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Y2S2- Genetics, Renal, Endocrine > Renal > Flashcards

Renal Flashcards

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1
Q

cause of nephrotic syndrome

A

damage to the clusters of small blood vessels in your kidneys that filter waste and excess water from your blood

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2
Q

4 stages of diabetic nephropathy:

A
  1. hyperfiltration
  2. microalbuminuria
  3. macroalbuminuria
  4. end stage renal failure
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3
Q

nephrotic syndrome

A

Triad of:

  1. Proteinuria (> 3g/24hr) causing
  2. Hypoalbuminaemia (< 30g/L) and
  3. Oedema
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4
Q

complications of nephrotic syndrome

A

increased risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine
hyperlipidaemia
chronic kidney disease
increased risk of infection due to urinary immunoglobulin loss

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5
Q

Upper urinary tract infection-

Lower urinary tract infection-

A

pyelonephritis

cystitis

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6
Q

Risk Factors for UTIs:

A
  • Females
  • Recurrent UTI
  • Sexual activity
  • Vaginal infection
  • Diabetes
  • Obesity
  • Genetic susceptibility
  • Older age
    o Oestrogen deficiency
    o Cognitive impairment
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7
Q

Risk Factors for Complicated UTIs:

A

Patients with factors that compromise the urinary tract or host defence
- Urinary obstruction, e.g. prolapse, prostatic enlargement
- Urinary retention caused by neurological disease
- Immunosuppression
- Renal failure
- Renal transplantation
- Pregnancy
- Presence of foreign bodies
o eg indwelling catheters (CAUTI) or other drainage devices

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8
Q

Organisms causing UTIs:

A
  • Most common: E.coli UPEC
  • Klebsiella pneumoniae
  • Staphylococcus saprophyticus- common in sexually active young women
  • Enterococcus spp.
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9
Q

Pathophysiology of UTIs

A
  1. Infection of urethra by pathogen
  2. Colonisation of urethra & organism swims up to bladder- colonisation and invasion of bladder wall, pili and adhesins allow them to hold onto wall despite system flushing urine through
    Bacteria infiltrate neutrophils & multiply in cytoplasm of bladder wall- subvert immune system, form biofilms, epithelial damage,
    Inflammation= pain in suprapubic region
  3. Bacteria ascend to kidney and multiple there- they can infiltrate into the bloodstream > bacterial bloodstream infection
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10
Q

Biofilms are important in

A

allowing persistence infections causing relapses and acute prostatitis.

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11
Q

bacterial mechanisms in UTIs

A

Invades bladder cell wall using Type 1 pili.
Multiplication to form intracellular bacterial communities (IBC) and these exfoliate or form quiescent bacterial reservoirs (QIR).
To cause pyelonephritis bacteria must express pyelonephritis associated (P) pili.

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12
Q

MOST common cause of secondary bloodstream infections

A

CAUTI

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13
Q

what can UTIs cause?

A
  • Bacteraemia common in pyelonephritis
  • Perinephric abscesses
  • Can rarely lead to remote deep seated infection
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14
Q

bacterial virulence factors

A
  • Adherence: pili, adhesins
  • Toxin production- haemolysins
  • Immune evasion- capsule
  • Iron acquisition
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15
Q

presentation of pyelonephritis

A

Pyelonephritis: Loin pain/flank tenderness, fever/rigors, sepsis

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16
Q

presentation of cystitis

A

Cystitis: Dysuria, frequency, urgency, suprapubic tenderness

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17
Q

presentation features of UTI in infants and elderly

A 
In infants (<2yrs) –vomiting/fever
In elderly - less localised symptoms – confusion/falls
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18
Q

most common causes of dysuria in elderly women

A

Atrophic vaginitis and oestrogen deficiency are the most common causes of dysuria in elderly women and often mistreated.

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19
Q

location of dysuria and differentials

A

o End of stream- external vagina

o Throughout- urethritis

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20
Q

Urine dipstick

A

The dipstick is only to be used in patients under 65
- useful only in presence of clinical UTI symptoms- presence of nitrites indicate a UTI as a possible diagnosis but it have 75% sensitivity

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21
Q

why can urine dipsticks only be used in people <65?

A
  • can only be used <65 as elderly people often have asymptomatic bacteriuria which may be mistaken for UTI
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22
Q

when is urine culture bacteriuria significant?

A

• Generally significant if >105 CFU/mL

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23
Q

when is asymptomatic bacteriuria treated?

A

pregnant women- thought to decrease risk of development of pyelonephritis (pregnancy can dilate the ureters) which can lead to pre-term labour

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24
Q

when does bacteriuria signify a UTI?

A

Symptomatic bacteriuria: UTI

• Culture results SUPPORT clinical diagnosis only

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25
Q

Rapid Detection of UTI- point of care tests

A

• Flexicult – for primary care – culture at the bedside in 24 h.
• Rapid detection using molecular markers
- check for presence of bacteria (resistant) or inflammation
o >50% of elderly women have asymptomatic bacteriuria
o Urgent clinical need for indication of active inflammation specifically in urinary tract

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26
Q

• Nitrofurantoin should only be used for

A

cystitis

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27
Q

when should IV antibiotics be used over oral?

A

• If there are any signs of SIRS or sepsis, IV should be used over oral
o Some MDR organisms only have IV choices available

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28
Q

antimicrobial use increases

A

risk of recurrent UTI and antimicrobial resistance

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29
Q

Management of Upper UTI:

A

take blood cultures before giving IV antibiotics

gentamicin and consider adding amoxicillin

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30
Q

Diagnosis and Management of Catheter Associated UTI

A

review need for catheter

  • Do not use urine dipstick for diagnosis
  • Urine culture is often positive in catheterised patient, this does not differentiate between colonisation and infection
  • Diagnosed clinically
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31
Q

Managment of Lower UTI

A

only for aamelioration and shortening of symptom duration in cystitis
Trimethoprim (if resistant then Nitrofurantoin)

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32
Q

All children with confirmed UTI need

A

investigation and consideration of vesico-ureteric reflux

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33
Q

recurrent UTI

A

Recurrent UTI occurs in ¼ women, antimicrobial exposure is a risk factor and it is often MDR organisms.

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34
Q

recurrent UTI management

A

advice- fluid intake, diet, lubrication, STI, supplements like cranberry extract
trial methenamine and high dose Vit C for 12 months

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35
Q

Most common causes of Chronic Kidney Disease

A 
Diabetes
Hypertension
Chronic glomerulonephritis
Polycystic kidney disease
Renovascular Disease
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36
Q

how is estimated GFR found?

A

MDRD equation

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37
Q

GFR in each stage of CKD

A 
Stage 1 CKD if eGFR is >90 ml/min/1.73m2 
Stage 2 CKD- 60-89 
Stage 3 CKD-  30-59
Stage 4 CKD- 15-30 
Stage 5 CKD- <15
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38
Q

what else is required to diagnose stage 1&2 of CKD?

A

demonstrable kidney damage (e.g. haematuria or proteinuria)

biopsy or radiologically proven

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39
Q

strategies to prevent progression of CKD

A

Control blood pressure (RAS inhibition) Reduce proteinuria (RAS inhibition)
If diabetes, optimise glycaemic control

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40
Q

process of interstitial fibrosis in diabetes

A

normally protein in filtrate taken up into lysosomes and broken down into amino acids then taken up into peritubular capillaries
in diabetes, heavy proteinuria overloads the system and the tubular cell dies, it is cleared by fibroblasts -> scarring

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41
Q

marker of chronic progressive kidney disease

A

lots of interstitial fibrosis

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42
Q

toxic drugs in CKD

A

NSAIDs, contrast, gentamicin (aminoglycoside)
phosphate enemas- atopic bowel absorbs large amounts of phosphate
antibiotics in lower dosing

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43
Q

__% of elderly patients may have CKD

A

> 25%

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44
Q

consequences of hypertension in end stage renal disease

A

left ventricular hypertrophy, stroke, end organ damage- eyes, kidney

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45
Q

BP treatment goals in CKD

A

“normal” - 130/80

DM / Proteinuria 125/75

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46
Q

what potassium abnormality is present in CKD?

A

Hyperkalaemia common as GFR declines < 25

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47
Q

Causes of hyperkalemia in CKD:

A

–Diabetes and type 4 renal tubular acidosis - low renin and Aldo level
- ACE inhibitors
- High K Diet
reduced distal sodium delivery- increase potassium absorption

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48
Q

examples of potassium binders

A

patiromer, sodium zirconium

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49
Q

Acidosis in CKD- cause and management

A

Much acidosis in CRF is due to animal protein in food.
– Inability to acidify urine in CKD
• Aim to keep Serum HCO3 >22
• Replace with NaHCO3 / Sodium Bicarbonate

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50
Q

biochemical findings in CKD patients with anemia

A

Hb<12inmales/<11infemales

– Generally normochromic normocytic anaemia

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51
Q

why do CKD patients have anemia?

A

decreased response of EPO to a hypoxic stimulus (kidney) and decreased RBC survival, iron deficiency, blood loss
aluminum / hyper PTH / B12+Folate defic

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52
Q

EPO replacement criteria

A

All pts with Hb <105 and adequate iron stores should be on Epo
• Target Hb 100-120

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53
Q

EPO and relationship with aluminum / hyper PTH / B12+Folate defic

A
  • PTH negative regulator of EPO
  • aluminium stimulate eryptosis
  • B12+Folate- required by erythroblasts for proliferation during their differentiation
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54
Q

features of renal osteodystrophy

A

Reduced bone density (Osteoporosis)
Reduced bone mineralisation (Osteomalcia)
Secondary/Tertiary Hyperparathyroidism
May get spinal osteosclerosis: Rugger Jersey spine

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55
Q

Pathophysiology of renal osteodystrophy

A

CKD: reduced calcitriol produced and reduced phosphate clearance –> low serum calcium
Secondary hyperparathyroidism to restore calcium levels–> bone resorption leading to osteoporosis
Calcitriol continues to reduce –> oesteomalacia

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56
Q

renal osteodystrophy management

A 
Phosphate restrict (0.8-1.0g/kg/day) 
• binders- calcium or non-Ca binders
– Vitamin D therapy (alfacalcidol) 
• increases Ca / decreases PO4
– Monitor PTH regularly
– Parathyroidectomy may be required
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57
Q

consequences of hyperphosphatemia

A

Vessel calcification – Non-compliant vessels
– Systolic hypertension – L Vent Hypertrophy
– Diastolic hypotension - Myocardial ischaemia
• Calciphylaxis

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58
Q

medial calcification is a result of

A

hyperphosphatemia and hypercalcemia, doesn’t obstruct lumen

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59
Q

as CKD progresses, there is an increased risk of

A

CV death and death from all causes

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60
Q

malnutrition in CKD

A

common- dietary restrictions, decreased appetite

malnourished pts do worse on dialysis

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61
Q

Who should you refer to renal clinic?

A

Any patient with rapid increase in creatinine/ hypertension
• Stage 3 CKD with hypertension/proteinuria /haematuria/ rising creatinine
• Any stage 4/5 CKD who is suitable for treatment

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62
Q

choice of treatment in CKD

A
  • haemodialysis
  • peritoneal dialysis
  • kidney transplant
  • conservative care- no dialysis, symptomatic
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63
Q

body fluid compartments

A

intracellular- interstitial fluid, plasma and transcellular fluid.
extracellular

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64
Q

majority of body fluid is in which compartment?

A

intracellular

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65
Q

What happens when you add salt to the extracellular compartment?

A

raised osmolarity in extracellular compartment

Water will move out to balance osmolarity which depletes cellular water

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66
Q

external and internal osmotic pressures

A

pull water into compartments

sodium is principal extracellular osmotic pressure

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67
Q

internal hydrostatic pressure

A

pushing water out of compartment

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68
Q

external hydrostatic pressures

A

pull water into compartment

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69
Q

If you add water into the vascular space >

A

expand vascular space > flow into interstitial space > flow into cellular space because of dilution and raised hydrostatic pressure (increased volume) > water will move out to each compartment equally

dilution hyponatremia

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70
Q

define eu-, hypo- and hyper- volemia

A

Euvolaemic/normovolaemic: normal 55-60% total body water
Hypovolemic: volume deplete
Hypervolemic: volume overloaded

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71
Q

Clinical Signs of Hypovolemia

A
  • Postural hypotension
  • Tachycardia
  • Absence of jugular venous pulse at 45
  • Reduced skin turgor/ dry mucosa
  • Supine hypotension
  • Oliguria
  • Organ failure
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72
Q

Clinical Signs of Hypervolemia:

A
  • Hypertension
  • Tachycardia
  • Raised JVP
  • Gallop rhythm
  • Peripheral and pulmonary oedema (pitting oedema- different to adipose tissue)
  • ‘third space gains’- excessive fluid in body cavities eg. pleural space
  • Organ failure
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73
Q

Hypervolaemic hyponataemia

A

in which water gains exceed sodium gains

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74
Q

Causes of Hypervolaemic hyponataemia

A

Renal failure
Heart failure
Liver failure
Nephrotic syndrome

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75
Q

Hypovolaemic hyponatremia-

A

excessive sodium losses and water losses are insufficient to concentrate sodium back up, depends on volume of water loss

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76
Q

Causes of Hypovolaemic hyponatremia-

A 
Burns
Sweating
Diarrhoea
Vomiting
Fistulae
Addison's disease
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77
Q

Euvolemic hyponatremia

A

water evenly distributed across all compartments, hyponatremia is dilutional

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78
Q

Causes of Euvolemic hyponatremia

A

hypotonic IV fluids, hypothyroidism, SIADH

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79
Q

Why does SIADH cause euvolemic hyponatremia?

A 
ADH secretion in excessive
-	Not suppressed by reduced tonicity
-	Water reabsorption is excessive (and inappropriate)
-	Sodium is diluted
-	Hyponatremia results
Clinically euvolaemic
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80
Q

Treatment of Hypovolemia:

A 
-	Restoration of volume state
o	Blood if necessary
o	Crystalloid
-	Cessation of diuretics
-	Steroids for Addison’s
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81
Q

Treatment of Hypervolemia:

A
  • Diuretics
    o Usually loop diuretics eg. furosemide/ bumetanide
    o Fluid restriction
    o Treatment of underlying cause eg. Heart attack
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82
Q

Treatment of Euvolaemic Hyponatraemia:

A 
-	Treat underlying cause
o	Stop IV fluids
o	Thyroxine replacement
-	Fluid restriction down to 500ml/day
-	Rarely demeclocycline- reduces tubular sensitivity to ADH
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83
Q

Correcting sodium faster than 12mmol/L/day leads to a significant risk of

A

central pontine myelinosis because of fluid shifts.

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84
Q

Recommended rate of sodium correction:

A

o 4-10mmol/L/day if asymptomatic
o 8-12 mmol/l/day if symptomatic
o with careful monitoring / observation, needs to be brought up slowly

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85
Q

what is mostly commonly the underlying cause of hypernatremia?

A
  • Hypovolaemia is almost always the case (concentration) > increased serum concentration due to loss of fluid
  • The list of potential aetiologies is very similar to that for hypovolaemic hyponatraemia
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86
Q

renal clearance

A

volume of plasma cleared of a substance per unit time

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87
Q

GFR

A

volume of fluid filtered from the glomerular capillaries into the Bowman’s capsule per unit time

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88
Q

what is needed to estimate GFR?

A

substance completely lost from the plasma to urine
endogenous: creatinine, cystatin C
exogenous= inulin, radioisotope tracers

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89
Q

accuracy of creatinine clearance at low GFR

A

inaccurate- amount creatinine secreted becomes proportionally much larger
inconvenient for patient as requires urine collection

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90
Q

ACR

A

albumin: creatinine ratio, used in classification of CKD

severe= >30

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91
Q

NICE guideline for AKI

A

Rise in creatinine of ≥ 25 micromol/L in 48 hours
Rise in creatinine of ≥ 50% in 7 days
Urine output of <0.5ml/kg/hour for > 6 hours

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92
Q

what is AKI commonly characterised by?

A

oliguria & increases in plasma urea & creatinine often accompanied by a loss in ability to regulate water, electrolyte & acid-base balance.

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93
Q

acute on chronic kidney injury

A

acute insult on a background of chronic existing renal impairment

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94
Q

An increased risk of AKI is associated with:

A 
Chronic kidney disease
Diabetes with chronic kidney disease
Heart failure
Renal transplant
Age 75 or over
Hypovolaemia
Contrast administration
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95
Q

renal tubular acidosis type 1

A

inability to generate acid urine (secrete H+) in distal tubule
causes hypokalaemia
complications include nephrocalcinosis and renal stones

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96
Q

causes of renal tubular acidosis

A

idiopathic, rheumatoid arthritis, SLE, Sjogren’s, amphotericin B toxicity, analgesic nephropathy

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97
Q

what can be used to confirm RTA T1?

A

ammonium chloride loading test

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98
Q

measures of electrolyte homeostasis

A 
Spot urine- however urine conc varies throughout the day
24hr urine collection
Measure creatinine (or osmolality) to correct for
variability in urine conc.
99
Q

plasma sodium is an indicator of

A

indicator of fluid balance, rather than total body sodium e.g. hypernatraemia tends to reflect water deficit, rather than sodium overload

100
Q

Urine Na+ >30 mmol/L can signify

A

inappropriate loss – tubular dysfunction / damage / inadequate aldosterone action
e.g. intrinsic /established renal failure caused by un- treated pre-renal failure

101
Q

urine concentrating ability is assessed by measuring

A

urine osmolality (and plasma osmolality for comparison)

102
Q

loss of urine concentrating ability may be accompanied by

A

polyuria

103
Q

dipstick urinalysis can include

A

Glucose (diabetes?)
• Ketones (ketoacidosis?)
• Protein (albumin) – not as sensitive as lab measurement
• Blood (detects Hb: calculi, glomerulonephritis)
pH

104
Q

how can renal pathology be related to proteinuria?

A

• Increased glomerular permeability – increasing urinary albumin, detectable levels
of large MW proteins not normally found in urine
• Decreased tubular protein reabsorption – increased conc. of low MW proteins eg. Fancuni Syndrome

105
Q

Proteinuria may be detected by

A

dipstick testing (not as sensitive as lab urine)
• lab-based albumin / protein measurement, sometimes 24hr collection but usually a spot urine using creatinine to adjust for urinary conc:
o protein:creatinine ratio (PCR)
o albumin:creatinine ratio (ACR) – used to classify CKD

106
Q

microalbuminuria

A

Refers to abnormal level of albumin, usually too low for detection by urine dipstick
ACR > 3.5 mg/mmol in men, >2.5 mg/mmol in women
- confirmed with collection on 2/more sep occasions

107
Q

transient causes of microalbuminuria

A

post-trauma, surgery, pyrexia, vigorous physical exercise

108
Q

acid production- cellular and metabolic

A

cellular respiration produced CO2- react with water to make carbonic acid
metabolic processes- non volatile acids (can’t be removed by lungs) eg. ketones, lactate

109
Q

countermeasures in acidosis

A

rapid buffers bind H+ and reduce acidity eg. proteins, bicarb
lungs- remove CO2, limited by bicarb reserves
slow kidneys- excrete H+, regen and recover bicarb

110
Q

respiratory acidosis- sign, compensatory mechanism and consequence of decompensation

A
  • raised CO2
  • slow renal resorption of bicarbonate
  • acidaemia consequence
111
Q

respiratory alkalosis- sign, compensatory mechanism and consequence of decompensation

A
  • low CO2
  • renal excretion of bicarb (marginal)
  • alkalemia consequence
112
Q

metabolic acidosis- sign, compensatory mechanism and consequence of decompensation

A
  • low bicarb
  • increase RR to lower CO2, increased renal resorption of bicarb
  • acidaemia consequence
113
Q

metabolic alkalosis- sign, compensatory mechanism and consequence of decompensation

A
  • raised bicarb
  • lowered RR to increase CO2, renal excretion of excess bicarb (marginal)
  • alkalemia consequence
114
Q

What can be used to calculate pH/bicarb?

A

Henderson Hasselbalch equation

115
Q

Which aspect of ABGs can tell you if a pt is adequately oxygenated?

A

pO2, FIO2, [Hb]

116
Q

When only should BE be deranged?

A

BE should only be deranged where a metabolic disorder is present:
• metabolic acidosis -> neg BE
• metabolic alkalosis -> pos BE

117
Q

When only should standard bicarb be deranged?

A

Std bicarb should only be deranged where a metabolic disorder is present:
• purely resp. disorder -> ref range std bicarb
• purely metabolic disorder -> approx equiv to actual bicarb
• mixed resp-met disorder -> significant difference with actual bicarb

118
Q

Causes of metabolic acidosis with raised anion gap

A 
Methanol
uremia
diabetic ketoacidosis (DKA)
paraldehyde, phenformin
iron, isoniazid
lactic (ie, carbon monoxide [CO], cyanide)
ethylene glycol
salicylates.
119
Q

anion gap

A

difference between most abundant [cations] and [anions]

= [Na+] – [Cl-] – [HCO3-]

120
Q

What does the anion gap depend on?

A

no change: replaced with Cl- ions (hyperchloraemic acidosis)

• elevated: replaced with anions corresponding to lactate, keto-acids etc.

121
Q

Causes of respiratory acidosis

A

COPD
Decompensation in other respiratory conditions e.g. Life-threatening asthma / pulmonary oedema
Neurological
Sedative drugs: benzodiazepines, opiate overdose

122
Q

Causes of respiratory alkalosis

A

Usually acute
- asthma, COPD exacerbation, pulmonary embolism
- pain, panic attack
- iatrogenic (over-ventilation while under intubation)
- inappropriate stimulation of respiratory centre (brain stem): head injury, local tumour
- metabolic: hepatic encephalopathy, salicylate poisoning
Pregnancy- chronic

123
Q

causes of metabolic alkalosis

A 
Vomiting / aspiration (e.g. Peptic ulcer leading to pyloric stenosis, nasogastric suction)
Diuretics
Liquorice, carbenoxolone
Hypokalaemia
Primary hyperaldosteronism
Cushing's syndrome
124
Q

Stages of AKI

A

tage 1: creatinine rise of 1.5x compared to baseline or urine output <0.5 ml/kg/hour for 6 hours.
Stage 2: creatinine rise of 2x compared to baseline or urine output <0.5 ml/kg/hour for 12 hours.
Stage 3: creatinine rise of 3x compared to baseline or urine output <0.3 ml/kg/hour for 24 hours (or anuria for 12 hours) or serum creatinine >354umol/dl

125
Q

pre renal causes of AKI

A

Inadequate blood supply to kidneys reducing filtration of blood, may be due to:
VOLUME DEPLETION → diarrhoea, bleeding, 3rd space fluid losses, diuresis, sepsis
HYPOTENSION → HF, sepsis, oedematous states, drugs (ACEi/ARBs)
RENAL ISCHAEMIA → hepatorenal syndrome, arterial occlusion
DRUGS → NSAIDs, calcineurin inhibitors, ACEi/ARBs

126
Q

renal causes of AKI

A 
intrinsic disease in the kidney leading to reduced filtration of blood, may be due to:
Dysfunction in the glomeruli (acute glomerulonephritis)
Tubules (acute tubular necrosis)
Interstitial (acute interstitial nephritis)
Renal vessels (haemolytic uraemia syndrome or vasculitis)
Rhabdomyolysis
127
Q

post renal causes of AKI

A 
obstructive uropathy
Obstruction may be caused by:
Kidney stones
Masses such as cancer in the abdomen or pelvis
Ureter or uretral strictures
Enlarged prostate or prostate cancer
MUST BE IN ALL PRESENT KIDNEYS
128
Q

obstructive uropathy

A

obstruction to the outflow of urine from the kidney, causing back-pressure into the kidney and reduced kidney function

129
Q

myeloma kidney

A

obstruction of lumen of tubules, some patients can form casts that cause intratubular obstruction

130
Q

investigation that all patients with significant AKI must have

A

ultrasound to exclude or demonstrate obstruction to renal tract

131
Q

most common cause of AKI

A

acute tubular necrosis

132
Q

can acute tubular necrosis be reversible?

A

in early stages, yes

133
Q

two main causes of ATN

A
  1. ischaemia: shock, sepsis

2. nephrotoxins

134
Q

nephrotoxic drugs

A
  • aminoglycosides
  • myoglobin secondary to rhabdomyolysis
  • radiocontrast agents
  • lead
  • NSAIDs
  • ACEi e.g. Ramipril
  • ANGII receptor blocker e.g. Candesartan
  • statins
135
Q

Histopathological features of ATN

A

tubular epithelium necrosis: loss of nuclei and detachment of tubular cells from the basement membrane
dilatation of the tubules may occur
necrotic cells obstruct the tubule lumen

136
Q

what can be seen in the urine in ATN?

A

muddy brown casts in urine

137
Q

acute allergic interstitial nephritis

A

drug related eg. PPIs, antibiotics, diuretics, NSAIDs
may have an eosinophilia (no rash)
often responds well to steroids

138
Q

rapidly progressive glomerulonephritis is characterised by

A

haematuria, proteinuria, autoimmune aetiology and glomerular crescents- mass of inflammatory cells outside glomerulus in Bowman’s space

139
Q

Hemolytic uremic syndrome (HUS) is a clinical syndrome characterized by the triad of

A

thrombotic microangiopathy, thrombocytopenia, and AKI

140
Q

How does E.coli cause intravascular thrombosis?

A

generates shiga toxin which is toxic to the vascular endothelial bed causing intravascular thrombosis (kidney is particularly susceptible)

141
Q

creatinine kinase is a marker of

A

muscle damage

142
Q

rhabdomyolysis

A

damage to muscle from statins/being unwell releasing muscle contents into blood, myoglobin is nephrotoxic

143
Q

Investigations in AKI

A
  • Urine dipstick – simple BUT important (blood, protein)
  • Urine culture
  • Renal Ultrasound - if obstructed then decompress •Renal biopsy (AKI and normal sized kidneys)
  • Angiography ± intervention
144
Q

autoantibodies in SLE, vasculitis, Goodpasture’s syndrome

A
  • Anti-nuclear factor (ANA) - SLE
  • Anti-neutrophil Ab (ANCA) - vasculitis
  • Anti-GBM Ab - Goodpasture’s syndrome,
145
Q

Management of AKI

A

Fluid rehydration with IV fluids in pre-renal AKI
Stop nephrotoxic medications
Relieve obstruction in a post-renal AKI, for example insert a catheter for a patient in retention from an enlarged prostate

146
Q

Drugs that may have to be stopped in AKI as increased risk of toxicity (but doesn’t usually worsen AKI itself)

A
  • Metformin
  • Lithium
  • Digoxin
147
Q

Renal replacement therapy (e.g. haemodialysis) is used when

A

patient is not responding to medical treatment of complications, for example hyperkalaemia, pulmonary oedema, acidosis or uraemia.

148
Q

Complications of AKI

A

Hyperkalaemia
Fluid overload, heart failure and pulmonary oedema
Metabolic acidosis
Uraemia (high urea) can lead to encephalopathy or pericarditis

149
Q

Class I molecules

A
  • Expressed by most somatic cells of body
  • If Class 1 HLA molecule is associated with virus-derived protein then the cell is recognised as infected and killed by cytotoxic T cells
150
Q

Class II molecules

A
  • Expressed by Antigen Presenting Cells (DCs etc) that constantly ’sample’ their microenvironment
  • Used to present antigenic peptides derived from digested material (including pathogens, abnormal or foreign cells)
151
Q

transplant rejection is

A

directed at specific antigens and an be cell/antibody mediated
it is donor specific

152
Q

how does transplant rejection exhibit memory?

A

a 2nd similar Tx is rejected MORE RAPIDLY and this results from the rapid generation of cytotoxic antibodies that recognise the Tx

153
Q

HLA profiling

A

Used to allocate kidneys but less important for other organs such as liver (less immunogenic)

154
Q

levels of kidney mismatch

A

If all HLA-A, -B and –DR loci are the same the it is a 0-0-0 mismatch
If they are all different then it is a 2-2-2 mismatch

155
Q

drugs used in immunosuppression treatment in transplants

A
  • corticosteroids
  • calcineurin inhibitors- tacrolimus
  • antiproliferative agents
156
Q

What are monoclonal and polyclonal antibodies in immunosuppression treatment
directed against?

A
  • IL-2 receptor blockers (IL-2 stimulates clonal expansion of T cells)
  • T cells (cytotoxic complement fixing Abs)
  • Co-stimulatory molecules
157
Q

calcineurin inhibitors

A

Inhibit T cell activation by interfering with intracellular signaling pathways

158
Q

types of transplantation

A 
Cadaveric Tx (commonest) e.g. subarachnoid haemorrhage
•DCD = donated after cardiac death
•DBD = donation after brain death

Living related donor Tx
• Sibling, spouse, altruistic • Typically a kidney Tx

159
Q

patient assessment for transplant

A

age, primary cause of renal failure eg. polycystic kidneys versus conditions which can recur in a Tx (e.g. aHUS, FSGS)
Comorbidities, History of infections & tumours, Urological disease

160
Q

Which vessels and organs are the transplanted kidney attached to?

A

iliac vessels and bladder

renal vein anastomosis

161
Q

criteria for a kidney Tx to go ahead

A 
Blood group (ABO) compatible 
Immunological ‘X-match negative’- there are no antibodies in circulation against cells
162
Q

What does a positive immunological X match mean?

A

there are antibodies in circulation against cells- the complement used during flow cytometry allows a lytic process to occur and green dye signifies dead cells
No Tx

163
Q

sensitisation- production of HLA antibodies

A

If a person is exposed to a foreign HLA molecule, they can produce an HLA antibody against this e.g. patient is A1, A24 and with exposure to A31 generating an anti-A31 antibody

164
Q

What can high sensitisation be derived from?

A 
Highly sensitised patients exhibit high levels of cytotoxic Abs to many HLA antigens
may be derived from:
• Previous transfusions (WBC filtered) 
• Pregnancies- paternal antigens in baby
• Previous Transplantation
165
Q

Do anti-HLA antibodies matter?

A

HLA antibody status requires careful consideration

  • make a successful X-match less likely (long wait for Tx)
  • can lead to antibody mediated rejection
  • Consider desensitisation/antibody removal or paired exchange Tx
166
Q

Which HLA is most significant in transplantation?

A

DR > B > A

Based on mismatch effect

167
Q

Types of transplant rejection

A

Hyperacute rejection (should not happen)
•Acute rejection- first few months
•Chronic rejection

168
Q

What is hyperacute rejection?

A

total destruction due to pre-existing antibodies against ABO or HLA antigens
an example of a type II hypersensitivity reaction

169
Q

treatment of hyperacute rejection?

A

no treatment is possible and the graft must be removed

170
Q

Hyperacute Rejection- cellular mechanism

A

Cytotoxic antibodies bind endothelial cells and induces complement activation, platelet aggregation and intravascular thrombus formation → ischaemia and necrosis of the transplanted organ

171
Q

Acute rejection (< 6 months) features

A
  • Rise in creatinine (often only indication)
  • Reduced urine output
  • Tender transplant
  • Fever
172
Q

What must be excluded to diagnosis acute rejection?

A

Dehydration, renal obstruction, vascular catastrophe, drug toxicity (tacrolimus- nephrotoxic)

173
Q

cellular features of acute rejection

A

tubulitis, vasculitis, large vessel involvement

174
Q

treatment of acute rejection

A
  • High dose methyl prednisolone (anti-inflammatory, kills lymphocyte etc)
  • Change to more potent immunosuppressive agent or an increased dose
  • ‘Anti-T cell’ antibody (increased risk of infection, tumours)
  • Plasma exchange (severe acute Ab mediated rejection)
175
Q

features of chronic rejection

A
  • Progressive renal dysfunction

* Interstitial fibrosis and vascular disease on renal biopsy

176
Q

What must be excluded to diagnosis chronic rejection?

A
  • Recurrent disease (membranous, MCGN)
  • Obstruction (ultrasound)
  • Renal artery stenosis (Doppler of renal artery +/- MRI angiography)
177
Q

Causes of chronic graft failure (> 6 months)

A

both antibody and cell mediated mechanisms cause fibrosis to the transplanted kidney (chronic allograft nephropathy)
recurrence of original renal disease (MCGN > IgA > FSGS)
poor drug compliance (tacrolimus)

178
Q

Cold ischaemia time impact on Tx

A

prolonged CIT of kidney prior to surgery increases risk of chronic rejection (CIT of living donor &laquo_space;cadaveric donor)

179
Q

Factors promoting graft failure

A
  • Delayed graft function- doesn’t work for a few days bc of adverse impact of ischaemia on early graft function
  • Cytomegalovirus (CMV) infection
  • Age of donor and ‘donor disease’
  • Poor BP control
  • Proteinuria
180
Q

Management of chronic Tx rejection

A

Most patients will eventually require dialysis and potentially a further Tx
• Optimise immunosuppression
• Proactive treatment of BP, lipids, proteinuria etc

181
Q

Infective risk of immunosuppression- bacterial

A

UTI, chest infection

can be given prophylactic cotrimoxazole

182
Q

Infective risk of immunosuppression- viral

A

CMV, herpes virus, parvo virus, BK virus (causes renal dysfunction)
can be given prophylactic valgancyclovir if recipent CMV –ve and donor CMV +ve

183
Q

tumour risks of immunosuppression

A

increase incidence of all cancers and skin cancers common (skin surveillance, UV block)

184
Q

Post Tx Lymphoproliferative Disorder (PTLD)

A

secondary to infection with Epstein Barr virus (reduce immunosuppression, may need chemotherapy)

185
Q

side effects of immunosuppressive drugs in transplant

A

Plasma levels of tacrolimus (nephrotoxic) are measured regularly
Increased risk of diabetes (steroids and tacrolimus)
Hypertension (steroids and CNI)
Osteoporosis (steroids)

186
Q

What mechanisms are affected in hypovolemia?

A

SNS- tachycardia, vascoconstriction
RAAS- vasoconstriction, Aldo stimulates salt and water retention
increased ADH, reduced urine output

187
Q

initial treatment for hyperkalemia in AKI

A

IV calcium salts if ECG abnormal- protects myocardium

188
Q

best investigation to confirm post renal AKI

A

USS renal tract- show bladder, estimate bladder volume

189
Q

hydronephrosis

A

swelling of kidney due to build-up of urine when urine cannot drain out from the kidney to the bladder due to obstruction
more damage to cortex- CKD + loss of renal function

190
Q

Benign prostatic hypertrophy

A

encroaches the bladder

  • urine isn’t adequately excreted
  • urine accumulation and increased pressure -> back pressure goes up to kidney
191
Q

Complications of Benign prostatic hypertrophy

A

dilation of renal pelvis, hydronephrosis, hydroureter, renal impairment

192
Q

treatment in benign prostatic hypertrophy

A

urinary catheter- decompression of renal tract, may become polyuric (can’t conc urine)
alpha blocker eg. tamsulosin- enable sphincter to be capable of relaxing
transurethral prostatic resection surgery (TURP)

193
Q

compliance of the bladder

A

Bladder pressure remains constant despite increase in volume due to visco-elastic properties (elastin/collagen; detrusor relaxation without change in tension)
• Bladder filling- sensors detect increase in wall tension

194
Q

volitional micturition controlled by?

A

Spino-bulbar reflex
• Modulation by Pontine Micturition Centre (Barrington’s nucleus)
• Onuf’s nucleus in intermediolateral S2,3,4

195
Q

volume at which bladder is full

A

Fullness at 250ml; Uncomfortable at 500ml (detrusor contractions)

196
Q

3 causes of black eyes

A

directly injured in eye
tracking of blood down to tissues around eye
raccoon eyes from base of skill fracture

197
Q

micturition positive feedback loop

A

detrusor contraction -> wall tension rises -> afferent signals to PMC -> efferent signals increase detrusor contraction

198
Q

central coordination of micturition

A

PMC- takes afferent and produces efferent signals

prefrontal, thalamic, hyperthalamic, cerebellar areas

199
Q

excitatory neurones in micturition

A

cholinergic (Ach)

200
Q

inhibitory neurones in micturition

A

GABA and glycine neurones

201
Q

facilitation of voiding of bladder involves

A

contraction of detrusor and relaxation of sphincter when bladder less than full

202
Q

inhibition of bladder allows

A

postponement of voiding

203
Q

protein: 2+ or more implies

A

intrinsic renal disease and very unlikely to be explained by asymptomatic infection

204
Q

congenital nephrotic syndrome is due to

A

mutation in podocyte specific gene eg. nephrin

symptoms: ascites, oedema, low levels of protein in body

205
Q

The presence of blood and protein in the urine implies?

testing and differentials?

A

glomerular disease and an urgent need to test excretory kidney function, consider systemic diseases (eg vasculitis, lupus)

206
Q

in hypertension, albuminuria suggests

A

primary renal cause

207
Q

albuminuria is a risk factor for?

A

cardiovascular- aggressive management of cardiovascular risk is indicated

208
Q

symptoms of nephrotic syndrome

A

severe lethargy, reduced exercise tolerance, nausea, loss of appetite

209
Q

haematuria can be a sign of

A

serious systemic disease for which diagnosis and treatment is very urgent, whether or not there is also albuminuria

210
Q

if you find proteinuria, what should you not do?

A

send MSU to exclude infection

211
Q

diseases where the glomerulus is damaged (may have proteinuria/haematuria)

A

DM, vascular disease/ischameia, vasculitis, glomerulonephritis, deposition disease eg. amyloid, myeloma

212
Q

storage lower urinary tract symptoms

A
  • Urgency
  • Frequency
  • Nocturia
  • UI: urinary incontinence
213
Q

voiding LUTS

A
  • Hesitancy
  • Poor flow
  • Intermittency
  • Terminal dribbling
214
Q

What is nocturia an effect of?

A

ageing, renal concentrating ability decreases with age increased renal blood flow at night (lying down) leading to increased urine production

215
Q

Difference between nocturia and nocturnal polyuria

A

nocturia- <2x night

nocturnal polyuria- production of more that 1/3 of 24-hour urine at night

216
Q

Causes of decreased bladder capacity and polyuria

A

DM/DI, polydipsia
reduced compliance, reduced functional capacity,
neurogenic bladder, irritation

217
Q

What is post-void dribble?

A

Release of small amount of urine after micturition- Due to release of urine retained in bulbar/prostatic urethra

218
Q

Straining in mictruition

A

Use of abdominal muscles to void (Valsalva only normally required at end of voiding)

219
Q

decreased force of mictruition is usually secondary to

A

bladder outlet obstruction

220
Q

urge incontinence

A

Involuntary loss of urine associated with strong desire to void (detrusor contraction)

221
Q

stress incontinence

A

Involuntary loss of urine when intra-abdominal pressure rises without detrusor contraction eg with coughing, sneezing

222
Q

IPSS

A

International Prostate Symptom Score assessing severity of LUTs

223
Q

Uroflow Meter

A

subsequent bladder scan assesses residual volume

poor flow= bladder outflow obstruction

224
Q

When is a urodynamic assessment indicated?

A

suspected neuro abnormality, complex voiding patterns, young patients with severe issues

225
Q

What is a urodynamic assessment?

A

pressure transducers on bladder and rectum
Pressure from bladder and rectum measured during filling and voiding
• Patient asked to cough periodically to check transducers
• Subtracting rectal (abdominal) pressure from bladder = detrusor activity

226
Q

bladder outlet obstruction presentation in urodynamic assessment

A

No unstable contractions during filling
• No leak whilst coughing during filling
• Very high pressure and low flow during voiding

227
Q

urethra causes of LUTs

A

Strictures -the narrowing of the urethra

can be congenital or result from iatrogenic trauma- urethral instrumentation or anastomosis- or non-iatrogenic trauma

228
Q

symptoms of outflow obstruction

A

storage symptoms may come before voiding symptoms
decompensation fo detrusor leading to:
- residual urine, chronic retention
- bladder failure
- renal failure from obstructive nephropathy

229
Q

management of overactive bladder

A

Lifestyle (alcohol), anti-muscarinics (Solifenacin, Fesoterodine), selective β-3 adrenoreceptor agonist (Mirabegron), Intradetrusor Botox

230
Q

management of stress incontinence

A

Pelvic floor exercises, weight loss, surgery (autologous rectus abdominis sling, artificial sphincter)

231
Q

management of bladder outlet obstruction

A

Medical therapies: alpha- blockers (Tamsulosin), 5ARI (Finasteride), surgery (TURP, laser prostatectomy)

232
Q

first line treatment for urge incontinence

A

bladder retraining

233
Q

hyaline casts in the urine are seen in

A

normal urine after exercise, during fever or with use of loop diuretics

234
Q

ECG signs of hyperkalaemia

A

small or absent P waves, tall-tented T waves, and broad bizarre QRS complexes- very broad QRS complexes form sinusoidal wave pattern

235
Q

nephritic syndrome characterised by

A

haematuria with red cell casts, proteinuria (>3g/day), hypertension, oliguria, oedema

236
Q

Indiacations for dialysis

A 
A - Acidosis
E - Electrolyte imbalance
I - Intoxication (e.g. Aspirin, Barbiturates, Lithium, Alcohol, Salicylates and Theophylline)
O - Overloaded with fluids
U - Uraemia
237
Q

IgA nephropathy is the most common

A

cause of glomerulonephritis in general

238
Q

IgA nephropathy presents with

A

classically presents as macroscopic haematuria in young people following an upper respiratory tract infection.

239
Q

cause of IgA nephropathy

A

caused by mesangial deposition of IgA immune complexes

240
Q

Differentiating between IgA nephropathy and post-streptococcal glomerulonephritis

A
  • post-streptococcal glomerulonephritis is associated with low complement levels
  • main symptom in post-streptococcal glomerulonephritis is proteinuria (although haematuria can occur)
  • typically an interval between URTI and the onset of renal problems in post-streptococcal glomerulonephritis
241
Q

Minimal change disease presentation

A

common cause in children, presents as nephrotic syndrome
highly selective proteinuria- only intermediate-sized proteins such as albumin and transferrin leak through the glomerulus

242
Q

Pathophysiology of Minimal change disease

A

T-cell and cytokine-mediated damage to the glomerular basement membrane → polyanion loss
the resultant reduction of electrostatic charge → increased glomerular permeability to serum albumin

243
Q

Adult polycystic kidney disease increases the risk of

A

brain haemorrhage due to ruptured berry aneurysms

244
Q

high UCR indicates

A

pre-renal cause of AKI

Y2S2- Genetics, Renal, Endocrine (6 decks)

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