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Y6 Senior Med COPY > Renal > Flashcards

Renal Flashcards

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1
Q

define AKI

A
  • Increase in serum creatinine by ≥26 micromol/L within 48 hours
    *o Urine volume < 0.5 mL/kg/hour for 6 hours
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2
Q

pre renal vs renal vs post renal aki urea: creatinine ratio

A
  • pre renal: **urea rise&raquo_space; ** creatinine rise
  • renal and post renal: urea rise &laquo_space;creatinine rise
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3
Q

What are causes of pre-renal AKI

A
  • hypovolaemia (bleeding, shock, dehydration)
  • Oedema (cardiac /liver failure, nephrotic syndrome
  • Renal hypoperfusion –> reduced GFR (renal artery stenosis, vasculitis, drugs)
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4
Q

What are causes of renal AKI

A

intrinsic kidney damage, classified on location (vasculitis, glomerulonephritis, tubular, interstitial)

**Vascular **
* Vasculitis
* Cholesterol embolism

Glomerular
* Glomerulonephritis (IgA nephropathy, post-streptococcal etc)
* Haemolytic uraemic syndrome

Tubular:
* Acute tubular necrosis (ATN): secondary to ischaemia of pre-renal AKI or tubular toxins
* Nephrotoxins: aminoglycosides, cephalosporins, ACEi, ARBs, NSAIDs, gentamicin, contrast, cisplatin, heavy metals
* Rhabdomyolysis: myoglobin is nephrotoxic
* Multiple myeloma

Interstitial:
* Acute tubulointerstitial nephritis (penicillin, NSAIDs) Autoimmune (SLE)
* Infiltrative disease (lymphoma, sarcoidosis)
* Eclampsia

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5
Q

INTRINSIC acronym for renal causes of AKI

A

**INTRINSIC **
* Ischaemia (pre-renal AKI  ATN)
* Nephrotoxic ABx (gentamicin, vancomycin, tetracyclines)
* Tablets (ACEi, NSAIDs)
* Radiological contrast
* Injury (rhabdomyolysis)
* Negatively birefringent crystals (gout)
* Syndromes (glomerulonephritis)
* Inflammation (vasculitis)
* Cholesterol emboli

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6
Q

What are causes of post-renal AKI

A

Post-Renal: obstruction to urinary flow

  • In lumen ~ Luminal (i.e. stones)
  • In wall ~ Mural (i.e. transitional cell carcinoma, urethral stricture)
  • External pressure ~ Extra-mural (i.e. BPH)
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7
Q

risk factors for AKI

A

o **Age > 75 **
o CKD (acute-on-chronic)
o Comorbidities: **heart failure, peripheral vascular disease, chronic liver disease, diabetes mellitus **
o Sepsis
o Hypovolaemia (Poor fluid intake/increased losses)
o Nephrotoxic drugs

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8
Q

what are A>E findings for AKI

A

A. Vomiting
B. Tachypnoea, cough (pulmonary oedema), bibasal crackles
C. Tachycardia, fluid overload, dehydration, hypotension
D. Confusion (uraemia), oliguria (abrupt anruia ~ post renal)
E. Abdominal pain (palpable bladder ~ retention), M+V, diarrhoea, fatigue

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9
Q

what is workup for AKI

A

Bedside: ECG (hyperkalaemia), urine dipstick, catherise, urine sample (MC&S, ACR), ABG (acidosis, hyperk)

Bloods: U&E, calcium, phosphate, FBC, CRP/ESR, LFTs, CK (for rhabdo), renal screen

Imaging: bladder scan, renal uss

Renal biopsy (if unsure of cause - rarely done)

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10
Q

which drugs to stop in initial management of AKI

A

Stop drugs that:
* reduce renal perfusion –> NSAIDs, ACEi/ARBs, diuretics), are nephrotoxic (aminoglycosides, cephalosporins, tetracyclines
* are renally excreted –> metformin (lactic acidosis), sulphonylureas and insulin (hypoglycaemia), penicillins, beta blockers, lithium, digoxin
* can cause hyperK –> ACEi/ARBs, K-sparing diuretics, NSAIDs

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11
Q

What is management for AKI

A
  1. Fluid resuscitation – to treat oliguria
  2. Catheterisation: relieve bladder outflow obstruction and/or accurately monitor urine output
  3. Treat the CAUSE
    o Hypovolaemia > IV fluids
    o Retention > catheterise
    o Pulmonary oedema > cautious use of furosemide
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12
Q

Managment of hyper k with explanations

A
  1. Stabilize of the cardiac membrane –>
    IV calcium gluconate
    (does NOT lower serum potassium levels)
  2. Short-term shift in K from ECF to ICF
    compartment –>
    combined insulin/dextrose infusion and
    nebulised salbutamol
  3. Removal of potassium from the body –>
    calcium resonium loop diuretics and
    dialysis
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13
Q

investigations for acute urinary retention

A

bedside: post-void bedside bladder scan (assess residual volume)
bloods: routine - FBC, CRP, U+E
post catherisation CSU (catherised specimen of urine) for infection
US for hydronephrosis

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14
Q

causes of acute urinary retention

A

most common = BPH
others = urethral stricture, prostate cancer, UTI constipation

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15
Q

What are indications for dialysis

A
  • Acidosis (refractory to treatment / severe <7.2)
  • Electrolyte imbalance (refractory hyperkalaemia >7)
  • Intoxication (CKD stage 5; GFR <15)
  • Oedema pulmonary or fluid
  • Uraemia complications (encepalopathy, nausea, pruritus, pericarditis)
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16
Q

How can you define AKI

A

KDIGO guidelines:

  • increase serum creat >26 within 48hours
  • increase serum creat >1.5x baseline within past 7 days
  • urine vol <0.5ml/kg/h for 6 hours
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17
Q

How can you classify AKI

A

Based on creatinine compared to baseline or based on URINE OUTPUT

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18
Q

What is presentation of AKI

A 
oliguria / anuria
dehyrdation, thirst, dry mouth 
confusion 
uraemia: malaise, nausea, vomiting, pruritus, drowsiness 
hypotension, hypovolaemia (if prerenal) 
palpable bladder (if postrenal) 
renal bruits (if renovasc disease)
dehydration
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19
Q

What are two blood markers of renal function

A

Urea

Creatitinine

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20
Q

What is creatinine

A

breakdown of protein metabolism within muscles

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21
Q

How does creatinine travel through kidneys

A

creatinine enters the blood

is freely filtered through kidneys

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22
Q

what pathology can alter creatinine amount in the blood

and why

A

Creatinine is produced and excreted through kidneys at constant rate

So if RENAL FUNCTION DECREASES

You reduce creatinine excretion > increased in creatinine in blood

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23
Q

what is eGFR

A

Serum creatinine + age + sex + ethnicity

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24
Q

What is creatinine clearance

A

eGFR + height + weight

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25
why is creatinine clearance importannt
because the amount of creatinine produceed is dependent on our muscle mass
26
What is urea
a nitrogenous waste product
27
what conditions can cause urea to be elevated in the blood
DEHYDRATION - as urea is reabsorbed by kidneys when dehydrated UGI BLEED - as RBC breakdown cause increased urea
28
What is classification of AKI
KDIGO stages 1-3 Stage1: serum creatinine 1.5 to 1.9x reference; bodyweight in urine mLs every 2 hours for <12 hours Stage 2: serum creatinine 2.0 to 2.9x reference; bodyweight in urine mLs every 2 hours for over 12 hours Stage 3: serum creat >3; anuric >12h
29
Drugs that need to be stopped in AKI
DAMN Diuretics ACEi, ARB Metformin NSAID
30
What are three forms of renal replacement therapy
Haemodialysis Peritoneal dialysis Renal transplant
31
How does peritoneal dialysis work
Peritoneum is used as semipermeable membrane. Dialisate is instilled in peritneum
32
What is advantage and disadvantage of peritoneal dialysis
Advantage: can be done at home Disadvantage: risk of infection
33
Explain how haemodialysis works
Access via **AV fistula** / tesio line Takes blood out, passes it through dialysate. It is separated from dialysate via a semipermeable membrane Electrolyte imbalances are corrected via **diffusion**; fluid overload is corrected via **negative pressure in the dialysate** (draws out water from blood)
34
What are problems that occur with renal failure (link back to the specific renal function)?
Fluid balance >> FLuid overload Electrolyte homeostasis >> hyperkalaemia, acidosis Waste excretion >> uraemia Hormone production >> anaemia, hypercalcaemia (hyperphosphataemia)
35
CKD definition
irreversible progressive reduction in renal function over months- years (reduced GFR to < 60 ml/min/1.73m^2 for >3mo)
36
stages of CKD
1: eGFR >90 2: eGFR >60 3: eGFR >30 4: eGFR >15 5: eGFR <15
37
ix for CKD
- assess renal function = **eGFR** (isotopic GFR id gold standard but expensive), **creatinine** is better than urea (which varies based on hydration and diet) - boods: **FBC, U+E, low Ca, high phosphate, PTH, blood glucose** - urine: **ACR, dipstick** - CXR: heaart failure signs - US: check for structural abnormalities - **renal biopsy**: if rapidly proressive disease
38
How do you manage CKD
*slow progression of disease*: modify RF => antihypertensives (**ACEi, ARB**), good **glycaemic** control), **statins**, **stop smoking, exercise, good BMI** treat *complications* - sodium and fluid balance => **restrict fluid + salt, furosemide** - potassium = **diet restriction, sodium bicarb (if acidosis), potassium binding resins** - renal osteodystrophy and Ca/PO4 imbalance => **diet phosphate restriction, phosphate binders (sevelamer), alfacalcidol** - Anaemia => IV/SC **erythropoietin** Consider **renal replacement therapy**
39
complications of CKD
***'CRF HEALS'*** **C**VS: accelerated **atherosclerosis, pericarditis, uraemic cardiomyopathy** **R**enal Osteodystrophy: **osteoporosis, osteomalacia**, secondary or tertiary **hyperPTH**ism **F**luid overload **H**TN **E**lectrolyte disturbance **A**naemia **L**eg restlessness: unknown cause. Consider Clonazepam (with care as renal excretion) **S**ensory Neuropathy
40
Nephritic syndrome 4 key features
**Haematuria Proteinuria Hypertension Oliguria**
41
What are causes of nephritic syndrome
Immune-mediated - IgA nephropathy (e.g **Berger disease**, HSP)~ most common - **Post streptococcal glomerulonephriitis** - **Rapidly progressive glomerulonephritis (e.g Goodpastures**) CAUSE INFLAMMATION OF GLOMEROLUS AND NEPHRON > CAPILLARY BECOMES LEAKY -> blood and protein leak through
42
Describe what occurs in IgA nephropathy
Resp/GI infection -> abnormal IgA is produced -> antibodies made against it -> Sticky immune complexes are produced -> IgA an C3 deposited in glomerular membrane
43
Explain how IgA nephropathy presents
* 5-7 days post (resp or gi) infection * young male * recurrent episodes of macroscopic haematuria
44
how does henoch-schonlein purpura present
**Haematuria Rash on extensors (non-blanching raised palpable purpura) Scrotal Swelling Polyarthritis Abdo Pain**
45
What is Post-Streptoccal Glomerulonephritis
Occurs** 4-6 weeks** following **Group A beta-hemolytic Streptococcus (skin or throa**t) infection **Streptococcus pyogenes**!
46
differentiate IgA nephropathy from post strep glomerulonephritis
47
What must you manage in Post-Strep Glomerulonephritis
HTN
48
what is triad of nephrotic syndrome
**Proteinuria Hypoalbuminaemia Oedema** + Thrombosis (due to loss of antithrombin III thhrough kidneys) + Hypercholesterolaemia ( Due to hepatic synthesis in response to low oncotic pressure)
49
Causes of nephrotic syndrome
Minimal change diisease Focal segmenral glomerulonephritis (MOST COMMON) Membranous glomerulonephritis
50
investigations for glomerulonephritis
* Bloods: **FBC, U&Es, Ceatinine, LFTs** (albumin), **Lipid profile, Complement studies, Antibodies**: ANA, Anti-dsDNA, ANCA, Anti-GBM * Urine: **Dipstick, PCR, Microscopy** (red cell casts), 24 hr collection (creatinine clearance and protein) * Imaging: **CXR**: (infiltrates in Goodpasture’s and Wegener’s), **Renal tract ultrasound** (exclude other pathology) * **Renal Biopsy** (for microscopy)
51
management for nephrotic syndrome
* Monitor: **U&Es, BP, fluid balance and weight** * **Treat underlying cause** * Symptomatic relief and treat complications o **Oedema: salt and fluid restriction + furosemide** o **Proteinuria: ACEi/ARB** o **Lipids: statins** o **VTE: tinzaparin** o **Treat infections** * Refer to nephrology
52
management of nephritic syndrome
- **Monitor U+E, BP , fluid balance, weight**. - Post-streptococcal: **Supportive management** - RPGN: **Urgent referral, Immunosuppressive therapy (steroids, cyclophasamide), plasmapheresis** - Ig A: **Supportive + prednisolone if severe**
53
what are causes of CKD
- MOST COMMON = **DM and HTN** (long term renal injury) - chronic inflammation = **glomerulonephritis** - amyloid, IgA nephropathy , **vasculitis**, tubulointerstitial disease (**pyelonephritis**)
54
clinical features of CKD
55
what is mode of inheritance for PKD
Autoomal dominant
56
what occurs in PKD
multiple renal cysts develop and cause damage to adjacent nephrons
57
how and when does PKD present
in **> 30 years old** **flank pain (renal stones are more common), haematuria (cyst rupture), HTN** berry aneurysm: **SAH** **Mitral valve prolapse**
58
investigations for PKD
**ultrasound** (first line) = multiple cysts bilaterally in enlarged kidneys
59
HOw can you manage PKD
give TOLVAPTAN to slow down progression
60
what is the usual cause of RAS
atherosclerosis
61
what occurs to renal enzymes in RAS
**Stenosis** --> **Renal hypoperfusion**> stimulates RAS --> **increased angiotensin 2, increased aldosterone** > **increased BP**
62
whhat drug is AWFUL if you have RAS and wy
ACEi in RAS, renal perfusion is maintained by **constriction of the efferent** arteriole **ACEi remove that constriction** > glomerular filtration pressure drops > little blood flows to kidey > **severe AKI**
63
clincal features of RAS
hypertension refractory to treatment worsened by ACEi renal artery bruits weak leg pulses
64
Gold standard Ix for RAS
Digital subtraction renal angiography | done after CT angiogram/MRI as invasive
65
WHAT IS fibromuscular dysplasia
Proliferation of cells in the walls of the arteries --> **vessels bulge or narrow** --> RAS This most commonly affects **YOUNG WOMEN** On **MR angio:** **'string of beads'** appearance.
66
treatment for RAS
lifestyle modification: stop smoking, lose weigtht, low salt diet ANTI-HTN (target <130/90) = ARB + diuretic atorvastain and aspirin | consider renal artery stent and post stent clopidigrel
67
What are stimuli for renin secretion
low Na low perfusion sympathetic stimulation (beta adrenergic receptors)
68
how does renin act on the RAS
Renin releasedd from JGA | Renin converts angiotensinogen to Angiotensin 1
69
What occurs to angiotenssin 1
Angiotensin 1 is cleaved in lung by ACE to At2
70
What is function of At2
Stimulates adrenal production of aldosterone | also constricts arterioles
71
how do you distinguish glomerulonephritis from AIN on urine dip
glomerulonephritis = NEPHRITIC syndrome = blood and protein in urine AIN = NePHROTIC syndrome = protein and WCC
72
what do you do if a patient has CKD but needs a scan with contrast?
give IV saline before and after - this reduces the risk of precipitating an AKi
73
what CK levels are you expecting for rhabdomyolysis
CK >10 000 otherwise (if lower than that) it could just be a soft tissue injury
74
what histopathological findings do you expect with a carcinoma
nuclear enlargement hyperchromasia pleomorphism
75
difference between IgA and post infection nephropathy in terms of timing
IgAA is FEW DAYS | post-infectious is FEW WEEKS
76
How does urinary sodium differ between prerenal and renal AKI, and why?
prerenal: LOW urinary sodium because the kidney works fine and is desperately trying to hold on to sodium to raise BP renal: HIGH urinary sodium because the kidney is damaged so loses lots of sodium
77
classify and name causes or intrinsic renal AKI
VASCULITIS - affects the blood vessels - small vessels (microangiopathic): HUS, TTP, DIC, GPA - large vessel (obstructive): renal artery / vein thrombosis or embolus GLOMERULONEPHRITIS - affects the glomerolus - minimal change disease (in children) - membranous glomerulonephritis (in adults) ATN - affects tubules - rhabdomyolisis, post-hypovolaemia AIN - affects intersttium - NSAIDS, PENICILLIN, SULFA-DRUGS, PPI, CIPROFLOX, ALLOPURINOL, FUROSEMIEDE
78
most common extarenal presentation of PKD
cystic liver > hepatomegaly
79
what is a dangerous unique complication of haemodysalisis
Dialysis disequilibrium syndrome | causes cerebral oedema (headache, drowsiness)
80
why do you need to STOP LITHIUM in AKI?
because may cause toxic accumulation of lithium (although lithium itself does not actually cause AKI)
81
what dose of aspirin can you continue for AKI
low dose (75 mg)
82
how do you treat cranial DI
DESMOPRESSIN
83
how do you treat nephrogenic DI
thiazide
84
when does a GP need to refer to nephrology someone with CKD
if; - eGFR below 30 - eGFR falls progressively by > 15 in a year
85
what else other than GFR do you need to diagnose CKD stages 1 and 2
you need supportive evidence (e.g. from urine dip, USS, symptoms) otherwise likely not CKD, as GFR is simply variable in peoopke
86
what dose of potassium is safe to give IV per hour WITHOUT CARDIAC MONITORING
10mmol / h
87
what must a patient be on if receiving 20mmol KCl /h
requires cardiac monitoring | via central line preferred
88
what is the pathophysiology of goodpasture
anti-GBM antibodies against T4 collagen
89
what are symptoms of goodpasture syndrome/anti gbm disease
- rapidly progressive glomerulonephritis > NEPHRITIC syndrome (**proteinuria + haemoaturia**) - pulmonary haemorrhage > **haemoptysis** | more common in men, exacerbated by resp tract infection
90
how much does creatininee need to increase by to recognise an AKI
>26 micromol / L
91
what are the three ways of removing potassium from the body (rather than merely shifting it into cells) in hyperkalaemia
calcium resonium (enema > oral) loop diuretics dialysis
92
what electrolyte imbalance can large volumes of NaCL cause
hyperchloraemic metabolic acidosis
93
which vit D supplement is good for end stage kidney disease a
alpha calcidiol
94
risk factors for AKI
o **Age > 75 ** o **CKD (acute-on-chronic)** o Comorbidities: **heart failure, peripheral vascular disease, chronic liver disease, diabetes mellitus ** o **Sepsis** o **Hypovolaemia** (Poor fluid intake/increased losses) o **Nephrotoxic drugs**

Y6 Senior Med COPY (29 decks)

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