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Year 3 > Block 34 Week 2 > Flashcards

Block 34 Week 2 Flashcards

1
Q

advantages of renal transplantation?

A
  • removes burden of life long dialysis
  • improves renal clearance - dialysis only provides GFR of around 10ml/min
  • improves life expectancy
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2
Q

+ of transplantation - renal clearance?

A
  • improves renal clearance - dialysis only provides GFR of around 10ml/min
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3
Q

disadvantages of renal transplantation?

A
  • sig perioperative mortality risk - largely cardiovascular mortality or sepsis
  • 2% of perioperative mortality
  • new onset post transplant diabetes (NODAT) - 10-20%
  • assoc w sig inc risk of graft loss and early death
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4
Q

disadvantages of renal transplantation - immune related?

A
  • lifelong burden of immunosuppression
  • risk opportunistic infections - espec viral, pneumocystitis
  • cancer risk - non-melanoma skin cancer, cervical, lymphoma
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5
Q

absolute CI for renal transplants?

A
  • active infections
  • active cancer - wait 2-5 yrs following cure
  • active drug misuse
  • uncontrolled major psychiatric disease that would disrupt ability to take meds
  • active non-concordance w treatment
  • short life expectancy - under 5 yrs
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6
Q

organ transplantation is governed by?

A
  • Human Tissues Act 2004
  • main change to prev legistlation - facilitated live donor transplantation between unrelated ppl
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7
Q

Human tissues act 2004?

A
  • regulates activities concerning the removal, storage, use and disposal of human tissue
  • consent is the fundamental principle
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8
Q

key points of the HTA?

A
  • Reg storage, removal and use of human tissues
  • makes it lawful to take minimum steps to preserve the organs of a deceased person for use in transplantation while steps are taken to determine the wishes of the deceased
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9
Q

offences under the HTA?

A
  • removing storring or using human tissue without consent
  • storing or using donated tissue for a scheduled purpose for something else
  • trafficiking in human tissue for transplant purposes
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10
Q

types of transplants from cadaveric donors?

A
  • heart beating - DBD
  • non-heart beating - DCD
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11
Q

heart beating (DBD) transplant?

A
  • heart beating (DBD) - donation after brain death. Traditionally the more common one
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12
Q

non heart beating donation?

A
  • non-heart beating (DCD) - donation after cardiac death, organs no longer perfused at the time of transplantation
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13
Q

main diff between heart beating and non heart beating transplants?

A
  • main difference between DBD and DCD is that in DBD the kidneys are still perfused at the time of retrieval but aren’t in DCD
  • With DCD youre more likely to get delayed graft function which means that the kidneys dont intially work on implantation
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14
Q

changes in donation overtime?

A
  • increase in donations from living donors over time up until 2014/2015 and then has tailed off - may be due to increased risk in end stage CKD in live donors
  • DBD donors stayed the same
  • DCD increased
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15
Q

live donors?

A
  • related - blood or emotional relation
  • unrelated
  • paired or pooled donor - organs exchanged between pairs to overcome incompatibility to obtain best immunological match
  • altruistic donor - person donates to anyone
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16
Q

how are live donations done?

A
  • in paired or pooled transplants the organs are exchanged between donor-recepient pairs to overcome blood group or HLA incompatibility
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17
Q

blood groups

A
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18
Q

the independent assessor?

A
  • All donors and organ recipients are required to see an Independent Assessor (lA) who is trained and accredited by the HTA.
  • The lA interviews the donor and recipient both separately and together on our behalf and is independent of the healthcare teams who are involved with the medical parts of the process.
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19
Q

independent assessor interviews?

A
  • The purpose of the interviews is to ensure that donors are not forced to do something against their wishes, to ensure that no reward has been sought or offered and to ensure that the donor has the capacity to make an informed decision.
  • Donors and recipients will be asked to bring along proof of their identity and proof of their relationship.
  • It is a criminal offence to carry out a transplant operation between two living people if the conditions of the HT Act are not met.
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20
Q

blood supply for the transplanted kidney?

A
  • blood supply for the transplanted kidney is usually from the external iliac artery and vein usually, into the iliac fossa
  • only the upper 1/3 of the ureter can be implanted when the kidney is transplanted bc its supplied by the renal artery
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21
Q

types of organ rejection?

A
  • hyperacute rejection: blood group incompatbility
  • acute rejection or chronic rejection MHC antigens
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22
Q

what is the MHC?

A
  • genes coding for HLA, inherited
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23
Q

Class 1 HLA?

A
  • Class I antigens (HLA-A, B, Cw) - expressed on all nucleated cells
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24
Q

Class II HLA?

A
  • Class ll antigens (HLA-DR, DQ, DP) - expressed on antigen presenting cells, B lymphocytes and activated T cells
  • can also be expressed on endothelial cells of BVs especially in the kidney
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25
Q

HLA and renal transplantation?

A
  • as we have 2 copies of each HLA type, 6 different HLA antigens need to match (2 A, 2 B and 2 DR)
  • If HLA types are all the same, there’s a 0,0,0 mismatch
  • if 1 A, 1 B and 2 DR are the same there is a 1,1,0 mismatch
  • if none of the antigens are the same theres a 2,2,2 mismatch
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26
Q

Triggering an immune response in transplants?

A
  • donor antigen is presented to recepient T cells by APCs - commonly dendtitis
  • the APC may be of donor origin (direct) or recipient origin (indirect)
  • antigen must be presented in association w a class 2 MHC w co-stim molecules in order to initate an immune response
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27
Q

what are the 3 signals in the immune response?

A
  • -> T cell activation via recognition of the antigen by the CD3 receptor - signal 1
  • -> associated w costimulatory molecule CD80,86 and CD28: signal 2
  • -> T cells undergo IL-2 mediated clonal proliferation
  • -> CD25 is the IL2 receptor - signal 3
  • -> production of cytokines to recruit more inflammatory cells
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28
Q

summary of the 3 signals?

A
  • signal 1: CD3
  • signal 2: CD28, CD80
  • signal 3: IL2, CD25
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29
Q

What are costim molcules?

A

CD40 and CD154

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30
Q

what are the calcineurin inhibitors?

A

Cyclosporin and tacrolimus:

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31
Q

axathioprine?

A

purine synthesis inhibitor

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32
Q

leflunomide?

A

pyridimine synthesis inhibitor

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33
Q

anti CD52?

A

alemtuzumab - depletes T cells

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34
Q

what is hyperacute rejection?

A
  • Hyperacute rejection occurs when the recipient has pre-formed antibodies to the donor kidney (for example with a blood group incompatible transplant) - occurs immediately
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35
Q
A
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36
Q

what happens during hyperacute rejection?

A
  • Antibody binds directly to antigens on the endothelium lining the capillaries of the kidney
  • Complement activation and inflammatory cell infiltration result in endothelial damage
  • Platelet adhesion and vascular thrombosis lead to renal infarction
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37
Q

hyperacute rejection is?

A

immediate

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38
Q

what is acute rejection?

A
  • Antigen presentation leads to T cell activation
  • Activated T cells undergo clonal proliferation and infiltrate tubules -> ATI -> cell death
  • ‘Helper’ T cells recruit
  • Cytotoxic T cells leading to direct cellular toxicity - Predominantly tubular rejection
  • B cells leading to donor specific ab production - predom vascular rejection
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39
Q

what are the major causes of late graft loss?

A
  • chronic rejection
  • recurrent disease
  • death w a functioning graft
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40
Q

what is the definition of kidney failure?

A
  • reduction in kidney function
  • usually identified from: decrease in urine output, increase in serum creatinine, decrease in eGFR
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41
Q

AKI =

A

sudden decrease in kidney function over days to weeks

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42
Q

CKD =

A
  • CKD: there has been a persistent decline in kidney function over a longer time
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43
Q

Acute on C kidney failure

A

means that there has beena sudden decrease in kidney function in someone with chronic kidney disease

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44
Q

end stage kidney disease

A

End stage kidney disease means that there is insufficient kidney function to maintain life without renal replacement therapy

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45
Q

reversibility of kidney disease

A
  • AKI or acute on chronic kidney disease -> potential to restore kidney function to normal (acute) or baseline abnormal (acute on chronic) function
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46
Q

stage 1 of CKD?

A

normal GFR

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47
Q

Stage 2 of CKD?

A

60-89 ml/ min

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48
Q

Stage 3 of CKD?

A

3a) 45-59 ml/min
3b 30-44 ml/min

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49
Q

Stage 4 of CKD?

A

15-29ml/min

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50
Q

stage 5 of CKD?

A

<15 ml/ min or RRT

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51
Q

RIFLE classification of CKD

A
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52
Q

Oliguria =

A
  • Oliguria is an abnormally low urine output
  • in adults <400mls/day or <0.5ml/kg body weight/hour)
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53
Q

anuria =

A
  • Anuria is no urine output
  • <50mls/day
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54
Q

Pre-renal injury?

A
  • this implies decreased blood flow either because of a fixed obstruction (renal artery stenosis) or far more commonly a decreased circulating volume or blood pressure
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55
Q

site of intra-renal injury?

A
  • This means that the injury is within the kidney itself
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56
Q

site of post-renal injury?

A
  • This means that there is an obstruction somewhere between the
    renal pelvis and the urethra - obstruction has to affect both kidneys to cause renal failure
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57
Q

causes of pre-renal failure - true hypovolaemia?

A

– History of volume loss
* GI – diarrhoea and/or vomiting diarrhoea and/or vomiting
* Burns
* Haemorrhage

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58
Q

causes of pre renal failure - relative hypovolaemia?

A

– Heart failure
– Septic shock
– Hepatorenal failure

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59
Q

Clues for pre-renal failure?

A
  • cause for volume depletion
  • signs of hypovolaemia - tachycardia, hypotension - espec postural hypotension
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60
Q

clues to renovascular disease?

A
  • Atherosclerotic vascular disease elsewhere
  • Hypertension
  • Vascular bruits on abdominal examination
    * Deteriorating renal function with ACE-inhibition
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61
Q

causes of intra-renal failure - glomerular?

A

Glomerulonephritis

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62
Q

tubular causes of intrarenal failure?

A
  • Ischaemic ATN (prolonged pre‐renal/contrast nephropathy)
  • Nephrotoxic ATN (gentamicin/amphotericin/paracetamol)
  • Intratubular obstruction (crystals/myoglobin/myeloma)
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63
Q

intersitial causes of tubular renal failure?

A

– Acute pyelonephritis
– Acute interstitial nephritis (drugs/infection)

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64
Q

vascular causes of intra-renal failure?

A
  • Vasomotor (drugs including NSAID’s/ACE‐I’s)
  • Malignant hypertension, scleroderma
  • Vasculitis
  • Microvascular obstruction (atheroemboli/cholesterol emboli/HUS/ TTP)
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65
Q

volume depletion and ACE

A
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66
Q

NSAIDs

A
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67
Q

features suggestive of intra-renal AKI?

A
  • proteinuria - suggestive of glomerular disease
  • haematuria
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68
Q

proteinuria - microalbuminuria?

A
  • Microalbuminuria (measured by an albumin:creatine ratio) is an indicator of early diabetic nephropathy and capillary injury indicator of early diabetic nephropathy and capillary injury secondary to hypertension or vascular disease
  • The urine dipstick test will be negative
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69
Q

proteinuria ?

A
  • Proteinuria (measured by a protein:creatinine ratio) is an indicator of glomerular disease (glomerulonephritis)
  • The urine dipstick test will be positive
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70
Q

visible haematuria?

A
  • visible (macroscopic) - more commonly indicates bleeding within the urinary tract
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71
Q

invisible haematuria?

A
  • invisible - more commonly indicates glomerular haematuria
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72
Q

post-renal renal failure - in order to cause renal failure?

A
  • in order to cause renal failure, the obstruction needs to be bilateral or affect a single functioning kidney e.g. kidney transplants
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73
Q

sites of obstruction - PUJ?

A
  • Bilateral pelvicoureteric junction (PUJ)
  • Bilateral ureteric - tumour /retroperitoneal fibrosis / bilateral stones / bilateral sloughed papilla
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74
Q

Sites of obstruction - bladder outflow?

A
  • Prostatic hypertrophy / stone / tumour / neurogenic bladder
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75
Q

sites of obst- urethra?

A
  • Tumour / valves / stricture/ foreign body
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76
Q

clues to obstructive picture

history of:

A
  • urinary tract surgery
  • pelvic malignancy/radiotherapy - bladder symptoms
  • polyuria (early obstruction)
  • anuria (very late obstruction
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77
Q

clues to obstructive picture:

Signs of

A
  • palpable bladder - prostatic enlargement
  • abnormal rectal or vaginal examination
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78
Q

absence of ? makes obstruction unlikely

A

hydronephrosis on renal US

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79
Q

roles of the normal kidney

A
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80
Q

signs and symptoms of uraemia

A
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81
Q

Treatment of severe renal failure?

A
  • dialysis
  • transplantration
  • conservative care of ESRF - symptom management
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82
Q

cautions of ACE/ ARB

A
  • hyperkalaemia
  • fall in GFR
  • renal artery stenosis
  • volume depletion
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83
Q

Tx of water/ sodium retention?

A
  • dietary salt restriction
  • loop diuretic
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84
Q

anemia?

A
  • less EPO -> anaemia
  • treat w recombinant EPO if sympptomatic
  • target hb: 100-120
  • avoid overcorrection - risk of excess cardiovascular mortality
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85
Q

pathophys of sodium retention?

A
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86
Q

consequences of severe hyperkalaemia?

A
  • can cause cardiac arrest
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87
Q

Pathophys of bone disease

A
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88
Q

pathophys of acidosis and hyperkalaemia

A
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89
Q

Staging of CKD

A
  • Stage 1: Normal GFR; GFR >90 mL/min/1.73 m2 with other evidence of chronic kidney damage
  • Stage 2: Mild impairment; GFR 60-89 mL/min/1.73 m2 with other evidence of chronic kidney damage
  • Stage 3: Moderate impairment; GFR 30-59 mL/min/1.73 m2
  • Stage 3 CKD should be split into two subcategories defined by (2):
  • GFR 45-59 ml/min/1.73 m2 (stage 3A)
  • GFR 30-44 ml/min/1.73 m2 (stage 3B)
  • Stage 4: Severe impairment: GFR 15-29 mL/min/1.73 m2
  • Stage 5: Established renal failure (ERF): GFR < 15 mL/min/1.73 m2 or on dialysis
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90
Q

other evidence of chronic kidney damage may be one of the following:?

A
  • persistent microalbuminuria
  • persistent proteinuria
  • persistent haematuria (after exclusion of other causes, e.g. urological disease)
  • structural abnormalities of the kidneys demonstrated on ultrasound scanning or other radiological tests, e.g. polycystic kidney disease, reflux nephropathy
  • biopsy-proven chronic glomerulonephritis (most of these patients will have microalbumuria or proteinuria, and/or haematuria)
91
Q

The definition of CKD is the presence of either of the following for 3 months (i.e. chronicity) or more:

A
  • Marker of kidney damage:
  • Albuminuria (> 3 mg/mmol, i.e. A2/3)
  • Abnormalities (including electrolyte derangement) secondary to tubular disorders
  • Structural abnormalities
  • Abnormalities on histology
  • History of kidney transplant
  • Reduced GFR: GFR < 60 ml/min/1.73 m2(i.e. G3a-G5)
92
Q

CF of CKD?

A
  • patients generally asymptomatic but develop non specific symptoms at more advanced stages - GFR under 45
93
Q

symptoms of CKD?

A
  • Frequently asymptomatic in early stages
  • Anorexia & nausea
  • Fatigue & weakness
  • Muscle cramps
  • Pruritus
  • Dyspnoea
  • Oedema
94
Q

Signs of ckd?

A
  • Pallor(secondary to anaemia)
  • Hypertension
  • Skin pigmentation
  • Excoriation marks
  • Peripheral neuropathy​
95
Q

signs of overload with CKD?

A

(e.g. raised JVP, peripheral & pulmonary oedema)

96
Q

uraemic encephalopathy?

A
  • in severe renal impairment patients can develop high urea levels -> uraemic encephalopathy - seizures, confusion, low consciousness
97
Q

other things that can arise from CKD?

A
  • pericarditis (e.g. pericardial effusion and clinical rub on auscultation)
  • and defective platelet function (causes bruising)
98
Q

Diagnosis of CKD?

A
  • serum creatine and urinary ACR
  • Serum creatinine levels have a high individual variation changing with disease states, muscle mass, pregnancy and dietary intake.
99
Q

investigations for CKD?

A
  • urine dipstick
  • urine microscopy
  • ACR - spot test or 24 hr collection
  • electrophoresis (e.g. myeloma)
100
Q

Screening for CKD?

A
  • FBC, U&Es, PTH, myeloma screen
101
Q

imaging for CKD

A
  • renal US
  • MR angiography
  • echo
  • ECG - high risk of CVS disease
102
Q

Management of CKD involves?

A
  • blood pressure control and reducing proteinuria
  • standard target - >140/90 for CDK
103
Q

when is there a lower target for BP w CKD?

A

f the ACR is > 70 mg/mmol then a tigher blood pressure control may be targeted (< 130/80 mmHg).

104
Q

How is HTN with proteinuria on a history oc CKD managed?

A
  • ACE/ ARB for CKD hypertension with proteinuria
105
Q

SGLT2 inhibitor?

A
  • dapaglflozin
  • decreases renal intraglomerular pressure and inhibiting RAAS
106
Q

other therapies for CKD?

A
  • statins
  • smoking cessation
  • antiplatelets for secondary prevention of CVS disease
107
Q
A
108
Q

complications of CKD - potassium

A
  • hyperkalaemia - NSAIDs and potassium-sparing diuretics, may worsen hyperkalaemia
  • Acute rises in potassium should be managed as a medical emergency.
108
Q

Complications of CKD - anemia?

A
  • anemia - A normocytic normochromic anaemia is typical of CKD.
  • treated using erythropoietin-stimulating agents (ESA) such as epoetin alfa.
109
Q

management of acute hyperkalaemia?

A
  • This involves stabilisation of the myocardium (with calcium gluconate) and
  • driving potassium into the intracellular compartment (with insulin/dextrose).
110
Q

management of chronic hyperkalamia?

A
  • Chronic elevations in serum potassium can be managed with low potassium diets, potassium-binding resins and correction of acidosis.
111
Q

electrolyte abn associated w reduced kidney function?

A
  • In disease, reduced kidney function (usually associated with a GFR < 30ml/min) leads to hypocalcaemia, hyperphosphataemia and hyperparathyroidism (secondary hyperparathyroidism
  • can lead to osteomalacia, osteoporosis and osteitis fibrosa cystica - renal osteodystophy
112
Q

management of hypocalccaemia?

A

dietary supplements and calcitriol

113
Q
A
113
Q

management of hyperphosphateaemia?

A
  • Hyperphosphataemia: dietary restriction and phosphate binders (e.g. calcium acetate).
114
Q

management of hyperparathyroidism?

A
  • Hyperparathyroidism: calcimimetics or surgery.
115
Q

complications - fluid overload?

A
  • hypervolaemia and patients may have evidence of peripheral oedema, ascites, raised JVP, gallop rhythm and bilateral pleural effusions.
115
Q

management of fluid overload?

A
  • Fluid overload can be managed with a combination of fluid restriction, reduced sodium intake and the use of oral diuretics (e.g. furosemide).
116
Q

metabolic ? with CKD?

A
  • tendency to retain H+, acidosis can exacerbate hyperkalaemia
117
Q

Renal replacement therapies?

A
  • haemodialysis
  • peritoneal dialysis
  • renal transplantation
118
Q
A
118
Q
A
118
Q
A
119
Q

haemodialysis involves?

A
  • Haemodialysis involves the removal of waste products and other substances by passing blood through a dialysis machine.
  • Blood comes into contact with a semi-permeable membrane, which contains the dialysate on the other side.
  • Substances may then diffuse between the two fluids (blood and dialysate).
120
Q

what does haemodialysis require?

A
  • Haemodialysis requires intravenous access in the form of an arteriovenous fistula or an artificial line (e.g. portacath).
  • Patients usually have haemodialysis 3-4 times a week for several hours.
121
Q

peritoneal dialysis?

A
  • Peritoneal dialysis is achieved by using the peritoneal cavity as the primary site of ultrafiltration.
  • A catheter (e.g. Tenckhoff catheter) is inserted into the abdominal cavity, which allows the infusion of the dialysate.
  • The dialysate then dwells within the abdomen using the peritoneum as a semi-permeable membrane for the transfer of waste products.
  • The dialysate can then be removed after a certain amount of time and the procedure repeated.
122
Q

Ways in which peritoneal diaysis can be carried out?

A
  • In general, peritoneal dialysis can be achieved by continuous ambulatory peritoneal dialysis (CAPD) where multiple exchanges are made each day, or by automated peritoneal dialysis (APD) where the exchange is made overnight when the patient sleeps.
123
Q

Renal transplantation is the?

A

gold standard for RRT

124
Q

Complications of transplantation?

A
  • complications: graft rejection, complications from immunosuppressive agents (e.g. malignancy, infection) anddisease recurrence.
125
Q

Obstructive uropathy?

A
  • obstructive uropathy is a disorder of the urinary tract which occurs due to obstructured urinary flow and can be either structural or functional
  • back up of urine causes hydronephrosis
126
Q

most common cause of obs uropathy?~

A

BPH

127
Q

other causes of obst uropathy?

A

constipation, urethral stricture, colonic endometriosis, parasitic obstructions, prostatic adenocarcinoma

128
Q

who does obst uropathy affect more?

A
  • obstructive uropathy is more common in men in their 60s
  • Obstructive uropathy is significantly less common in females.
129
Q

symptoms of BPH?

A
  • Nocturia, dysuria, urinary urgency or frequency, and decreased force of urinary stream should suggest benign prostatic hypertrophy/hyperplasia or prostatic adenocarcinoma.
130
Q

Fever + BPH symptoms?

A
  • Fever should increase your concern for concomitant urinary tract infection and, possibly, septicemia.
131
Q

prostatic malignancy should be considered when?

A
  • Prostatic malignancy should be considered in the presence of recent unintentional weight loss, night sweats, and hematuria with a nodular prostate on examination.
132
Q

what can cause scarring -> obs uropathy?

A
  • Radiation and other treatments for prior malignancies can increase scarring in the GU tract and produce obstruction.
133
Q

GI features that can contribute to obst uropathy?

A
  • Gastrointestinal symptoms of constipation, nausea, vomiting, and diarrhea may aid in diagnosing fecal impaction, bowel obstruction, or a colonic mass as contributing factors to the urinary tract obstructions.
134
Q

obst uropathy: what can suggest uretral injury?

A
  • Recent surgeries (e.g., appendectomy, hysterectomy) can suggest ureteral injury
135
Q

An upper urinary tract obstruction (i.e. in the ureters) presents with:

A
  • Loin to groinorflankpain on the affected side (due to stretching and irritation of ureter and kidney)
  • Reduced or no urine output
  • Non-specific systemic symptoms, such as vomiting
  • Impaired renal function on blood tests (i.e. raised creatinine)
136
Q

Lower urinary tract obstruction (i.e. in the bladder or urethra) presents with:

A
  • Difficulty or inability to pass urine (e.g., poor flow, difficulty initiating urination or terminal dribbling)
  • Urinary retention, with an increasingly full bladder
  • Impaired renal function on blood tests (i.e. raised creatinine)
137
Q

Common causes of UT obstruction?

A
  • Kidney stones
  • Tumours pressing on the ureters
  • Ureter strictures (due to scar tissue narrowing the tube)
  • Retroperitoneal fibrosis (the development of scar tissue in the retroperitoneal space)
  • Bladder cancer (blocking the ureteral openings to the bladder)
  • Ureterocele
138
Q

ureterocele?

A

(ballooning of the most distal portion of the ureter – this is usually congenital)

139
Q

common causes of LUT obstruction?

A
  • Benign prostatic hyperplasia (benign enlarged prostate)
  • Prostate cancer
  • Bladder cancer (blocking the neck of the bladder)
  • Urethral strictures (due to scar tissue)
  • Neurogenic bladder
140
Q

Management of a urinary obstr?

A
  • nephrostomy: to bypass an obstruction in the upper UT e.g. a ureteral stone
  • A nephrostomy involves surgically inserting a thin tube through the skin at the back, through the kidney and into the ureter.
  • This tube allows urine to drain out of the body, into a bag.
141
Q

How can an obstruction in the lower UT be bypassed?

A
  • Aurethralorsuprapubic cathetermay be used to bypass an obstruction in the lower urinary tract (e.g., a urethral stricture or prostatic hyperplasia).
  • Aurethral catheteris a tube, inserted through the urethra, into the bladder.
  • Asuprapubic catheteris a tube, inserted through the skin just above the pubic bone, directly into the bladder.
142
Q

Hydronephrosis?

A
  • due to obstruction of the urinary tract leading to back pressure into the kidneys
  • Idiopathic hydronephrosisis the result of a narrowing at thepelviureteric junction
  • can be congenital or develop later
143
Q

features of hydronephrosis?

A
  • Typical presenting features of hydronephrosis are vague renal angle pain and a mass in the kidney area.
  • It may be seen on anultrasound,CT scanorintravenous urogram(x-ray with IV contrast collecting in the urinary tract).
144
Q

Ix of obst uropathy?

A
  • urinalaysis - infection, haematuria
  • creatinine
  • FBC - anemia, sepsis
  • prostate specific antigen - BPH, prostate cancer
145
Q

BPH is caused by?

A
  • Affects men over 50
  • It is caused by hyperplasia of the stromal and epithelial cells of the prostate.
  • It usually presents with lower urinary tract symptoms.
146
Q

in BPH proliferation occurs in the?

A
  • proliferation occurs primarily in the transition zone of the prostate, this leads to restriction of the prostatic urethra and urinary flow.
147
Q

What are the LUTS?

A
  • Hesitancy– difficult starting and maintaining the flow of urine
  • Weak flow
  • Urgency– a sudden pressing urge to pass urine
  • Frequency– needing to pass urine often, usually with small amounts
  • Intermittency– flow that starts, stops and varies in rate
  • Strainingto pass urine
  • Terminal dribbling
  • Incomplete emptying
  • Nocturia
148
Q

scoring system for severity of LUT symptoms

A

The international prostate symptom score(IPSS) is a scoring system that can be used to assess the severity of lower urinary tract symptoms.

149
Q

assessment of BPH?

A
  • digital rectal examination
  • abd examination - palpable bladder
  • PSA
  • urine dipstick
  • urinary frequency volume chart
150
Q

PSA -?

A
  • high false positive rate
151
Q

Common causes of a raised PSA?

A
  • Prostate cancer
  • Benign prostatic hyperplasia
  • Prostatitis
  • Urinary tract infections
  • Vigorous exercise (notably cycling)
  • Recent ejaculation or prostate stimulation
152
Q

what does a benign prostate feel like?

A
  • A benign prostate feels smooth, symmetrical and slightly soft, with a maintained central sulcus
153
Q

what does a cancerous prostate feel like?

A
  • A cancerous prostate may feel firm/hard, asymmetrical, craggy or irregular, with loss of the central sulcus
154
Q

management of BPH - 2 drug classes?

A
  • alpha blockers
  • 5 alpha reductase inhibitors
155
Q

alpha blockers?

A
  • Alpha-blockers(e.g.,tamsulosin) relax smooth muscle, with rapidimprovement in symptoms
156
Q

5-alpha reductase inhibitors?

A

(e.g.,finasteride) gradually reduce thesize of the prostate by blocking DHT production

157
Q

Ix of BPH?

A
  • dipstick
  • bloods - FBC, UEs, LFTs - ALP may be elevated in prostatic cancer w bony mets
158
Q

imaging for BPH?

A
  • USS - size of prostate and evaluate for hydronephrosis
  • MRI prostate - diagnosis of malignancy
159
Q

physical side effects of haemodialysis?

A
  • hypotension - one of the most common
  • nausea and dizziness
  • sepsis
  • muscle cramps - usually in the lower le
  • itchy skin
  • loss of libido and erectile dysfunction
160
Q

psychological side effects of haemodialysis?

A
  • mental fatigue
  • drowsiness
  • tiredness
  • light headedness
  • lack of motivation
161
Q

impacts of haemodialysis on social wellbeing?

A
  • low self esteem
  • loneliness
  • depression
  • anxiety
  • repeated hospital trips - impact on work and social life
162
Q

concern w peritoneal dialysis?

A

peritonitis

163
Q

signs of peritonitis?

A
  • abdominal pain
  • a high temperature
  • feeling and being sick
  • experiencing chills
  • the used dialysis fluid becoming cloudy
164
Q

other risks of peritoneal dialysis?

A
  • hernia - inc strain on the abdominal muscles
  • weight gain
165
Q

psychological issues of peritoneal dialysis?

A
  • depression
  • loss of sexual function -> relationship issues
  • family burden
  • loss of independence
166
Q

which type of immunity are B cells involved?

A
  • humoral/ antibody mediated immunity - activated by TH2 cells
  • fights extracellular infections, includingmost bacteria and fungi, protozoans such as Giardia, and parasitic worms such as Schistosoma.
167
Q

types of B cells?

A
  • plasma cells
  • memory B cells
168
Q

IgM?

A
  • IgM– this has a pentameric structure.
  • It is expressed on B cell surfaces andproduced earlyin the immune response whilst IgG is being generated.
169
Q

IgG?

A
  • Monomeric structure
  • It is found mainly incirculating bloodandtissues
  • it also crosses the placentato provide passive immunity to the fetus
170
Q

IgA?

A
  • forms a dimeric structure once it reaches its target tissues.
  • It is found in mucosal areas such as the GI, respiratory and urinary tracts.
  • It is also secreted in saliva, tears and breast milk.
171
Q

IgE?

A
  • IgE– this has a monomeric structure
  • It binds to allergens and mediates allergic reactions, as well as providing immunity against multicellular organisms such as parasitic worms.
172
Q

IgD?

A
  • IgD– this has a monomeric structure and is rather mysterious.
  • It is found in very low levels in the serum, and appears to interact with basophilsand mast cell
173
Q

all T cells express?

A
  • all T cells express CD3 on their surfaces, along with T cell receptors(TCRs) which recognise specific antigens presented in an MHC I or MHC II molecule
174
Q

Helper T cells?

A
  • helper Tcells (CD4)facilitate the activation of the immune response and stimulate division and differentiation of various effector cells
175
Q

cytotoxic T cells?

A
  • cytotoxic T cells (CD8)– also known as killer or effector T cells – providecell-mediatedimmunityby targeting and killing infected cells
176
Q

regulatory T cells ?

A
  • regulatory Tcells (CD25+FOXP3)– also known as suppressor T cells – play a vital role in limiting the immune response to prevent excessive damage to tissues and organs
177
Q

memory t cells?

A
  • memory T cells (CD62 + CCR7)“remember” what has happened to allow the immune system to mount a faster, more effective response
178
Q

How is cell mediated immune response activated?

A
  • activated by TH1 -> activation of APC and cytotxic T cells
  • designed to fightintracellular infections, includingviruses,some bacteria and fungi, andprotozoanssuch asPlasmodiumandToxoplasma.
179
Q

steps of T cell development?

A
  • T cells undergo education in the thymus gland
  • tested with self cell antigens
  • anycells which have generated a receptor thatreacts to these undergonegative selectionand are destroyed
  • this prevents the immune system from reacting to the body and is known as immunological tolerance or self tolerance
180
Q

T cells - graduation from the thymus?

A
  • In order to graduate successfully from the thymus, T cells must also express CD3and CD4 or CD8 (but never both), and bind to self MHC
    complexes(but not too strongly?
181
Q

steps of the cell mediated resp?

A
  • First step of the cell mediated response is the activation of APCs
  • TH1 cell encounters an infected APC and recognises the MHC-2 restricted antigen on its surface
  • this activates the APC by providing aCD40 ligand second signaland secretinginterferon-gamma(IFNγ)
182
Q

2: once activated, APCs are able to increase production of?

A
  • increase their production ofnitric oxideandsuperoxide radicals,
  • which optimises their killing mechanisms and allows them todestroy ingested pathogensmuch more effectively
183
Q

3: cytoxic T cell response?

A
  • next step is the activation of antigen specific cytotoxic T cell response
  • activated APCspresent their antigen to the specificcytotoxicT cell receptorwithin anMHC I, along with a variety ofsecond signals, includingB7 + CD28and/or4-IBB + 4-IBBL
184
Q

APC presentation to cytotoxic T cells is helped by?

A
  • this process is helped along by the secretion ofIL-2– a potentT cell growth factor–byTH1 cellsand thecytotoxic T cellsthemselves
185
Q

how do activated CT cells recognise infected cells?

A
  • activated cytotoxic T cells recognise infected cells by recognising the MHC1 presenetd antigen
186
Q

how do T cells damage cells?

A
  • T cells secrete perforin to create holes in the cell wall
  • They then use this hole to releasegranzymesandgranulysininto the cell, which induceapoptosisandDNA fragmentation.
  • Fas ligand interactionsbetween the cell surfaces can also produceapoptosisof theinfectedcells via the aptly named death-inducing signalling complex (DISC)
187
Q

T cells can also release?

A
  • interferon gamma
  • is able toblock intracellular viral replicationwithout killing the cell itself
188
Q

Memory T cells?

A
  • after the infection subsides, most antigen specific cytotoxic T cells will remain as dormant memory T cells
  • during reinfection, only the first signal (MHC + antigen) is required to activate the cytotoxic T cell response; no second signal is necessary
  • this means that any antigen- presenting cell(not just dendritic cells) can activate cytotoxic T cells directly, reducing the need for TH1 cell help and resulting in a much swifter and more efficient cell- mediated immune response.
189
Q

extracellular infections–>

A

TH2–>humoral immune response with B cells and antibodies

190
Q

intracellular infections–>

A

TH1–> cell- mediated immune response with activated APCs and cytotoxic T cells

191
Q

blood group A?

A

has A antigens on the red blood cells with anti-B antibodies in the plasma

192
Q

blood group B?

A

has B antigens with anti-A antibodies in the plasma

193
Q

gr O?

A

has no antigens, but both anti-A and anti-B antibodies in the plasma

194
Q

gr AB?

A

has both A and B antigens, but no antibodies
\

195
Q

Group A genotype?

A
  • Group A: can be IAIA or IAi genotypes
196
Q

Group B genotype?

A
  • Group B: can beIBIBorIBigenotypes
197
Q

Group AB genotype?

A
  • Group AB: can only beIAIBgenotype
198
Q

group O genotype?

A
  • Group O: can only be ii genotype
199
Q

which alleles are codominant?

A
  • A and B alleles are codominant but O is recessive
200
Q

Universal donor and universal recipent?

A
  • O is the universal donor
  • AB is the universal recipient
201
Q

which blood can safely given in emergencies?

A
  • O Rh - blood can be safely given to anyone
  • used in emergencies
202
Q

All blood donations are routinely tested for?

A
  • All donations are routinely tested for hepatitis B, hepatitis C, hepatitis E, human immunodeficiency virus, syphilis and for first time donors, human T-lymphotropic virus,
203
Q

Blood transfusion w ? is the best practice?

A

identical ABO and rh

204
Q

group and hold test?

A
  • Screening for antibodiesis part of the standardgroup and holdpathology test (also known as a type and screen).
  • Any subsequent crossmatch involves testing the units to ensure there is no clinically detectable agglutination reaction between the patient’s blood sample and the blood product to be crossmatched.
205
Q

haemolytic transfusion reaction?

A
  • Transfusion of an incompatible blood product can cause ahaemolytic transfusion reaction, where the antibody-antigen reaction causes the affected cells to be destroyed. This haemolysis could be either intravascular or extravascular, depending on whether the classical complement pathway is activated.
206
Q

Matching?

A
  • kidney donor and recepients are matched by blood group and tissue type
  • people from the same ethnic background are more likely to have matching blood groups and tissue types.
207
Q

HLA typing?

A
  • blood test to determine the HLA type of the patient and the potential donor to see how well they matc
  • 6 antigen match is the best but is very rare to get, especially if they are unrelated - zero mismatch
  • second blood test is to measure antibodies to HLA - done for the patient only
208
Q

Serum crossmatch?

A
  • donor cells mixed w patients serum
  • If your serum has antibodies against the donor’s cells, the antibodies will bind the donor cells and be detected using a fluorescent detection method.
  • If these antibodies are at high levels, the donor cells will be destroyed.
  • This is called a positive crossmatch and it means that the transplant cannot take place.
209
Q

five ab classes image

A
210
Q

role of the HTA 2004?

A
  • regulates activities concerning the removal, storage, use and disposal of human tissue
  • The Human Tissue Act 2004 also created an offence of DNA ‘theft’.
  • It is unlawful to have human tissue with the intention of its DNA being analysed, without the consent of the person from whom the tissue came
211
Q

Offences under the HTA

A

1) Removing, storing or using human tissue for Scheduled Purposes without appropriate consent.

2) Storing or using human tissue donated for a Scheduled Purpose for another purpose.

3) Trafficking in human tissue for transplantation purposes.

4) Carrying out licensable activities without holding a licence from the HTA (with lower penalties for related lesser offences such as failing to produce records or obstructing the HTA in carrying out its power or responsibilities).

5) Having human tissue, including hair, nail, and gametes, with the intention of its DNA being analysed without the consent of the person from whom the tissue came or of those close to them if they have died.

212
Q

key functions of the HTA?

A
  • establish the Human Tissue Authority (HTA) to regulate activities concerning the removal, storage, use and disposal of human tissue
  • make appropriate consent a legal requirement for the removal, storage and use of body parts, organs, tissue and cells (“relevant material”). The Human Tissue Act lists the purposes for which consent is required ( these are called “scheduled purposes”)
  • introduce licensing requirements for the removal, storage and use of bodies, organs, tissue and cells
  • sets out offences and penalties for breaching the requirements
213
Q

arguments for an opt out system?

A
  • increases number of organ donations -> reducing number of patients dying whilst awaiting an organ transplantation
  • families are consulted before the donation occurs
  • faith and religious beliefs considered
  • argued that opt-out systems overcome many traditional barriers to deceased organ donation – such as perceived religious or socio-cultural preclusions, lack of education or transplant awareness and challenges in communicating with families who are grieving a loved one.
214
Q

arguments against an opt out system?

A
  • insufficient consent - explicit consent not sought before the person dies
  • unethical - taking away rights of people
  • can be seen as a bodily violation
  • implies that bodies belong to the state
  • safeguaring issues - as patients haven’t directly said they do want their organs to be donated and those that want to refuse could feel pressured by social norms to comply.
215
Q

Principles guiding organ and tissue donation ?

A
  • should be voluntary and altruistic
  • free and consented
  • respect for donor and receptient autonomy
  • confidentiality and protection of donor’s and recipients data
216
Q

Ethical issues in organ donation?

A
  • insufficient donors- shortage of obtainable and useable organs
  • use of organs from cadavers, infants and organs
  • internet and global transplant tourism
  • use of organs from living donors - could lead to manipulation, coercion, emotional suffering, morbidity
  • financial payments to encourage donation - organs moving from poor to rich
  • organ black market
217
Q

Blood donation ethical issues?

A
  • unacceptable for some e.g. Jehovas witnesses
  • absolute safety of the blood cannot be guaranteed
  • patient rejection of blood transfusions - autonomy
  • coercion. financial gain
  • anonymity between donor and recipient
218
Q

Discuss the healthcare resource implications of organ transplantation and blood donation

A
  • reduced need for dialysis which is more expensive long term -> reduced health care spending
  • lifelong immunosuppressants required - cost
219
Q
A

Year 3 (45 decks)

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