

A

Wegener’s granulomatosis

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2
Q

First line renal Ix

A

USS

+ urinalysis for blood and protein (+urine microscopy)

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3
Q

Red cell casts are diagnostic of what two conditions?

A

Glomerulonephritis

Vasculitis

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4
Q

3 things cANCA means

A

It is associated with Wegener’s granulomatosis

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5
Q

Microscopic vasculitis can cause?

A 
Episcleritis
Skin rashes
Joint pains
Nosebleeds
GI bleeding
Acute kidney injury
Chronic kidney disease
Pulmonary haemorrhage
Mono neuritis multiplex - pins and needles etc
Seizures due to intracerebral haemorrhage
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6
Q

Crescents on renal biopsy indicates

A

Severe glomerular injury

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7
Q

Why act quick in rapidly progressive glomerulonephritis (RPGN)?

A

Patients can rapidly become unwell with multi-system symptoms
All c ANCA positive patients are at risk of developing pulmonary involvement
Rapid aggressive immunosuppression may salvage damaged nephrons and restore useful renal function

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8
Q
  1. Duration of ABx in UTI
  2. Most common pathogen?
  3. Uncomplicated UTI first line Ix
  4. After recurrent UTIs what Ix?
  5. Non drug methods to reduce UTIs
  6. Prophylaxis for UTIs?
A
  1. 3 day
  2. E.coli then S. saprophyticus
  3. Urinalysis
  4. USS
  5. Pee after sex, Avoid barrier contraception, cranberry, increase fluids, probiotics
  6. Low dose, once daily ABx or single dose post sex
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9
Q

CKD
Definition
Stages

A

Kidney damage OR GFR <60
For >3 months

1 = 60-89
2 = 45-59
3 = 30-44
4 = 15-29
5 = <15
5D = On dialysis
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10
Q

AKI criteria (2 ways and all within 1 week)

A

Serum creatinine rise of >26 over 48hrs OR rise of 1.5fold

Low urine output for over 6 hours

all occurred within 1 week

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11
Q

Indications for dialysis

A

Hyperkalemia

Acidosis

Fluid overload

Uraemic encephalopathy

Pericarditis

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12
Q
  1. First line Ix if suspected CKD/AKI to exclude obstruction
  2. Size of kindeys in CKD
  3. Asymmetry of renal tract =
  4. Unilateral enlargement of kidney
  5. diabetic drug CI in CKD
A
  1. USS
  2. Smaller
  3. Renal artery stenosis
  4. Hydronephrosis
  5. Metformin - lactic acidosis
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13
Q
  1. For nephrotic syndrome what must be known

2. How is proteinuria measured

A
  1. Low serum albumin. Proteinuria >3g/24hr. ACR or PCR

2. No longer 24hr collection. Now on the spot ACR or PCR

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14
Q

Biopsy in renal disease

A

Pre existing conditions such as DM mean that biopsy unneeded as likely to be DM nephropathy

Useful to detect glomerulonephritis (haematuria is a clue)

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15
Q

Transferrin saturation is low thus meaning that acute blood loss is unlikely and cause is more liekly to be?

A

CKD

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16
Q

The most common explanation for anaemia in CKD is

A

Poor bioavailability of iron (uraemia reduces iron absorption aim for 20% saturation

EPO deficiency

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17
Q

EPO must be given in conjunction with?

A

Iron

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18
Q

What enzyme is affected in CKD which causes Vitamin D deficiency and then raised PTH to try and counteract the low calcium (secondary hyperparathyroidism - primary is where both are high)

A

1α hydroxylase

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19
Q

why metabolic acidosis in CKD?

A

A metabolic acidosis is common in CKD due to reduced capacity to excrete the acid load generated during metabolism

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20
Q

CKD is irreversible?

A

True

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21
Q

Reduce what from diet in CKD?

A

Phosphate and potassium and salt

22
Q

DM BP targets

A

130/80

normally <130/85

23
Q

Treat hyperphosphataemia in CKD

A

Yes - unpleasnt chalkty taste

24
Q 
CKD complication and management
Anaemia
Hyperkalemia
Hyperphosphotaemia
Sodium and fluid retention
Hyperparathyroidism
A

EPO + Iron

Restrict diet + dialysis if severe

Restrict diet + phosphate binders

Diuretics + antihypertensives

Vitamin D

25
Absolute indications for dialysis
GFR <15 OR aeiou A > Acidemia pH <7.1 E > electrolyte imbalance > hyperklaemia I > Intoxication (drug or posion removal) O > Oedema/overload (pulmonary oedema U > Uraemia (encephalopathy and pericarditis
26
CKD Causes - District general hospital renal physician Sx Ix
Diabetes, Glomerulonephritis, Hypertension, Reflux, Polycystic kidneys From stage 4 Loss of appetite, fatigue, sleepy, anuria, itching, HTN Bloods: anaemia, low calcium, high phosphate, high ALP, high PTH Urine: ACR/PCR, culture, dipstick Imaging: USS - shrunken Histology: If rapid or normal sized kidney and unclear cause
27
Glomerulonephritis: Eosinophils + RBC casts Renal tubular casts + pigmented cells RBCs + proteinuria >3g
Allergic interstitial nephritis Acute tubular necrosis Glomerulonephritis > Biopsy Multiple myeloma > Serum and urine immunoelectrophoresis
28
AKI Prerenal - hyaline casts Intrinsic Postrenal
Transient hypoperfusion - hypotension, HF Acute glomerulonephritis - inflammation of glomerular membrane Allergic interstitial nephritis - allergic reaction to drugs Acute tubular necrosis (>50%) - nephrotoxic agents causing prolonged renal hypoperfusion Obstruction of urinary tract
29
NSAIDS, ACEi and diuretics on prerenal AKI
1. NSAIDs constrict afferent arterioole = Reduced GFR 2. ACEi dilate efferent arteriole = reduced GFR ... never give in RENAL ARTERY STENOSIS 3. Diuretics reduce plasma volume and GFR
30
Acute tubular necrosis - muddy brown! Cause Sx Dx
AKI with renal cellular injury Prolonged hypoperfusion, myeloma, drugs such as aminoglycosides, rhabdomyolysis Oliguria ? polyuria > recovery Urinary Na and FeNa are high as kidneys cannot reabsorb Na because tubules are damaged Normal urinalysis MUDDY BROWN CASTS Coarsely granular casts Biopsy: Abnormal tubular epithelium
31
Allergic interstitial nephritis Cause Sx - TRIAD Dx
Inflammation of the interstitium of the kidney causing AKI Drugs - penicillin Infection: Pyelonephritis TRIAD: Myalgia, pyrexia and rash ``` Eosinophilia in urine and serum Pyuria White cell casts NO BLOOD Biopsy for definitive ```
32
When are hyaline casts seen?
Prerenal
33
High potassium =
ECG!
34
A 65 year old women is admitted with back pain, fatigue and dehydration. Her Hb is 98, her Ur 18, her Cr is 250, adjusted Ca 3.1. What investigation will most help in the diagnosis?
Urine electrophoresis
35
4 things when considering is this an AKI?
Monitor change in Cr – rise = AKI, maintained = CKD Look for previous bloods to see Cr level– same = CKD Ultrasound – Cortex is thin and kidney overall is shrunken = CKD AKI if comes with NSAIDs or vomit/diarrhea
36
CKD pathophysiology
Renal disease + proteinuria = loss of nephrons to fibrous tissue These nephrons get poor perfusion and so blood is diverted to surviving glomerulus = increases filtration and pressure on remaining glomeruli = damages them further = vicious cycle
37
Although ACEi are dangerous to AKi they are protective in CKD as they reduce ?
Proteinuria
38
In CKD whats is gold standard treatment?
Transplant NOT haemodialysis
39
Detailed CKD pathophysiology
Nephron number decreases in CKD so other nephrons increase their GFR to try and compensate (doesn’t work). So as hyperfiltration occurs more glomerular permeability occurs which lets through the filtration of more proteins, macromolecules and debris which = proteinuria > secondary dyslipidemia due to stimulation of liver synthesis across the board. AND nephrotoxic inflammation and remodeling due to the increased junk that filtered and cytokines such as TGF = fibrosis. ALSO RAAS is activated which causes hypertension. These combine to cause tubulointerstiail fibrosis and secondary Focal segmental glomerulo sclerosis which in turn causes anuria, low GFR and systemic complications such as uremia.
40
Nephrotic syndrome | Definition and Sx
>3.5g in 24h proteinuria This level causes clinical hypoalbuminemia > decreased oncotic pressure > Oedema > liver produces more proteins to compensate some of which are lipoproteins which carry cholesterol = hyperlipidemia Loss of anticoagulation factor = pro-thrombotic state = DVT, PE – anticoagulant once albumin is below 20 Lipoproteins from liver = increases cholesterol = rampant CVD Loss of antibodies = increased risk of infection
41
AKI definition
>26.5 Cr rise in Cr within 48hours or low urine output. There are 3 stages of Cr level/AKI severity
42
AKI causes accumulation of which toxins
Urea: Pericarditis Acidosis Hyperkalemia: Tented T waves and wide QRS Salt and water: Fluid overload
43
How does quantity of proteinuria dictate cause
>1g proteinuria = Significant = Glomeruloneprhitis and systemic diseases such as diabetes <1g proteinuria = Modest = Tubulointerstitial disease, upper and lower UTI, kidney stones
44
Post strep glomerulonephritis versus IgA nephropathy
Both come after URTI PSGN presetns week after URTI, IgA is at the same time PSGN shows immune complex and LOW complement + streptolysin O in blood IgA nephropathy shows mesangial expansion with immune complexes
45
Steps to quantifying proteinuria
1. Urinalysis with dipstix 2. Urine albumin/creatinine ratio >30 3. 24 hour urine
46
Proteinuria algorithm
1. Assess BP 2. Quantify proteinuria 3. Assess GFR 4. USS 5. Special blood tests 6. Biopsy
47
ACEi and diabetic nephropathy
ACEi can help reduce proteinuria in CKD – dilatation of efferent arteriole HOWEVER don’t use in renal artery stenosis as they need to maximize GFR blood flow to kidney
48
``` Nephrotic syndrome Minimal change disease Presentation Ix Biopsy ```
Children with atopy + hodgkins Can't see podocyte problem on light microscope NEED electron microscope Responds well to steroids
49
``` Nephrotic syndrome Focal Segmental Glomerulonephritis Presentation Ix Biopsy ```
Young adult with HIV + FH Antibodies test are negative Segments of glomerular SCLEROSIS + IgM + Complement in basement membrane
50
``` Nephrotic syndrome Membranous glomerulonephritis Presentation Ix Biopsy ```
Older adults with malignancy IgG deposits + thickened GBM
51
Post renal Cause Sx Ix
Stones or cancer Nocturia, poor urinary flow, double micturition, oliguria, suprapubic mass Raised Cr + large kidney on ultrasound
52
Pre renal
Reduced renal perfusion Low BP

Stage 4 (12 decks)

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