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Phase 3A > Renal > Flashcards

Renal Flashcards

1
Q

Why does nephrotic syndrome increase clot formation?

A

Antithrombin 3 and plasminogen is lost in the urine

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2
Q

Why does nephrotic syndrome increase risk of heart disease?

A

Liver compensates for loss of proteins buy increasing synthesis of lipids - causes hyperlipidaemia

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3
Q

Why is there an increased infection risk in nephrotic syndrome?

A

Loss of antibodies in the urine

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4
Q

What would you look for on a blood film that would distinguish AKI from CKD?

A

Hypocalcaemia - wouldn’t happen in AKI, but would in CKD (vitamin D conversion reduced due to damage, also lost in the urine, vit D regultes calclium - therefore CKD a cause of secondary hyperparathyroidism)

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5
Q

What is diabetes inspidus?

A

Decreased ADH (brain) or lack of response to ADH (nephrogenic)

Cannot reabsorb water

Presentation: Polyuria and thirst (increasing serum osmolality), dehydration, postural hypotension, +++Na+ (because low water)

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6
Q

What is the role of ADH?

A

Allows for water reabsorption in the collecting ducts

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7
Q

What is a differential for diabetes inspidus?

A

Drinking too much water!

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8
Q

What is the cause of cranial diabetes insipidus?

A
  • Hypothalamus does not produce ADH (can be caused by tumours, infections, head injuries, brain surgery / radiotherapy)
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9
Q

What tests would you do for diabetes inspidus?

A
  • Urine osmolality LOW (lots of water not many solutes)
  • Water deprivation test –> don’t give water for 8 hours, then give desmopressin (synthetic ADH( and measure urine osmolality again.
    Used to distinguish between cranial and nephrogenic.
    Cranial - after desmopressin urine becomes less dilute (Can still respond to ADH just have problems making it). In nephrogenic - no response to the ADH as problem with the response to it).
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10
Q

What are the causes of nephrogenic diabetes?

A
  • Lithium - most known cause
  • Genetics
  • Electrolytes
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11
Q

What medication should be prescribed for those with CKD?

A

ACEi

ACEi first line for diabetics, not Ca2+ blocker - due to co-existing diabetic nephroptathy

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12
Q

What is the mechanism of action of spironolactone?

A

Aldosterone antagonist

Adverse effects: hyperkalaemia and gynaecomastia (switch to eplenerone if troublesome)

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13
Q

What type of blood gas distrubance would you see in a patient with diarrhoea?

A

Metabolic ACIDOSIS

*loosing bicarb in the faeces

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14
Q

What type of. blood gas disturbance would you see in vomitting?

A

Metabolic alkalosis

Would be loosing H+ in the vomit

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15
Q

What drugs should stopped in AKI?

A
  • NSAIDs
  • Antibiotics
  • ACE inhibitors
  • ARB2’s
  • Diuretics
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16
Q

What happens to potassium in AKI?

A

Shoots up

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17
Q

How would you distinguish between AKI and dehydration?

A

Both cause a reduced urine output

AKI: creatinine rise

Dehydration: urea (BUN) will rise much more than the creatinine, causing reduced urine output

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18
Q

What would you look for on the bloods of a patient presented with dehydration?

A

Urea (BUN)

Will be raised

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19
Q

What are the maintenance fluids for a healthy adult?

A
  • 25-30ml/kg/day water
  • 1 mmol/kg/day K+, Na+, Cl-
  • 50-100g/day glucose
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20
Q

How much potassium does 0.9% saline have in it?

A

154 mmol Na and Cl

21
Q

What does hartmaans solution have in it?

A

Na, Cl, Bicarb, K+

22
Q

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

A

Minimal change disease

23
Q

What is the treatment of minimal change disease?

A

Prednisolone

24
Q

A man comes in with haemoptysis, fever, and joint pain. Investigations show an AKI. What antibody would you want to test for?

A

Anti GBM

Signs of lung and kidney problems
Nephritis is usually rapid and progressive - happens within a couple of days

25
Q

What are antiGBM antibodies against?

A

Type 4 collagen

26
Q

List 4 causes of rhabdomyolysis

A
  • After a fall, long lie
  • Seizure
  • Statin use
  • Crush injury
27
Q

What would you expect to see on the bloods of someone with rhabdomyolysis?

A
  • Myoglobinuria
  • Calcium low (myglobin binds calcium)
  • Elevated CK
  • Hyperkalaemia - why you have to be really careful - ECG
28
Q

What is the treatment of rhabdomyolysis?

A

Lots and lots of IV fluids

29
Q

How can you differentiate between post-strep glomerulonephritis and IgA glomerulonephritis / bergers?

A

Bergers = URTI in last couple of days

Post-strep = URTI 2-3 weeks ago

30
Q

What things in the history would point towards Alports syndrome?

A
  • Hearing problems
  • Eye problems
  • Haematuria
31
Q

What causes post-strep glomerulonephritis?

A

Strep pyogenes

32
Q

What is a commonly recognised caution in those with nephrotic syndrome?

A
  • Increased risk of VTE
    Antithrombin 3 is lost in the urine (therefore unnopposed action of thrombin)
  • Infection rates increased - loose antibodies
  • AKI
  • Hypovolaemia
  • CV complications (increase lipids due to loss of proteins)
33
Q

What are the symptoms of amyloidosis?

A
  • Progressive weakness and SOB
  • Commonly causes loss of renal function and proteinuria
  • Hepatosplenomegaly
34
Q

What is the most common cause of kidney disease?

A

Diabetic nephropathy

35
Q

What things would you ask about in a LUTS history?

A

Frequency

Before stream - incontinence, urgency, trouble starting
During - weak flow, stop and starting of urine, dysuria
Following - dribbling, incomplete emptying

Urine - smelly, frothy, any blood

Fever, loin to groin pain, rigors, generally unwell

Red flag: back pain, weight loss, night sweats

36
Q

What is the mist common extra-manifestation of PKD?

A
  • Hepatomegaly (cysts form in the liver)
  • Most people think berry aneurysms are the most common, however this is not true, but they are a common exam Q to ask about!
37
Q

What can happen as a result of correcting sodium quickly in someone that has low sodium?

A

Central pontine myelosis

38
Q

If you use large volumes of NaCl for fluid resus, what can be a complication?

A

Hyperchloraemic metabolic acidosis - too much Cl-

39
Q

What is the triad seen in HUS?

A
  • AKI
  • Haemolytic anaemia - fragmented RBC seen on blood film
  • Low platelets
40
Q

What two things should you NOT give people with HUS?

A
  • Molitlity agents e.g. loperamide

- Antibiotics

41
Q

How long does it take for an AV fistula to mature before use?

A

6 - 8 weeks

42
Q

What is the anion gap?

A

Used to work out whether metabolic acidosis has been caused by :

  1. Increased acid production / ingestion
  2. Reduced loss of acid / loss of bicarb (can’t mop up excess acid)

If the anion gap is normal, no extra acid being produced in the body (have situation 2) -

If the anion gap is high, indicates a new acid (such as lactate, ketones, urate, acid posioning), has been produced by the body

43
Q

How can you tell that there is a renal cause as apposed to pre/post-renal cause on a urine dip?

A

Raised protien in renal problems - would not see with pre or post

44
Q

How can you tell the difference between an acute intersitutal nephritis and an acute tubular acidosis?

A

ACN - inflammatory, therefore involves WBC - raised in the urine

ATA/N = not inflammatory, results in destruction of cells, no WBC (luecocytes) in urine

Glomerulonephritis cause = nephritic - would see lots of blood present in the urine

45
Q

List some causes of acute interstitual nephritis

A
  • Penicillin containing drugs
46
Q

Name 4 causes of intrinsic AKI

A 
Glomerulonephritis 
ATN (Acute tubular necrosis) 
AIN (Acute intersititual nephritis)
Rhabdomyloysis 
Tumour lysis syndrome
47
Q

How would you classify AKI?

A

Pre-renal
Intrinsic
Post-renal

48
Q

List some of the signs of AKI

A
  • Confused patient (particulrly elederly) - caused by the build up on uraemia, leading to encepalopathy
  • Reduced urine output
  • Oedema

Phase 3A (17 decks)

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