Renal Problems Flashcards

1
Q

Approach to AKI

A

Identify patient at high risk and optimise care l Stop all nephrotoxic agents
l Assess and optimise volume status
l Monitor creatinine and urine output
l Non-invasive diagnostic workup l Invasive diagnostic workup
l Revise drugs
l Diet

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2
Q

How do NSAIDs cause acute AKI

A
  • anti-inflammatories block the production of prostaglandins
  • PG - have a role in maintaining blood flow to the kidney (normally vasodilate blood vessels to kidney)
  • NSAIDS will block the production, we will get decreased PG2 and this will cause vasoconstriction, reduce renal blood flow and decrease GFR, this will result in an INCREASE in renin secretion
  • if already dehydrated or hypovolemic can cause AKI
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3
Q

How to check volume status

A
  • JVP
  • pulse
  • capillary refill
  • BP
  • peripheral oedema
  • listen to lungs
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4
Q

What could blood in the urine indicate?

A

could indicate glomerulonephritis

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5
Q

What could high urea, proteinurea be suggestive of?

A

means inflammation - and infection is probably the most common cause

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6
Q

What are some other tests you can perform?

A
  • streptococal serology
  • coagulation
  • ultrasound of kidney - see flow, shape, size
  • kidney biopsy (if creatinine continues to increase)

then need to monitor - weekly blood tests, no nephrotoxic medication

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7
Q
####??!?!?! 
Why does phosphate increase with kidney failure
A
  • Kidney actviates Vit D
  • hwoever if this is not working, then not much vit D - this is needed to absorb calcium
  • if have low calcium PTH is released, and this will try to icnrease calcium but also will increase phosphate as well
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8
Q

Why do we see anaemia in chronic kidney disease?

A

due to impaired renal function - get reduction in erythropoeitn

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9
Q

How can we lower phosphate levels?

A

can give calcium carbonate

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10
Q

Main causes of CKD and why?

A
  • Diabetes - excess glucose in the blood starts sticking to proteins on wall of blood vessels, effects efferent arteriol -stiff and narrow, causing obstruction to glomerulus and makes it hard for blood to leave glomerulus - increase s pressure leading to hyperfiltration, get increased extracellular matrix secreted expanding the glomerulus - can lead to chronic kidney disease
  • Hypertension - get renal artery walls thickend in hypertension which will narrow lumen, this means less blood and oxygen gets to kidney resulting in ischemic injury, immune cells - will get glomeruloclerosis due to increased extracellular matrix around damaged areas leading to chornic kidney disease
  • glomerulonephritis
  • obese, smoking (toxins), family history
  • infections
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11
Q

Main signs and symptoms of CKD

A
  • tired
  • hard concentrating
  • poor appetite
  • swollen feeet and ankels
  • dry itchy skin
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12
Q

Secondary factors caused by CKD and reason (hint -what does kidney do?)

A

enin released to try and increase BP, however this furhter damages kidney)

  • high potassium levels (can impair heart functioning) (because lower kidney function - less potassium is secreted) - builds up in blood
  • calcium increase, phosphate increase (weak bones) (kidney helps activate vit D- helps increase calcium absorption from diet, get hypocalcaemia, lead to increase PTH, bone loses calcium, - weak bones,
  • proteinuria
  • anaemia
  • uraemia (increased urea in blood because it cannot be filtered out - can cause anemia, fatigue, pericarditis, heart failure, GI upsets ect, itchy skin ) - increased bleeding, platelets cannot stick to each other as well
  • Anaemia - (erhythropoietin decreases, decreased production of RBCs)
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13
Q

Nephrotic syndrome

A
  • glomeruli more damaged, so can allow plasma proteins to get through - causing proteinuria
  • hypoalbuminemia
  • low oncotic pressure, low osmoitc pressure - get water drive out and into tissue - oedema
  • get increased levels of lipids in blood - hyperlipidaemia
  • lipids in urine
  • caused by immune complexes - autoantibodies causing reaction and damaging GBM - gets thicker
  • can lead to Chronic kidney failure
  • frothy urine
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14
Q

Nephritic syndrome

A
  • immune complexes lodge in capaillary and get immune response against this
  • white cells recruited due to inflammation
  • allows red blood cells to get through openeing and white blood cells
  • also protein
  • haematuria (blood in urine)
  • oliguria - low urine output due to damage of glomerulus
  • low GFR
  • high BP due to lack of filtration
  • more inflammation
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15
Q

Rapidly progressing GN

A
  • inflammation of glomeruli
  • causes proliferaiton of cells in bowmans space forming cresent shape
  • due to immune reactions of body e.g body bakign antibody agianst bowmans capsuel
  • get proliferation of epithelial cells - cause cresents
  • can lead to firbosis
  • cannot filter blood very well - lead to decrease GFR
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16
Q

What are cresents

A
  • taking up space in bowmans capsule
  • can go on to form fibrosis
  • non-specific response to injury in capillary wall- causing inflammation response
  • get increase amounts of gaps in filtration space to allow white blood cells and inflammatory cells
  • then can get plasma proteins as well to enter space
  • can look under light microscpoy
17
Q

Good pasture disease

A
  • linear igG lining membrane
  • when have coughing blood, and haematuire and proteinuiria

Treatment - prednisone, cyclophosphamide,

-if get chronic kidney disease - then may need dialisis

18
Q

How do we treat differences in people with hypertension if they are over 50 and under 50

A
  • under 50 - ace inhibitor - because normally have stimulation of renin-angiotensin system
  • over 50 - diuretics and calcium channel blocker
19
Q

If patients have other problems what can we treat them with?

A
  • IHD – B-blocker
  • CHF – Thiazide/ACEI/ARB/B-blocker
  • DM – ACEI/ARB/Thiazide
  • CKD – ACEI/ARB
20
Q

Resistant hypertension -

A
if not responsding to BP medicaiton , despite using 3 drugs 
Causes - suboptimal therapy 
-diuretic, dose, complementary drugs
non-compliance
-competing drug - sodium, NSAID, OCP

Secondary - endocrine- hyperthryoid , renal - gn

-Very important to use diuretic to treat HT

21
Q

Good combinaiton for BP

A

Good

Thiazide and ACEI ACE and CCB B-blocker and α-blocker Thiazide and CCB

22
Q

Bad combination

A

•Bad

ACEI and B-blocker ARB and B-blocker ACEI and ARB

23
Q

What can you do to confirem hypertension

A

do an abulatory blood pressure measuremnets

24
Q

What are symptoms of a UTI

A
  • old age, female, sexual intercorse - risk factors
  • white cell count increases
  • ecoli may be present
25
Q

Cystitis

Pylonephritis

A

Cystitis - infeciton of bladder

Pylonephritis - infection of upper urinary tract

26
Q

Bacturia

A

Smooth muscle relaxation and ureteral dilatation occur
• Increased risk of pre-term birth, low birth weight and perinatal mortality.
• Treatment reduces complications

Treat with ammoxiciliin

27
Q

What can you do if you get recurrent cysititis?

A

supressive therapy

  • can be due to change in microflora
  • pee after sex
  • probiotics
28
Q

End stage renal disease options

A

conservaiton
dialysis
-renal transplant