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Phase 3 > Week 14 > Flashcards

Week 14 Flashcards

1
Q

What are the functions of the kidney?

A
  • Metabolic waste excretion (urea, creatinine)
  • Endocrine functions (vitamin D, EPO, PTH)
  • Drug metabolism/excretion
  • Control of solutes and fluid status (sodium, potassium, fluid)
  • Blood pressure control
  • Acid/base
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2
Q

How is kidney function assessed?

A

Measure what is put out in urine or what’s left in blood

Urinalysis:

  • detects proteinuria
    • 24hr urine collection (grams/24h)
    • PCR ratio (mg/mmol)
    • albumin:creatinine ratio (mg/mmol)
  • haematuria
    • visible or non-visible (only detectable on dipstick)

U&Es: urea, creatinine and eGFR

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3
Q

Describe limitations of kidney function tests:

A
  • Creatinine is affected by muscle mass, so 2 people of same age with different muscle masses will have different creatinine
  • 15% of creatinine is secreted by tubule
  • Urea is not as sensitive as creatinine
  • eGFR assumes stable renal function
  • Not suitable in AKI
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4
Q

Describe the aetiology of GN:

A

Extrinsic causes: antibodies, immune complexes, complement
Intrinsic causes: cytokines, growth factors, proteinuria

Can be primary or secondary

Secondary causes

  • CV: subacute bacterial endocarditis
  • respiratory: bronchiectasis, lung cancer, TB, pulmonary renal syndromes
  • ID: hepatitis, HIV, chronic infections, abx, malaria
  • rheumatology: RA, SLE, amyloidosis, CT disease
  • drugs: NSAIDs, bisphosphonates, heroin
  • GI: ALD, IBD, coeliac disease
  • diabetes
  • haematological: myeloma, CLL, PRV
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5
Q

Discuss diagnosis of GN:

A

Approach:

  • presentation, history/exam
  • kidney biopsy (of cortex) findings
  • likely cause and specific management
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6
Q

Describe different clinical presentations of GN:

A

Rapidly progressive GN:

  • rapid rise in serum creatinine
  • crescentic damage
  • vasculitis/lupus/IgA; often have other clinical features

Nephritic:

  • blood and protein in urine, high BP, rising sCr
  • proliferative/acute inflammation
  • IgA/lupus/post-infectious

Nephrotic:

  • > 3.5g/d proteinuria, low sAlb, oedema
  • non-proliferative, podocyte damage (scarring)
  • minimal change/FSGC/membranous

Overlap:

  • blood/heavy proteinuria
  • IgA/MCGN/SLE

Other:

  • urinary abnormalities alone
  • hypertension
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7
Q

Outline treatment and prognosis of GN:

A

Possible therapeutic strategies:

  1. Control infection, CTD (cyclophosphamide, dexamethasone, thalidomide)
  2. Remove Ab/IC or block Ab
  3. Steroids, cytotoxics and anti-hypertensives
  4. Dialysis, transplantation

Treat:
IgA; antihypertensives, ACEi
Membranous; treat primary cause, supportive treatment (ACEi, statin, diuretics, salt restriction) or specific immunosuppression
Minimal change with high dose steroids

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8
Q

Describe the pathophysiology, presentation, and management of diabetic nephropathy:

A

Not diabetic nephropathy if no proteinuria and if not presenting with other microvascular symptoms

Pathology: hyperglycaemia -> volume expansion -> intra-glomerular hypertension -> hyperfiltration -> proteinuria -> hypertension and renal failure

Management:

  • good glycaemic control
  • good BP control
    • ACEi/ARB
  • SGLT2 inhibitors
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9
Q

Describe the pathophysiology, presentation, and management of vascular disease affecting the
kidneys:

A

Presentation: likely other vascular complications, PVD, hypertension, angina

Pathology:

  • progressive narrowing of renal arteries with atheroma
  • perfusion falls, stenosis progresses
  • cortical hypoxia causes microvascular damage and activation of inflammatory pathways
  • parenchymal inflammation and fibrosis progresses and becomes irreversible

Management:

  • medical: BP control (not ACEo/ARB), statin
  • lifestyle: smoking cessation, exercise, low sodium diet
  • angioplasty only in rapidly deteriorating renal failure, uncontrolled raised BP and flash oedema
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10
Q

Describe the pathophysiology, presentation and management of other diseases, such as lupus
and amyloidosis and their effect on the kidneys:

A

SLE:

  • multiple autoAbs directed against cells of the GBM
  • activation of complement
  • presents with nephritic syndrome and abnormal immunology results
  • management with immunosuppression
    • steroids
    • MMF
    • cyclophosphamide/rituximab

Amyloidosis:

  • depositions insoluble proteinous (beta-pleated sheets) material in extracellular space
  • high affinity for constituents of capillary wall
  • presents with hypoalbuminaemia, elevated uPCR, nephrotic syndrome
  • amyloid evident on biopsy
  • treat underling source of inflammation/infection or underlying haematological condition (myeloma)
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11
Q

Describe APKD:

A

APKD:

  • cysts arise from tubules
  • cysts gradually enlarge
  • kidney volume increases
  • some compensation
  • eGFR falls, usually 10yr before kidneys fail
  • genetic (PKD1 and 2 gene mutations)
  • code for polycystin 1 and 2, locate in renal tubular epithelia (liver and pancreas ducts)

Management is supportive
Early detection and management of BP
Treat complications
Renal replacement therapy

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12
Q

What are some other inherited kidney diseases?

A

Alport’s syndrome: X-linked kidney disease caused by collagen 4 abnormality (affects BM) and presents with deafness and renal failure

Fabry’s disease: X-linked storage disorder caused by alpha galactosidase deficiency resulting in accumulation of Gb3 in glomeruli- causing ESRF
Also has neuropathy, cardiac and skin features

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13
Q

What are presenting features of cystitis and pyelonephritis:

A 
Cystitis - infection of the bladder
dysuria
frequency
urgency
suprapubic pain
haematuria
Pyelonephritis - infection of the kidney
the above PLUS
fever (>38ºC)
chills/rigors
flank pain
costo-vertebral angle tenderness
nausea/vomiting
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14
Q

What are the clinical consequences of tubulointerstitial abnormalities?

A

Renal scarring in 10-15% of children with UTI in childhood
20% of children and adults with ESRD have scarring

Congenital abnormalities:

  • vesico-uretetic reflux
    • retrograde passage of urine from the bladder into the upper urinary tract
  • obstruction of urinary drainage tracts

Chronic renal failure, recurrent UTIs, renal scarring

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15
Q

What is glomerulonephritis?

A
  • Inflammation of glomerulus and tubules

- Affects both kidneys but not necessarily all of each

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16
Q

Describe specific aetiologies of GN:

A

IgA:

  • mesangial disease (proliferation caused by mesangial IgA)
  • can be precipitated by infection; synpharyngitic presentation
  • may be secondary to HSP, cirrhosis, coeliac disease

Membranous:

  • presents with nephrotic syndrome
  • 10% secondary to malignancy, CTD, drugs
  • variable natural history

Minimal change:

  • commonest form of GN in children
  • podocyte fusion
  • idiopathic but may be secondary to malignancy

Crescentic:

  • aggressive disease which quickly progresses to ESRF
  • commonly caused by ANCA vasculitis, and other immune conditions
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17
Q

What is nephrotic syndrome?

A
  1. 3.5g proteinuria per 24h
  2. Serum albumin <30
  3. Oedema
  4. Hyperlipidemia

Must have first 3 for diagnosis
Children get swollen eyes
Risk of VTE and increased risk of infection (loss of anti-thrombotic factors and immunoglobulins)

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18
Q

What are the clinical consequences of APKD:

A 
Renal complications: ESRD
Cyst accidents
Other:
- hypertension
- intracranial aneurysms
- mitral valve prolapse
- aortic incompetence
- colonic diverticular disease
- liver/pancreas cysts
- hernias
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19
Q

What are the risk factors for UTI?

A 
Infancy - boys and girls under 1 year 
Abnormal urinary tract - congenital or other abnormalities 
Females
  - Anatomy
  - Sexual intercourse
  - Pregnancy
Bladder dysfunction/incomplete emptying 
  - Constipation (‘dysfunctional elimination syndrome’)
  - Neurogenic bladder
  - Prostate enlargement in men
‘Foreign' body
  - catheters
  - stones
Diabetes mellitus
  - glycosuria promotes bacterial growth
Renal transplant
Immunosuppression
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20
Q

What factors can contribute to the development of AKI?

A

Pre-renal: anything that impairs renal perfusion

  • hypotension
  • hypovolaemia (burns, diarrhoea, haemorrhage)
  • hypoperfusion
  • hypoxia
  • sepsis (vasodilation so effective perfusion decreases)
  • drugs, toxins

Renal:

  • glomeruli: GNs, drugs (gentamicin)
  • tubules: tubule-interstitial nephritis, rhabdomyolysis

Post-renal: obstructive causes

  • calculi
  • tumours (ureter, bladder, prostate, cervix, ovarian)
  • lymph nodes (commpression)
  • prostate
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21
Q

What are the outcomes for AKI?

A

Acute tubular necrosis

  • Often polyuric phase for 48-72 hr
  • May be up to 6l urine/day
  • Often subsequent low K, Ca, Mg
  • Tubules can fail to concentration urine
  • ~10-15% will never recover renal function, may have chronic renal failure following ATN
22
Q

Outline the diagnostic process in patient presenting with AKI:

A

AKI or CKD?

History and exam (e.g. septic, rashes, haemoptysis, rhabomyolysis etc)
Drugs (prescribed, OTC, supplements, radio-contrast and abuse)
Urinalysis
Renal ultrasound- to exclude obstruction

‘GN’ screen – ANCA, ANA, Immunoglobulins + EP, complement, aGBM, Urine Bence Jones protein

Others blood film, lactate (LDH), CK etc

23
Q

Outline emergency management of the patient with AKI:

A

Immediate

Airway and Breathing

Circulation – shock - restore renal perfusion
- hyperkalaemia
- pulmonary oedema
Remove causes; drugs or sepsis

Exclude obstruction & consider ‘renal’ causes: are the pre-renal causes sufficient to account for ARF?

Ask for help: ICU or renal unit

K >6.5 is a medical emergency

  • treat with calcium gluconate 10ml 10% as cardiac membrane stabiliser
  • see CBL for other treatments
24
Q

How is the severity of CKD classified?

A

CKD = kidney damage or GFR<60ml/min per 1.73m2 for 3 months or more

With eGFR:
Stage 1: >90
Normal or increased eGFR with other evidence of kidney damage
Stage 2: 60-89
Slight decrease in eGFR with other evidence of kidney damage
Stage 3a: 45-59
Moderate decrease in eGFR
Stage 3b: 30-44
Moderate decrease in eGFR
Stage 4: 15-29
Severe decrease in eGFR
Stage 5: <15
Established renal failure

SEE NICE 2014 GUIDELINES

25
Q

Describe clinical features of CKD:

A

Symptoms:

Pruritus
Nausea, anorexia, weight loss
Fatigue
Leg swelling
Breathlessness
Nocturia
Joint/bone pain
Confusion

Signs:

Peripheral and pulmonary oedema
Pericardial rub
Rash/excoriation
Hypertension
Tachypnoea
Cachexia
Pallor &amp;/or lemon yellow tinge
26
Q

Outline clinical consequences of progressive CKD:

A

Anaemia:

  • common, when eGFR <30
  • iron absorption and utilisation suboptimal
  • replace iron, B12, folate first if low
  • then ESA

CKD mineral and bone disorder:

  • accumulation of phosphate
  • calcium reabsorption decreases
  • PTH is activated to compensate
  • further increases phosphate causing calcium decrease
  • treat with activated via D, phosphate binders, calcimimetic, parathyroidectomy
27
Q

How are patients with CKD managed?

A

General principles:

  • targeted screening for CKD
  • interventions to slow the rate of progression of CKD and reduce cardiovascular risk
  • medicines to replace impaired individual functions of the kidney
  • advanced planning for future renal replacement therapy (RRT)
  • renal replacement therapy
Slowing progression:
Aggressive BP control
Good diabetic control
Diet
Smoking cessation
Lowering cholesterol
Treat acidosis
28
Q

What are the indications for renal replacement therapy?

A
  1. Medically resistant hyperkalaemia
  2. Medically resistant pulmonary oedema
  3. Medically resistant acidosis
  4. Uraemic pericarditis
  5. Uraemic encephalopathy
    and specific drug overdoses
29
Q

Describe haemodialysis:

A

2 aims:
removal of solutes- e.g. potassium, urea by DIFFUSION
removal of fluid: ultrafiltration- pressure: HYDROSTATIC FILTRATION

Blood in=> blood out => diffusion removes solutes => filtration removes fluid => dialysate discarded

Often requires surgical creation of AV fistula or AV graft for ease of access

Complications: crash, access problems, cramps, fatigue, hypokalaemia, blood loss, dialysis disequilibrium, air embolism

30
Q

Describe peritoneal dialysis:

A

Dialysate (high glucose concentration)-filled peritoneal cavity with high osmolality
Blood in peritoneal capillaries with low osmolality
Water, urea, creatinine and electrolytes and macromolecules diffuse to peritoneal cavity where they are removed by catheter

Can be continuous ambulatory or automated

Complications:
Infection - peritonitis
Glucose load – development or worsening control of diabetes
Mechanical – hernia, diaphragmatic leak, dislodged catheter
Peritoneal membrane failure
Hypoalbuminaemia
Encapsulating peritoneal sclerosis

Some patients not suitable:

  • grossly obese
  • intra-abdominal adhesions
  • frail
  • home not suitable
31
Q

Describe renal transplantation:

A 
Pros:
No dialysis
Better level of renal function
Can live much more independently
Better life expectancy
Fertility better
Cons:
Immunosuppressive medication for duration of transplant
Increased cardiovascular risk
Increased infection
Post transplant diabetes
Skin malignancies and others
32
Q

Describe pathophysiology of UTI:

A 
Ascending
  urethral colonisation 
  female>male
  multiplication in bladder
  ureteric involvement
Descending/haematogenous 
  blood-borne infections
  involvement of renal parenchyma

CFs:

  • suprapubic discomfort
  • dysuria, urgency, frequency
  • cloudy, blood stained and smelly urine
  • low-grade fever
  • sepsis
33
Q

Describe the pathophysiology of pyelonephritis:

A 
Upper urinary tract infection
Moderate to severe infection
Ascending infection involving pelvis of kidney
Enlarged kidney
Abscesses on surface of kidney
34
Q

Describe the pathophysiology of prostatitis:

A 
Localised infection
Usually spontaneous
May follow urethral instrumentation
Fever, perineal/ back pain, UTI, urinary retention
Diffuse oedema, micro abscesses
Likely organisms
Gram negative bacilli, e.g. E.coli, Proteus sp.
S.aureus (MSSA, MRSA)
N.gonorrhoea  (less common)
35
Q

What organisms can cause UTI/PYN/PRT?

A

UTI:
G-ve bacilli: e coli, klebsiella, proteus, pseudomonas
G+ve: strep; enterococcus, gp B strep, S. aureus
Anaerobes
Candida sp

PYN:

PRT:

36
Q

Describe antimicrobial treatment of UTI:

A

UTI:
Uncomplicated
- in pregnancy amoxicillin and cefalexin relatively safe, avoid trimethoprim in 1st trimester, avoid nitrofurantoin near term
- recurrent; encourage hydration, short course therapy
- recurrent: if simple measures fail 6 monthly trimethoprim/nitrofurantoin prophylaxis

Complicated

  • catheter associated UTI
    • colonisation common, treatment not always required
    • related UTI treat with empirical abx (gent/ciprofloxacin), remove catheter if not needed
Complicated:
All patients
FBC, U+Es, CRP
  - Urine sample
     - Urethral, CSU, Suprapubic, Nephrostomy 
Blood culture if pyrexia or hypothermic
Renal ultrasound
CT KUB
Antibiotic therapy 14/7 or more
  - usually IV
    - amoxicillin/vancomycin
    - gent/aztreonam/temocillin
37
Q

What are the complications of pyelonephritis?

A

Renal abscess:

  • similar symptoms to PYN
  • usually positive urine and blood culture
  • G-ve bacilli likely organisms
  • can become life-threatening
  • poor response to abx
Perinephric abscess:
- uncommon
- risk factors
  - Untreated LUTI, anatomical abnormalities
  - Renal calculi
  - Bacteraemia, haematogenous spread
Common organisms
  - Gram negative bacilli, E.coli, Proteus sp.
  - Gram positive cocci, S.aureus, Streptococci
  - Candida sp.
- treat empirically as complicated UTI
- surgical management
38
Q

Define key pharmacokinetic variables:

A

Pharmacodynamics: what the drug does to your body
Pharmacokinetics: what your body does to the drug

Bioavailability: fraction of the administered dose of drug that reaches the systemic circulation

Clearance: volume of plasma ‘cleared’ of drug per unit time

Half life: time required for serum plasma concentration to decrease by half

Linear pharmacokinetics: concentration that results from a dose is proportional to the dose ie double the dose, double the concentration

Non-linear pharmacokinetics: concentration that results is not proportional to dose, rate of elimination is constant regardless of amount of drug present

Volume of distribution (VD) is the volume in which the amount of drug would need to be uniformly distributed to produce observed blood concentration

39
Q

How are these variables altered in renal and hepatic disease?

A

Renal disease:

  • same hepatic metabolism
  • same/increase VD and prolonged elimination (half life increased)
  • thus, increased dosing interval

Hepatic disease

  • same renal elimination
  • same/increased VD and slower rate of enzyme metabolism (half life/bioavailability increased)
  • decreased dosage and increased dosing interval
40
Q

Describe prescribing issues to using drugs in the elderly:

A

The more medications a person is on, the higher the risk of drug-drug interactions or adverse drug reactions

The more medications a person is on, the higher the risk of non-adherence

Drug-disease interactions (PD increased risk of drug induced confusion)

Drug-drug interactions: statins and erythromycin and other abx, ACEi increase hypoglycaemia effect of sulfonylureas

Undertreatment to avoid risk (ie anticoagulation in AF from fear of falls)

Polypharmacy/prescribing cascade:
NSAID => hypertension => antihypertensive therapy

41
Q

How are commonly prescribed drugs altered in renal and hepatic dysfunction?

A 
Renal important examples:
Antibiotics- nephrotoxic, uraemia (reduce dose)
LMWH (reduce dose)
Metformin (avoid)
NSAIDs- fluid retention (avoid)
Digoxin- electrolyte disturbances (reduce dose)
Phenytoin (reduce dose)
ACE Inhibitors (caution)
Hepatic:
High extraction
 - Metabolised at high rate by liver
 - Rate varies with delivery
 - Affected by changes in blood flow
 - Morphine, verapamil, lignocaine
Low extraction:
 - Metabolised at low rate by liver
 - Independent of blood flow
- Sensitive to changes in liver enzyme activity
 - Chloramphenicol, theophylline
42
Q

Describe pathophysiology of tumours in the kidney and lower urinary tract:

A

Prostate:

  • majority is adenocarcinoma, usually arising in peripheral zone of prostate
  • can metastasise to bone, can cause spinal cord compression or ureteric obstruction

Bladder:

  • transitional cell carcinoma most common (superficial and invasive), squamous carcinoma and adenocarcinoma
  • strongly associated with inhalation of polycyclic aromatic hydrocarbons and smoking; excretion of chemicals in urine and frequent exposure in bladder
  • often pulmonary mets

Renal:

  • usually renal cell carcinoma, can be transitional CC, sarcoma or mets
  • RFs: smoking, obesity, hypertension, haemodialysis

Testicular:

  • conventional or clear cell (80%), papillary (10%), chromophobe (5%), collecting duct or medullary cell rare
  • have paraneoplastic syndrome: polycythaemia, hypercalcaemia, hypertension, deranged LFTs, rarely ACTH
43
Q

Describe the presentation of tumours in the kidney and lower urinary tract:

A

Prostate:

  • local: often asymptomatic, painful or slow micturition, UTI, haematuria, urinary retention, lymphedema
  • mets: bone pain, renal failure
  • elevated PSA, present on DRE, can do TRUS biopsy

Bladder:

  • classically painless frank haematuria
  • should have cystoscopy, renal U/S or KUBS

Renal:

  • 80% incidental
  • <25% systemic symptoms: night sweats, fever, fatigue, weight loss, haemoptysis
  • 10% classic triad of mass, pain, haematuria
  • varicocele, lower limb oedema, paraneoplastic syndrome

Testicular:

  • majority present as painless lump
  • may be noticed after incidental trauma
44
Q

Describe the management of tumours in the kidney and lower urinary tract:

A

Prostate:

  • watchful waiting, active surveillance
  • radiotherapy
  • radical prostatectomy
  • cryotherapy
  • TURP if symptomatic
  • androgen ablation therapy (medical castration) if advanced

Bladder:

  • urgent TURBT
  • intravesical mitomycin reduces risk of recurrence
Renal:
- large renal mass: radical nephrectomy, If no absolute indication for NSS
-  Small Renal Mass
1. Biopsy
2. Treatment
Nephron sparing surgery
      Partial Nephrectomy
      Cryotherapy
Radical Nephrectomy
Surveillance
- Radical Nephrectomy: removal of kidney and gerota’s fascia, sparing adrenal gland
- Indications for NSS; single kidney, CKD, CV risk factors, pT1a tumours

Testicular:
- radical orchidectomy, chemotherapy, para-aortic node dissection, retro-peritoneal node dissection

45
Q

Describe pathophysiology of stones of the urinary tract:

A

Abnormal urine:

  • under-saturated; too much salt, not enough water, lack of inhibitors, abnormal proteins
  • abnormal blood: hypercalcaemia, acidosis
  • hypercalciuria or hyperoxaluria

Urinary obstruction

  • congenital; medullary sponge kidney, PUJ obstruction, mega ureter, uterocele
  • acquired; ureteric stricture, anastomotic stricture

Urinary infection

  • urease producing organisms
  • proteus mirablis, causing STRUVITE
46
Q

Describe presentation of stones of the urinary tract:

A 
Incidental
 - Imaging for another reason
Pain 
 - Colic, radiates from loin to groin, cannot settle, unable to stay still
Haematuria
 - Visible or non visible
UTI or Sepsis
 - Unknown source until imaged
47
Q

Describe management of stones of the urinary tract:

A

Where do stones cause pain?
Renal – asymptomatic
3 points – PUJ,VUJ, crossing iliacs

<4mm – 75% chance of passing
<7mm – 25% proximal, 45% mid, 64% distal ureter

Medical:
Analgesia
NSAIDs or opiates?
- NSAIDs reduce pain due to reduced glomerular filtration, renal pressure and ureteric peristalsis
Medical expulsive therapy- only beneficial in large distal stones

Surgical:
ESWL – extracorporeal shockwave lithotripsy
Rigid ureteroscopy and fragmentation/ basket extraction
FURS – flexible ureteroscopy
PCNL – percutaneous nephrolithotomy
Emergency stent or nephrostomy

48
Q

What is ATN?

A

Acute tubular necrosis

Any pre-renal cause of AKI if severe/of sufficient duration

ATN is always due to under perfusion of the tubules and/or direct toxicity:
Hypotension
Sepsis
Toxins
Or often, all three

Toxins can be exogenous: drugs, contrast, poisons or endogenous: myoglobin, haemoglobin, immunoglobulins, calcium, urate

49
Q

Describe management of acute pyelonephritis:

A 
Check previous/recent microbiology results
Send urine +/- blood culture+/- imaging
Community: 
Co-amoxiclav/ Ciprofloxacin/ /Trimethoprim     (NICE  guideline)
  - Options may be limited
  - Allergy
  - Drug interaction
  - Antimicrobial resistance

Hospital: often broad spectrum abx
May remain symptomatic for few days
No response warrants further investigation
Uncomplicated pyelonephritis, 7-14/7 antibiotic
Complicated pyelonephritis, ≥ 14/7 therapy
+/- radiological/surgical intervention

50
Q

What are the complication son acute bacterial prostatitis?

A 
Complications 
Prostatic abscess
Spontaneous rupture
Urethra, rectum
Epididymitis
Pyelonephritis 
Systemic sepsis
51
Q

Describe the antibiotic management of acute bacterial prostatitis:

A

Check recent/previous microbiology
Ciprofloxacin/ Ofloxacin (no streptococcus cover)
D/W microbiology in systemic infections

52
Q

What are the types of renal stones commonly seen?

A 
Calcium stones – 80% ( mixed )
  - Calcium oxalate monohydrate or dihydrate
  - Calcium phosphate 
Infection stones - 10% 
  - struvite (proteus)
Uric acid stone - 5%  
  - not seen on xray
Others -1% 
  - cystine, xanthine, silica, drug stones -indinavir (not seen on CT)

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