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YEAR 2 SEMESTER 2 > renology and urology - wk 5 > Flashcards

renology and urology - wk 5 Flashcards

1
Q

what conditions can cause problems with respiratory removal of Co2 effecting acid-base balance

A

Causing acidosis via hypoventilation

  • Lung disease eg COPD
  • Airway obstruction
  • Opioid overdose/ head injury

Causing alkalosis via hyperventilation

  • Panic attack
  • Reaction to pain
  • Respiratory disorders eg asthma
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2
Q

what metabolic issues can cause acidosis

A
  • Over-production of acid
    o lactic acidosis from inadequate oxygen supply to tissue
     Eg Hypovalaemia, anaemia,
    o Ketoacidosis due to inadequate cellular supply of oxygen
     Eg type 1 diabetes, starvation, alcohol intoxication
  • Impaired excretion (from global loss of kidney function
    o Eg AKI, end-stage CKD
    o Renal tubular acidosis – bad filtration of H+
  • Unusual losses of bicarbonate
    o Lost from bowel following severe diarrhoea
    o Formation of fistula in small bowel
    o Renal tubular acidosis
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3
Q

what metabolic issues can cause alkalosis

A 
-	Loss of hydrogen ions
o	Eg following protaractive vomiting
o	Severe hypokalaemia
o	Hyperaldosteronism
-	Unusual indigestion of bicarbonate
o	Eg overdose of sodium bicarbonate
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4
Q

what are the 4 questions you should consider when interpreting blood gases

A

1) Is patient adequately oxygenated? (pO2, FIO2, [Hb}
a. Even is pO2 good, low Hb could mean not enough O2 delivered to tissues
2) What is there pH or H+ - normal, or acidaemia/alkalaemia
3) Is there a pCo2 disturbance?
4) Is there a [HCO£-] disturbance?

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5
Q

whats base excess

A
  • The concentration of H+ per L of blood, required to return H+ to references range at a ref range pCO2 (~5.3kPa)
  • Negative in metabolic acidosis
  • Positive in metabolic alkalosis
  • Ref. range -3 -> 3 mmol/L
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6
Q

whats standard bicarbonate

A
  • What the HCO3 would be if pCO2 were ref range (~5.3pKa)
  • So should be in reference range for a purely respiratory disorder
    o Ref range 21-29 mmol/L
  • Should be the same as the actual bicarbonate conc. In a metabolic disorder
  • Mixed metabolic and resp = significant difference with actual bicarb
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7
Q

whats the anion gap

A

Can be useful to narrow differentials of metabolic acidosis
Anion gap = difference between most abundant [cations] and [anions]
= [Na+] – [Cl-] - [HCO3-]
Ref. range anion gap; 6-18 mmol/L
- Elevated in certain types of metabolic acidosis
- Value depends on what HCO3- ions are replaced with.
o No change – replaced with Cl- ions (hyperchloremic acidosis)
o Elevated – replaced with anions corresponding to lactate, keto-acids et

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8
Q

what are the systemic effects of metabolic acidosis

A

Cardiovascular
- Negative inotropic effect (if severe)

Oxygen delivery

  • Acutely – H+ causes R-shift of oxyHb dissociation curve (facilitates Os delivery)
  • After several hours H+ reduces 2,3 DPG causing L-shift of curve (impairs O2 delivery)

Nervous system
- Impaired consciousness (little correlation with H+)

Potassium homeostasis

  • Leakage from cells causing high plasma (k+), may also be lost renally
  • If above sustained, total body K+ may be depleted

Bone

  • If chronic acidosis get buffering by bone
  • Leads to decalcification
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9
Q

what are the systemic effects of respiratory acidosis

A

Hypercapnia (high CO2)

  • SOB – although drive impaired in chronic retention
  • Neurological – anxiety, coma, headache, extensor plantars, myoclonus
  • Cardiovascular – systemic vasodilation

Independent to acidosis, often also effects of

  • Underlying pathology
  • Hypoxia caused by that pathology eg SOB, drowsy, cyanosis
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10
Q

what are the systemic effects of respiratory alkalosis

A

Acute hypocapnia

  • Cerebral vasoconstriction – light-headedness, confusion, syncope, fits
  • Fall in ionised calcium – peioral, peripheral paraesthesia

Cardiovascular
- Increased heart rate, vasoconstriction (possibly chest tightness/ angina in those with background of CAD)

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11
Q

what are the systemic effects of metabolic alkalosis

A 
Not usually significant
-	May cause shift of K+ into cells
Beware effect of IV sodium bicarb in CKD
-	Metabolic acidosis common in CKD
-	Acute fall in acidity may reduce solubility of calcium salts and increase risk of systemic calcification
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12
Q

define acute kidney injury

A
  • Increase in serum creatinine by >26.5 umols/L in 48 hrs
  • Increase in serum creatinine by >1.5x baseline creatinine within last 7 days
  • Urine volume <0.5ml/kg/hr for 6 hours
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13
Q

define pre-renal AKI and state some causes

A
  • Reduced real or ‘effective’ blood volume

Causes…
o Hypovolaemia eg bleeding, 3rd space fluid losses, over-enthusiastic diuretic therapy
o Hypotension eg septic/ cardiogenic shock, liver failure
o Reduced renal blood supply secondary to severe renovascular disease (ACE inhibitors eg), dissection of abdominal aorta, renal stenosis

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14
Q

define renal AKI and state some cause

A
  • Glomerulus, tubules and interstitium

casues

  • Tubulointerstitial (tubules and the bit ‘in between’)
  • Glomerulus
  • Blood vessels
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15
Q

define post-renal AKI and state some causes

A
  • Obstruction – multiple levels (eg ureter, bladder etc)

Causes
o Note that bilateral obstruction or obstruction of a single kidney (transplant) Is required in order to result in AKI
o Prostate – hypertrophy(common), cancer
o Bladder lesions – tumour
o Ureter – calculi, tumour, extrinsic compression (retroperitoneal fibrosis, tumour)

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16
Q

why is myeloma an important cause of AKI

A
  • B cells can precipitate in the nephron forming ‘casts’
  • If this happens in many nephrons in the kidney = widespread intratubular obstruction and AKI
  • Urgent so Treated with chemotherapy for malignancy
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17
Q

what is the commonest cause of renal AKI and explain it

A

Commonest cause is ACUTE TUBULAR INJURY

  • Tubular toxins eg gentamicin, cisplatinum, NSAIDs, radio-contrast dye
  • Severe prolonged hypotension (sepsis, MI)

Renal hypoperfusion eg elderly patient on ACE inhibitor, diuretic who has D&V
o Become unwell with diarrhoea/ vomiting
o Combo limits perfusion to kidneys
o So develop acute tubular injury - AKI

Initial oliguria then may exhibit polyureic recovery phase (watch electrolytes)

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18
Q

what are some tubulointerstitial causes of AKI (renal)

A
  • Acute allergic interstitial nephritis
  • DRUG-RELATED eg PPIs (omeprazole), antibiotics, diuretics, NSAIDs
  • May have an eosinophilia (no rash)
  • Often have little symptoms and no obvious reaction
  • But if diagnosed and drug stopped respond well to steroids
  • To the right all the red cells are eosinophils
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19
Q

what are some glomerular causes of AKI (renal)

A

Rapidly progressive glomerulonephritis (RPGN); immune aetiology and characterised by ‘glomerular crescents’

  • Rarer
  • In tissue section we see crescents aka mass of inflammatory cells outside of glomerulus in bowman’s space
  • Caused by different conditions
  • In cross section looks like crescent – becomes bigger and bigger encircling glomerulus
  • Glomerulus on the right is doomed – will become small and scarred with little functions
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20
Q

vascular causes of AKI

A

Haemolytic uraemic syndrome (HUS)
- Haemolysis, damage to blood vessels, kidney failure, uraemia
Caused by
- E coli (shiga toxin toxic to particular vascular beds – kidney vasculature vv vulnerable – thrombosis in the kidney)
- Familial cases (genetic aetiology) – mutations, normally require second illness eg hypotension, pregnancy etc
Leads to capillary loops full of fibrin

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21
Q

what should we ask about in a clinical history of a patient with suspected AKI

A
  • Renal history – pre-existing renal disease, diabetes, family history
  • Urine volume - ?acute oliguria (low urine volume)
  • Drug history – new drugs, nephrotoxic drugs (NSAIDs, ACEI, antibiotics)
  • Systemic symptoms – diarrhoea, rashes etc
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22
Q

what areas are important in clinical examination of a patient with suspected AKI

A
  • Fluid status (jugular venous pressure, BP) dehydrated
  • Evidence of infections
  • Rash, joint pathology
  • Arterial bruits, underlying renovascular disease
  • Palpable bladder (obstruction)
  • Check drug chart
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23
Q

what investigations should be undergone in an AKI patient

A
  • Urine dipstick – simple BUT important (blood, protein in urine = infection/ immune disease eg lupus/ vasculitis)
  • Urine culture
  • Renal ultrasound – if obstructed – decompressed
  • Renal biopsy (AKI and normal sozied kidney
  • Angiography +- intervention (if you think it’s a vascular issue)
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24
Q

what blood tests are important in someone with AKI

A
  • FBC, blood film, clotting screen
  • Biochemistry including Ca2+, (PO4)2-, LFTs and albumin
  • Creatinine kinase (damage to muscles from long lie/ drugs – release muscle components into blood because myoglobin coming from muscles is toxic to kidneys)
  • Blood cultures
  • Virology and serology eg Hep B, ASOT
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25
Q

what does widespread muscle damage lead to

A

The urine of someone with rhabdomyolysis aka widespread muscle damage will be dark red

  • Could also be someone with malaria
  • CK will be very high – 100,000-200,000!!!!
26
Q

what is the general treatment of AKI

A
  • Optimise fluid balance and circulation
  • Stop exacerbating factors eg nephrotoxic drugs (check drug chart)
  • Appropriate prescribing (check BNF, discuss with pharmacist) eg opiates accumulate AKI
  • Supportive treatment eg dialysis, nutrition
27
Q

what are specific treatments to target specified causes of AKI

A
  • Obstruction – drain renal tract (catheter etc)
  • Sepsis – effective antibiotics
  • RPGN eg SLE – immunosuppression
  • Goodpasture’s syndrome – plasma exchange
  • Compartment syndrome – fasciotomy
28
Q

when should an AKI patient be put on dialysis

A 
Severe uraemia 
-	No prospect of immediate improvement
-	Uraemic encephalopathy or seizures
-	Uraemic pericarditis
Hyperkalaemia unresponsive to medical treatment (>6.5)

also if…

  • Fluid overload, especially pulmonary oedema, resistant to treatment with diuretics/ fluid restriction
  • Severe acidosis (results in myocardial depression and hypotension)
29
Q

whats the difference between intermittent and continuous haemodialysis

A
  • Intermittent for ~3 hrs a day or every second day
    o Requires someone to tolerate treatments
    o Challenging to cardiovascular patients
  • Continuous dialysis
    o Much more gentle
    o Better for very sick patients
30
Q

give a brief overview of what cells are part of the innate and adaptive immune systems

A 
Innate immune system
-	Macrophages
-	Neutrophils
-	Complement and natural antibodies (IgM)
Adaptive immune system
-	Dendritic cells (antigen presentation)
-	T cells (helper and cytotoxic T cells)
-	Natural killer cells (NK) – cytotoxic
-	B cells (antibody generation and memory)
31
Q

what is the major histocompatibility complex (MHC)

A
  • MHC in humans called histocompatibility Locus Antigen (HLA)
  • These molecules imprint ‘individuality’ on cells and are pivotal in the generation of immune responses
  • HLA genes are polymorphic i.e., there are many different variations possible at each gene locus
32
Q

describe class I and class II MHC molecules

A

Class I molecules – HLA-A , -B, -C

  • Expressed by most somatic cells of body
  • Used to present peptides from internally processed proteins

Class II molecules – HLA-DP, -DQ, -DR

  • 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)
33
Q

explain the role of HLA Class I molecules

A

HLA CLASS I MOLECULES – HLA-A, -B, -C

  • If class 1HLA molecule is associated with virus-derived protein, then the cell is recognised as infected
  • Infected cell will be killed by cytotoxic T cells
34
Q

explain the role of HLA Class II molecules

A

HLA CLASS II MOLECULES – HLA-DP, -DQ and -DR

  • Used by antigen presenting cells (DCs)
  • To present antigenic peptides derived from material digested or processed
  • Cell surface expression of a peptide derived from a pathogen or foreign cell will stimulate a T cell immune response
  • How immune responses are initiated
35
Q

explain the t cell receptor and costimulation mechanism

A
  • Don’t want immune response kicking off randomly
  • So other molecules must be engaged before signal is strong enough to engage T cells and make sure they’re activated
  • These accessory molecules are also used to target for immunosuppression in patients
  • So not a simple T cell receptor, instead it’s a range of receptors that must be brought together to = activation

When they are activated T-cells are very effective assassins
- When find abnormal cell has range of kill mechanisms
o Tumour necrosis factor induce cell death
o Fas ligand induces cell death
o Perforin and Gz B punch holes in membrane = cell death

36
Q

how does the immune system react to transplant organs

A
  • Dendritic cell finds abnormal pathogen/ cell from transplant
  • Presents this antigen to initiate T cell responses which are antigen specific
  • Facilitated by production of IL-2 which is an interleukin required for proliferation of T cells
  • Clonal expansion = army of T cells unique to attacking the organ cells
  • After infection eradicated these cells die through activation induced cell death
  • BUT LEFT WITH MEMORY
37
Q

what are the key principles of transplant immunology

A
  • Rejection of Tx is directed at specific proteins called antigens
  • Rejection is donor specific
  • Rejection may be both cell or antibody mediated
  • Rejection exhibits ‘memory’ ie a 2nd similar Tx is rejected MORE RAPIDLY and this results from the rapid generation of cytotoxic antibodies that recognise the Tx
38
Q

how is HLA profiling used in kidney transplant in relation to mismatch

A

HLA profiling is used to allocate kidneys but less important for other organs such as liver (less immunological)

  • Is all HLA-A, -B and -DR loci are the same then it is a 0-0-0 mismatch
  • If they are all different it’s a 2-2-2 mismatch
  • Transplant lasts longer is there’s less mismatch
39
Q

what immunosuppression treatments are used during transplantation

A

Corticosteroids
- Kill lymphocytes
- Interfere with T cell activation and gene transcription
- Powerful anti-inflammatory agents
Calcineurin inhibitors (CNI) – Tacrolimus
- Inhibit T cell activation by interfering with intracellular signalling pathways
Anti-proliferative agents – mycophenolate mofetil (MMF)
- Inhibit clonal expansion of T cells
Various Monoclonal and polyclonal antibodies
Directed against…
- IL-2 receptor blockers (IL-2 stimulates clonal expansion of T cells)
- T cells (cytotoxic complement fixing Abs)
- Co-stimulator molecules

40
Q

what are important factors of patient history when thinking about transplant

A
  • Age important (biological and chronological)
  • Primary cause of renal failure eg polycystic kidneys versus conditions which can recur in a transplant (eg aHUS, FSGS)
  • Comorbid disease eg cardiovascular disease (IHD, PVD), diabetes etc
  • History of infections
  • History of tumours (need tumour free period)
  • Urological disease (eg bladder dysfunction)
41
Q

explain the assay used to assess immunological x-match

A

 take cells from serum of recipient and cells from the donor
 add source of complement
 if antibody binds to an antigen then lytic process happens – holes punched in membrane and cell dies
 if you add a vital dye this enters the cells that are getting holes punched in them and you can see the dye colour in the interior of the cell
 if the donor has antibodies the cells will become green
 so if cells = green this signals a positive cross match meaning the kidney transplant can’t go ahead

42
Q

explain production of HLA antibodies ie sensitisation and give some possible reasons for this

A
  • if a person is exposed to a foreign HLA molecule, they can produce HLA antibodies against this eg if patient is A1, A24 they may be exposed to A31 and generate this antibody
  • approx.. 30% of patients on renal waiting list have anti-HLA antibodies
  • the ‘specificity’ of these antibodies has to be defined
    Highly sensitised patients exhibit high levels of cytotoxic Abs to many HLA antigens that may be derived from –
  • previous transfusions (WBC filtered but some white blood cells can get through)
  • pregnancies (foetuses’ antigens)
  • previous transplantation
43
Q

describe the steps of the luminex HLA antibody detection test

A

LUMINEX HLA ANTIBODY DETECTION
- 100 different colour coded polystyrene beads in a single well
- Each bead population coated with selected class I or class II antigens or pool of antigens for screening purposes
Procedure
1- Microbeads coated with HLA antigen incubated with patient serum
2- Wash beads
3- Incubate with PE conjugated anti-human IgG
4- Wash beads
5- Run beads on LabScan 100TM – assign assay reactivity and antibody specifities

  • So you mix beads with patient serum and if there’s antibodies for the antigen on the beads they will bind.
  • you can pick up the antibodies binding to the beads by adding anti-human immunoglobulin which binds to the antibody on the bead and gives a fluorescent signal
  • gives you this graph 
  • at the left the patient has high antibodies for these antigens so want to give patient a kidney with antibodies on the right side of the graph as they don’t have antigens against these ones
44
Q

whats hyperacute rejection

A
  • occurs when Tx carries antigens to which the recipient is already sensitised
  • cytotoxic antibodies bind endothelial cells and induces complement activation, platelet aggregation and intravascular thrombus formation
  • the Tx is often destroyed ‘on the operating table’
45
Q

what are some features of acute rejection and what conditions must be excluded upon these features after transplantation

A

Features

  • rise in creatinine (often only indication if immunosuppression potent)
  • reduced UO
  • tender transplant
  • fever

Exclude

  • dehydration (clinical exam, BP)
  • renal obstruction (US)
  • vascular catastrophe (doppler)
  • drug toxicity (tacrolimus levels – as its nephrotoxic)
46
Q

antibody mediated rejection signs histologically

A
  • when antibody binds to epithelium it’s not there vv long
  • but activates compliment forming C4d =.an antibody footprint
  • you can stain kidney and look for this
  • associated with inflammation = capillaritis
47
Q

how do we treat 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)
48
Q

what are features of chronic rejection and what conditions must be excluded upon these features

A

Features

  • Progressive renal dysfunction
  • Interstitial fibrosis and vascular disease on renal biopsy

Need to exclude

  • Recurrent disease (membranous, MCGN)
  • Obstruction (US)
  • Renal artery stenosis (doppler of renal artery +- MRI angiography)
49
Q

what are the mechanisms behind chronic rejection

A
  • Increased HLA mismatch (1-2-1 vs 0-0-1)
  • Previous acute rejection
  • Poor drug compliance (low tacrolimus levels)
  • Prolonger cold ischaemia time in kidney prior to surgery (CIT of living donor &laquo_space;cadaveric donor)
50
Q

what are some factors promoting graft failure in transplantation

A
  • Delayed graft function
  • Cytomegalovirus (CMV) infection
  • Age of donor and ‘donor disease’
  • Poor blood pressure control
  • Proteinuria
51
Q

management of chronic rejection

A
  • No specific treatment available
  • Most patients will eventually require dialysis and potentially further Tx
  • Optimise immunosuppression
  • Proactive treatment BP, lipids, proteinuria etc
52
Q

what are infective risks of immunosuppression

A

Bacteria

  • Urinary tract infection, chest infection
  • Prophylactic cotrimoxazole

Viral

  • CMV, herpes virus, parvo virus, BK virus (causes renal dysfunction)
  • Prophylactic valganciclovir if recipient CMV -ve and donor CMV +ve
  • TB (may require prophylactic treatment)
53
Q

what are tumour risks of immunosuppresion

A

Tumours

  • Incidence of all cancers increased
  • Skin cancers common (UV block, avoid sun, monitor skin)
  • Post Tx lymphoproliferative Disorder (PTLD) – secondary to infection with Epstein Barr Virus (reduce immunosuppression, may need chemotherapy)
54
Q

what are side effects of immunosuppressive drugs

A

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

55
Q

whats central pontine myelinolysis

A

Devastating / fatal condition associated with rapid correction of hyponatraemia

  • Related to water fluxes into and out of brain
  • Commoner in alcoholism and malnutrition and young women
  • Associated with the pons in the brain
56
Q

whats the main cause of hypernatraemia

A
  • Hypovolaemia is almost always the case (concentration)
  • The list of potential causes is vv similar to that of hyponatraemia
  • The difference is the sodium: water balance
57
Q

explain diabetes insipidus as a cause of hypernatraemia

A
  • Diuresis continues unabated
  • Free water loss occurs
  • Sodium is concentrated
  • Hypernatremia occurs
  • No/ failed feedback mechanism
58
Q

what are the 2 types of diabetes insipidus

A

Cranial/central DI – non/ reduced synthesis ADH
Eg – pituitary tumour, head injury, meningitis, genetic, idiopathic

Nephrogenic – reduced tubular response
Eg – inherited (receptors don’t work/ not there), drugs (lithium carbonate – treatment for bipolar defective disorder SE it blocks receptors on tubular cells for ADH)

59
Q

what’s the treatment for hypernatraemia stemming from diabetes insipidus

A
  • Can be very difficult
  • Hydration tends to simply cause polyuria
  • Synthetic ADH (DDAVP) exists
    o Works in central/ cranial DI
    o Supranormal doses might work in nephrogenic DI
  • NSAIDs might help
60
Q

what’s a hydronephrotic kidney

A
  • Renal pelvis is larger darker area because it’s fluid filled
  • Pressure builds up = dilated pelvis
  • As back pressure builds up over time there’s dilatation of ureter and renal pelvis over time
  • The longer it persists the worse the damage to the kidney
  • If reversed early no long-term consequences
  • But if persists = renal damage and CKD

YEAR 2 SEMESTER 2 (14 decks)

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