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Yr3 - General Medicine > Renal > Flashcards

Renal Flashcards

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1
Q

AAV

A

ANCA Associated Vasculitis

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2
Q

ACR

A

Albumin:Creatinine Ratio

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3
Q

ADPKD

A

Autosomal Dominant Polycystic Kidney Injury

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4
Q

APD

A

Automated Peritoneal Dialysis

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5
Q

ANA

A

Anti-Nucleic Antibody

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6
Q

ANCA

A

Anti-Neutrophilic Cytoplasm Antibody

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7
Q

ATN

A

Acute Tubular Necrosis

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8
Q

AVF

A

AterioVenous Fistula

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9
Q

CAPD

A

Continuous Ambulatory Peritoneal Dialysis

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10
Q

CKD

A

Chronic Kidney Disease

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11
Q

CMV

A

Cytomegalovirus

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12
Q

CNI

A

Calcineurin Inhibitors

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13
Q

CHr

A

Hypochormnic Red Cells

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14
Q

eGFR

A

Estimated Globerular Filtration Rate

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15
Q

ESA

A

Erythropoeitin Stimulating Agent

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16
Q

ESRF

A

End Stage Renal Failure

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17
Q

GN

A

GlomeruloNephritis

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18
Q

GPA

A

Glomerulomatous PolyAngitis

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19
Q

HUS

A

Haemolytic Uraemic Syndrome

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20
Q

MMF

A

Mycophenolate Mofetil

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21
Q

MPA

A

Microscopic PolyAngitis

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22
Q

NODAT

A

New-Onset Diabetes After Transplantation

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23
Q

PCR

A

Protein: Creatinine Ratio

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24
Q

PD

A

Peritoneal Dialysis

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25
PND
Paroxysmal Nocturnal Dyspnoea
26
RRT
Renal Replacement Therapy
27
RPGN
Rapidly Progressive GlomeruloNephritis
28
RTA
Renal Tubular Acidosis
29
SIADH
Syndrome of Inappropriate Anti-Diuretic Hormone
30
SLE
Systemic Lupus Erythematosus
31
SVCO
Superior Vena Cava Obstruction
32
TIN
TubuloInterstital Nephritis
33
TTP
Thrombotic Thrombocytopenic Purpura
34
Features to ask out dyspnoea
``` Exercise tolerance Triggers Relieving factors Diurnal variation Orthopnoea PND Associated symptoms ```
35
Features to ask about leg swelling
Site Severity Time of onset Amount of fluid intake
36
Features to ask about N+V
``` Triggers Relieving factors Able to keep down food Frequency Associated symptoms Bowel frequency ```
37
Features to ask about ENT symptoms
``` Nasal secretions Sinusitis Epistaxis Haemoptysis Sore throat Visual disturbances Hearing loss ```
38
Features to ask about constitutional symptoms
``` Fever Joint pains Muscle aches Weight changes Lethargy Night sweats Pruritus ```
39
Features to ask about lower urinary tract symptoms
``` Dysuria Frequency Quantity of urine Colour of urine Frothiness Haematuria ```
40
Features to ask about flank pain
``` Duration Radiation Associated symptoms Intensity Aggravating/relieving factors ```
41
Presenting complaints of renal history
``` Dyspnoea Leg swelling N+V Upper airway symptoms Constitutional symptoms Lower urinary tract symptoms Flank pain ```
42
Features of PMH of renal histroy
``` Previous AKI - hospitalisation, requiring dialysis CKD stage Cause of CKD/ESRD CVS risk factors - DM, HTN, Hypercholesterolaemia Recurrent UTIs Childhood infections Surgery Cancer ```
43
Types of haemodialysis lines
``` Perm-cath - tunelled under skin - long term Vas-cath - non-tunelled - short term ```
44
Signs of advanced renal disease
Brown nails Discolouration of skin from uraemia Under-nutrition leading to muscle wasting Uraemic frost - urea from sweat crystallises on the skin Hyper-reflexia, pericardial rub, GI ulceration and bleedin
45
How to calculate anion gap
[Na+] - ([Cl-] + [HCO3])
46
Normal anion gap
8-12
47
What does high anion gap mean
Acidosis caused by increased acid
48
Causes of high anion gap
``` Lactic acidosis - anaerobic exercise - sepsis - organ ischaemia Ketoacidosis - diabetic - alcohol abuse - starvation Toxins - ethylene glycol - methanol - isoniazid - aspirin - salicylate Renal failure ```
49
What causes a normal anion gap in acidosis
Reduced alkali
50
Causes of normal anion gap in acidosis
``` GI losses of HCO3 - vomiting - diarrhoea Renal losses of HCO3 - renal tubular acidosis - mineralocorticoid deficiency (Addison's) Toxins - ammonium chloride - acetazolamide ```
51
Causes of hypernatraemia
Usually water deficit - cellular dehydration - osmotic drag - vascular shear stress - bleeding and thrombosis
52
Symptoms of hypernatraemia
``` Thirst Apathy Irritability Weakness Confusion Reduced consciousness Seizures Hyperfreflexia Spasticity Coma ```
53
Causes of hypovolaemic high Na+
``` Renal free water losses - osmotic diuresis (NG feed) - loop diuretics - intrinsic renal disease Non-renal free water losses - excess sweating - burns - diarrhoea - fistulas ```
54
Causes of euvolaemic high Na+
``` Renal losses - diabetes insipidus - hypodipsia Extra-renal losses - insensible - respiratory losses ```
55
Causes of hypervolaemic high Na+
``` Primary hyperaldosteronism Cushing's syndrome Hypertonic dialysis Hypertonic sodium bicarbonate Sodium chloride tablets ```
56
Features of diabetes insipidus
Dilute urine - urine osmolatlity < 300 Polydipsia Polyuria - not always hypernatraemic
57
Causes of cranial DI
Impaired release of ADH - trauma/post op - tumours - cerebral sacroid/TB - infections - meningitis/encephalitis - cerebral vasculitis - SLE/Wegener's
58
Causes of nephrogenic DI
Resistance to ADH - congenital - drugs - lithium, amphoterecin, demeclocycline - hypokalaemia - hypercalcaemia - tubulointestinal disease
59
Treatment of hypernatraemia
Free water
60
Symptoms of hyponatraemia
``` Decreased perception and gait disturbance Yawning Nausea Reversible ataxia Headache Apathy Confusion Seizures Coma ```
61
Features of pseudohyponatraemia
Low plasma sodium (<135 mmol/L) due to increased plasma lipid and/or plasma protein concentration
62
Causes of hypovolaemic hyponatraemia
Renal loss - [Urine Na+ > 20 mmol/L] - diuretics - thiazides - osmotic diuresis - gluocse, urea in recovering ATN - Addison's disease - mineralocorticoid deficiency Non-renal loss - [Urine Na+ < 20 mmol/L] - diarrhoea - vomiting - sweating - third space losses - burns, bowel obstruction, pancreatitis
63
Treatment of hypovolaemic hyponatraemia
IV fluids - 0.9% NaCl at 1-3 nl/kg/hour | Give K+ if necessary
64
Causes of euvolaemic hyponatraemia
Hypothyroidism Primary polydipsia - urine osmolality < 100 Glucocorticoid deficiency - adrenal insufficiency, SIADH
65
Features of SIADH
Low serum osmolality Inappropriately concentrated urine - urine osmolality > 100 Urine Na+ > 20 Clinical euvolaemia Not on diuretics Diagnosis of elimination - normal renal, thyroid and adrenal function
66
Management of SIADH
Fluid restrict < 800 ml/day PO sodium chloride May give furosemide Demeclocycline induces DI - reversing ADH effect
67
Causes of hypervolaemic hyponatraemia
CCF Nephrotic syndrome Liver cirrhosis
68
Treatment of hypervolaemic hyponatraemia
Fluid restrict | Consider furosemide
69
Rate of correcting hyponatraemia
<12 mmol/L/day | - too rapid correction leads to central pontine/osmotic myelinosis
70
Treatment of hyponatraemia
Acute - 3% hypertonic salive IV bolus +/- furosemide Chronic - hypertonic saline bolus if having seizures - isotonic saline and furosemide Asymptomatic - water restriction - stop offending drug - restore volume if dehydrated - Na+, water restriction and diuretics if overloaded
71
Causes of hyperkalaemia
``` CKD - rich diet with CKD - dried fruit, potatoes, oranges, tomatoes, avocados, nuts Drugs - ACEi - ARBs - Spironolactone - Amiloride - NSAIDs - Heparin - B-blockers Hypoaldosteronism Addison's disease Acidosis DKA Massive haemolysis Rhabdomyolysis ```
72
Features of hyporeninaemic hypoaldosteronism
Decreased angiotensin 2 production as well as intra-adrenal dysfunction Hypertensive with increased extra-cellular fluid volume - renin down-regulated by fluid overload
73
Causes of hyporeninaemic hypoaldosteronism
``` Diabetic nephropathy NSAIDs Ciclosporin Sickle cell Lupus nephritis ```
74
Treatment of hyporeninaemic hypoaldosteronism
Low K+ diet | Loop diuretic if overloaded
75
ECG changes of hyperkalaemia
``` Tented T waves Prolonged QRS Slurring of ST segment Loss of P waves Asystole ```
76
Treatment of hyperkalaemia
Stabilising myocardium - prevent arrhythmias - 10mls of 10% calcium gluconate over 5-10 mins Shifting K+ back to intracellular space - 10 units fast acting insulin IV (actrapid) and IV glucose/dextrose 50% 50mls - 500mls 1.4% sodium bicarbonate - if acidotic - 5-10mg salbutamol via nebuliser Eliminating K+ from body - 15-45g oral or rectal Calcium Resonium - mixed with sorbitol or laculose - 20-80mg Furosemide - depending on hydration status - dialysis if resistant to medical treatment
77
Symptoms of hypokalaemia
``` Fatigue Constipation Proximal muscle weakness Paralysis Cardiac arrhythmias Worsened glucose control in diabetics Hypertension ```
78
Causes of hypokalaemia
``` Pseudohyokalaemia - acute leukaemia Extra-renal losses - inadequate PO intake - gut losses Redistribution - delirium tremens - beta agonists - insulin - caffeine - doxazosin Refeeding syndrome Primary hyperaldosteronism Cushing's syndrome Renal losses - diuretics - RTA - glucocorticoids - hypomagnesaemia ```
79
ECG changes in hypokalaemia
Small T waves U wave Increased PR interval
80
Treatment of hypokalaemia
Replace magnesium Oral K replacement IV K replacement - 0.9% NaCl
81
Risk factors for AKI
``` Diabetes CKD IHD / CCF Elderly > 75 Sepsis Medications - ACEi - ARBs - NSAIDs - Antibiotics ```
82
Stages of AKI
``` Stage 1 - 1.5-1.9 x baseline serum creatinine - or 26.5 μmol/L increase - urine output < 0.5ml/kg/hr for 6-12 hours Stage 2 - 2.0-2.9 x baseline serum creatinine - urine output < 0.5ml/kg/hr 12 hours Stage 3 - 3 x baseline serum creatinine - or 353.6 μmol/L increase - or initiation of renal replacement therapy - urine output < 0.3ml/kg/hr for > 24 hours - or anuria for > 12 hours ```
83
Prerenal causes of AKI
``` Hypovolaemia Decreased CO Decreased effective circulating volume - CCF - liver failure Impaired renal autoregulation - NSAIDs - ACEi/ARBs - Cycloporine ```
84
Postrenal causes of AKI
Bladder outlet obstruction | Bilateral pelvoureteral obstruction - unilateral obstruction of solitary functioning kidney
85
Intrinsic causes of AKI
``` Glomerular - acute glomerulonephritis Tubules and interstitium - ischaemia - sepsis - nephrotoxins Vascular - vasculitis - malignant hypertension - TTP-HUS ```
86
Nephrotoxins that can cause AKI
``` Exogenous - iodinated contrast - aminoglycosides - cisplatin - amphotericin B Endogenous - haemolysis - rhabdomyolysis - myeloma - intratubular crystals ```
87
Investigations in AKI
Urine dip - abnormal protein and blood Daily bloods - FBC, U&Es, LFTs, bone profile, CRP Urine - PCR, MC+S, USS KUB
88
Management of AKI
Discontinue nephrotoxic agents if possible Ensure volume status and perfusion pressure - if dehydrated give IV fluids - if overloaded give diuretics Be aware of 3rd space losses - patient may look overloaded but JVP and BP low Monitor urine output Avoid hyperglycaemia Treat underlying cause
89
Indications for renal replacement therapy in AKI
``` Resitant to medical therapy - hyperkalaemia - metabolic acidosis - fluid overload Uraemic pericarditis Uraemic encephalopahty Intoxications ```
90
Symptoms of uraemic encephalopathy
Vomiting Confusion Drowsiness Reduced consciousness
91
Features of nephrotic syndrome
Oedema Albumin < 30 Urine PCR > 350 Hypercholesteraemia
92
Complications of nephrotic syndrome
``` Higher risk of infection Venous thromboembolism Progression of CKD Hypertension Hyperlipidaemia ```
93
Causes of nephrotic syndrome
Minimal change disease - commonest form in children Focal segmental glomerulosclerosis Membranous nephropathy Membranoproliferative glomerulonephritis - commonly presents as nephritic syndrome Lupus nephritis
94
Presentation of nephritic syndrome
``` AKI Mild to moderate oedema Proteinuria < 3.5g/24hrs Hypertension Sometimes visible haematuria ```
95
Causes of nephritic syndrome
``` Post-infectious GN IgA nephropathy Small vessel vasculitis Anti-GBM disease Thin basement membrane disease Alport syndrome Lupus nephritis Membranoproliferative glomerulonephritis ```
96
Associations of post-infectious GN
``` Weeks after group A, B-haemolytic streptococci infections - 1-2 weeks post tonillitis/pharyngitis - 3-4 weeks post impetigo/cellulits Usually children 3-12 yrs Can lead to PRGN in some cases ```
97
Investigation findings of post-infectious GN
Postive anti-streptococcal antibodies Low serum C3 Biopsy - immune complex deposition - IgG, IgA, C3
98
Treatment for post-infectious GN
Usually self limiting Supportive therapy - ACEi/ARB for proteinuria and hypertension - low sodium diet
99
Associations for IgA nephropathy
Episodic gross haematuria during or directly after URT and GI infections or strenuous exercise Male > Female 2nd-3rd decade of life
100
Investigation findings for IgA nephropathy
Asymptomatic michrochaematuria with intermittent visible haematuria Increase serum IgA Normal C3 and C4 Biopsy - mesangial immune complex depositis in glomeruli
101
Treatment for IgA nephropathy
Supportive therapy | - ACEi/ARB for proteinuria and hypertension
102
Types of small vessel vasculitis (ANCA associated)
Granulomatosis with polyangitis (GPA) Microscopic polyangitis (MPA) Eosinophilic granulmatosis with polyangitis (Churg-Stauss syndrome)
103
Associations with GPA
Pulmonary and nasopharyngeal involvement - haemoptysis - nasal ulcers / polyps
104
Investigation findings for GPA
c-ANCA (PR3) Biopsy - segmental necrotising GN
105
Associations for MPA
Usually only mild respiratory symptoms
106
Investigation findings for MPA
p-ANCA (MPO) Biopsy - segmental necrotising GN
107
Associations for eosinophilic granulomatosis with polyangitis
Patients have - asthma - allergic rhinitis - purpura - peripheral neuropathy
108
Investigation findings for eosinophilic granulomatosis with polyangitis
``` p-ANCA Bloods - eosinophilia Biopsy - segmental necrotising GN ```
109
Treatment for ANCA associated vasculitis
Immunosuppression
110
Associations for anti-GBM disease (Goodpasture syndrome)
Two peaks - 3rd and 7th decade Antibodies against type IV collagen - react with pulmonary basement membrane causing pulmonay haemorrhage Can lead to PRGN
111
Investigation findings for anti-GBM disease
Anti-GBM antibodies Pulmonary infiltrates on CXR Biopsy - linear deposition of IgG along basement membrane
112
Treatment for anti-GBM disease
Plasma exchange | Immunosuppression
113
Associations for thin basement membrane disease
Heriditary Abnormalities of type IV collagen Good prognosis
114
Investigations for thin basement membrane disease
Persistent microscopic haematuria - possible intermittent visible haematuria Biopsy - diffuse thining of GBM
115
Treatment for thin basement membrane disease
Monitor renal function | Supportive treatment
116
Associations for Alport syndrome
X-linked - usually affects males Mutation in gene coding for type V collagen Associated with hearing loss and abnormalities of the eyes Often leads to ESRF
117
Investigation findings for alport syndrome
Persistent microscopic haematuria with intermittent visible haematuria Sensorineural hearing loss Biospy - splitting of GBM - alternating thickening and thinning of GBM Genetic studies - family history
118
Treatment for alport syndrome
Supportive treatment Renal replacement therapy Renal transplant - can lead to development of anti-GBM sdisease
119
Associations for lupus nephritis
Complication of SLE | Can be nephrotic or nephritic
120
Investigation findings for lupus nephritis
ANA and anti-dsDNA postitive Biopsy - 6 different classes have different presentation
121
Treatment for lupus nephritis
Supportive therapy | Immunosuppressive therapy based on classification/presentation
122
Management of glomerulonephritis
``` Supportive - ACEi/ARB for proteinuria - control BP - salt and water restriction if fluid overloaded - diuretics for fluid overload - statins for hypercholesterolaemia Immunosuppressive - specific to cause - oral corticosteriods, IV pulsed methylprednisolone, tacrolimus, ciclosporin, reiuximab, MMF, azathioprine Invasive - RRT / haemodialysis - severe AKI or ESRF - plasma exchange for AAV and anti-GBM ```
123
Definition of CKD
Presence of kidney damage - manifested by abnormal albumin excretion or decreased kidney function - quantified by eGFR - persists for more than 3 months
124
CKD classification
``` ACR categories - A1 = < 3 - A2 = 3-30 - A3 = > 30 GFR categories G1 = > 90 G2 = 60-89 G3a = 45-59 G3b = 30-44 G4 = 15-29 G5 = < 15 (kidney failure) ```
125
Causes of CKD
``` Diabetes Hypertension Glomerulonephritis Renovascular disease Polycystic kidney disease Obstructive nephropathy - urological problems Chronic/recurrent pyelonephritis ```
126
Complications of CKD
Anaemia of chronic kidney disease Chronic kidney disease - mineral and bone disease Secondary and tertiary hyperparathyroidism Hypertension CVS disease Malnutrition/sarcopenia Dyslipidaemia
127
Complications of advanced CKD
``` Electrolyte disturbances Fluid overload Metabolic acidosis Uraemic pericarditis Uraemic encephalopathy ```
128
Management of CKD
``` Treat underlying disease Reduced CVS risk - statin, control BP and diabetes, weight loss and exercise, stop smoking Reduce progression of CKD - reduce proteinuria - ACEi/ARB - monitor blood and BP Prevent complications - low phosphate/potassium diet - phosphate binders - IV iron/folate/vit B12 - EPO ```
129
Features of diabetic nephropathy
Type 1 or long duration type 2 Associated with other diabetic microvascular complications - retinopathy - peripheral neuropathy
130
Diagnosis of diabetic nephropathy
Most diabetic patients will undergo screening for diabetic nephropathy - raised urine albumin:creatinine ratio - evidence of long standing/poorly controlled DM - evidence of other microvascular disease
131
Treatment of diabetic nephropathy
ACEi/ARB - reduce proteinuria Anti-hypertensives - BP control CVS risk modification Screen for other microvascular complications
132
Features of hypertensive nephropathy
Chronic raised BP causing nephrosclerosis | - hard to tell if HTN caused renal impairment or renal impairment caused HTN
133
Investigations for hypertensive nephroapthy
24 hour urinary metanephrines - phaeochromocytoma Aldosterone:renin ratio - primary aldosteronism Cortisol and dexamethasone suppression test - Cushing's syndrome TSH - hyperthyroidism MRA - renal artery stenosis
134
Features of polycystic kidney disease
2 types - autosomal dominant - type 1 - PKD1 mutation on chromosone 16 - type 2 - PKD2 mutation on chromosone 4 Symptoms related to - size of kidney - infection of cysts - flank pain, haematuria, fever - asymptomatic
135
Diagnosis of polycystic kidney disease
Family history | USS
136
Treatment of polycystic kidney disease
Control BP Tolvaptan - vasopression recptor-2 antagonist Genetic counselling and testing
137
Features contributing to anaemia of chronic kidney disease
Decreased production of erythropoietin from the kidney Absolute iron deficiency - poor absorption and malnutrition Functional iron deficiency - inflammation, infection Blood loss Shortened red blood cell survival Bone marrow suppression from uraemia Medication induced Deficiency of vit B12 and folate
138
Management of anaemia of CKD
Measure haematinics - vitamin B12, folate, ferritin, iron, transferrin saturation, CHr Replacement of any deficiencies Aim for Hb 100-120
139
Diagnosis of CKD mineral bone disease
Abnormalities of calcium, phosphate, alkaline phosphatase, PTH or vitamin D metabolism Vascular and/or soft tissue calcification Abnormalities in bone turnover, metabolism, volume, linear growth or strength - low turnover states - adynamic bone disease - osteomalacia - high turnover states - osteitis fibrosa
140
Featues of CKD MBD
``` Increased fibroblast growth factor 23 Increased alkaline phosphatase and PTH Increased phosphate Decreased serum calcium Decreased 1,25-vitamin D ```
141
Causes of tertiary hyperparathyriodism
PTH release continues despite raised serum calcium levels - parathyroid gland nodular hyperplasia - advanced CKD
142
Management of CKD MBD
Reduce occurrence/severity of renal bone disease | CVS morbidity and mortality caused by elevated serum levels of PTH and high phosphate levels and calcium overload
143
Features of peritoneal dialysis
Reliant on patients own peritoneal membrane Solutes move from patients blood across peritoneal membrane, down concentration gradient Osmotic gradient created by high concentration of glucose in dialysate fluid - removes water from patient
144
Advantages of peritoneal dialysis
Quality of life Good when patients have some residual native renal function Regimes designed on a more individual basis
145
Disadvantages of peritoneal dialysis
Patients need to be able to manage technical aspects of dialysis Unsuitable in patients with stoma/previous surgery Risk of infection
146
Complications of peritoneal dialysis
``` Drianage problems Malposition Leaks Herniae Hydrothorax Long term use -> encapsulating peritoneal sclerosis ```
147
Features of automated PD
Automated cycler machine performed at night | - 10-12L exchanged over 8-10 hours
148
Features of continuous ambulatory PD
4-5 dialysis exchanges per day - 2L each | Regular intervals throughout day with long overnight dwell
149
Advantages of haemodialysis
Efficient | Unit-based - plenty of support from staff
150
Disadvantages of haemodialysis
Less freedom - fixed days at haemodialysis unit Food and fluid restrictions Use of needles
151
Complications of haemodialysis
``` Infection/bacteraemia Haemodynamic instability Reaction to dialysers Haematomas Risk of bleeding Muscle cramps Anaemia - clotted lines AVF steal syndrome SCVO - central lines ```
152
Advantages of renal transplantation
Near normal lifestyle | Better mortality/morbidity
153
Disadvantages of renal transplantation
``` Criteria to meet suitability to safely undergo operatio Compliance with lifelong medication Risk of rejection Risk of malignancies over time Risk of infection - immunosuppression Long waiting times for cadaveric organ ```
154
Active conservative management
When RRT offers no survival benefit | - insuitable for or choose not to have invasive therapy
155
Considerations for active conservative management
Age > 08 | WHO performance score of 3 or more
156
Features of active conservative management
``` Symptom control to enhance quality of life Respect patients preferred place of care Advanced care plan MDT approach Support for patient and family ```
157
Contraindications for kidney transplanation
Active infection or malignancy Severe heart disease - not suitable for correction Severe lung disease Reversible renal disease Uncontrolled substance abuse, psychiatric illness On-going treatment non-adherence Short life expectancy
158
Types of kidney transplant
Living related donor Living unrelated donor Cadaveric donor
159
Features of living related donor transplant
Best possible option - elective procedure - may have good compatibility Time to transplantation - months
160
Features of living unrelated donor transplant
Comparable outcomes to live-related donors | Time to transplantation - months
161
Types of living unrelated donor transplant
Live-donor paired exchange Live-donor/deceased-donor exchange Live-donor change Altruistic donation
162
Features of deceased donor transplant
60% Little time for preparation Time to transplantation - years Survival of kidney allograft and patients are significantly low compared to live donor transplantation
163
Induction treatment for renal transplant
At the moment of transplantation - potent immunosuppression to create tolerance of the graft - methylprenisolone - basiliximab - thymoglobulin - alentuzumab - rituximab
164
Maintenance treatment for renal transplant
``` Steroids - prednisolone Calcineurin inhibitors - tacrolimus - cyclosporine - voclosporin Antimetabolite medications - mycophenolate - azathioprine Rapamycin inhibitors - sirolimus - everolimus T-cell regulation - belatacept - belimumab ```
165
Long term care for renal transplant patient
Monitor GFR, CNI levels, proteinuria, Ca, phosphate, PTH, lipids and glucose Screen for infections Vaccination - except live or live attenuated viral vaccines Monitor CVS disease, bone and mineral metabolism disease Screen for malignancies - 3x more likley to have cancer - anunual skin checks Contraception obligatory in 1st year - counsel about pregnancy after
166
Causes of mortality for transplant patient
CVS disease Infections Malignancy
167
Acute complications of transplant
Surgical complications Infection - < 4 weeks - nosocomial infections or related to donor - 1-12 months - activation of latent infections, relapsed, residual or opportunistic infections - > 12 months - community aquired
168
Common pathogens in post transplant infection
``` CMV Hepatitis B HSV Varicella zoster EBV BK Aspergillus Listeria TB ```
169
Chronic complications post renal transplantation
New-Onset Diabetes After Transplant (NODAT) | Malignancy
170
Simultaneous kidney transplantation options
``` Liver-kidney - liver failure or cirrhosis and ESFR Pancreas-kidney - selected patients with type 1 DM - simultaneous or sequential Re-transplant - transplant patients who progress into ESRF ```
171
Examples of loop diuretics
Furosemide Bumetanide Torsemide
172
Main indications of loop diuretics
Fluid overload
173
Action of loop diuretics
Inhibits Na+K+Cl- transporter in Loop of Henle
174
Pharmacokinetics of loop diuretics
Metabolised - kidney and liver | Excreted - urine
175
Common side effects of loop diuretics
``` Hyponatraemia Hypokalaemia Diuresis Dehydration Alkalosis ```
176
Features of loop diuretics
Furosemide 40mg = Bumetanide 1mg IV better absorbed if gut oedema present Protein-bound = low volume of distribution
177
Examples of thiazide and thiazide-like diuretics
Bendroflumethiazide | Indapamide
178
Main indications of thiazide and thiazide-like diuretics
Hypertension | Fluid overload
179
Method of action of thiazide and thiazide-like diuretics
Inhibits NaCl channel in distal convoluted tubule
180
Pharmacokinetics of thiazide and thiazide-like diuretics
Metabolised - kidney | Excreted - urine
181
Common side effects of thiazide and thiazide-like diuretics
``` Hyponatraemia Hypokalaemia Dehydration Hypercalcaemia Hyperuricaemia Hypomagnesaemia Alkalosis ```
182
Examples of K-sparing diuretics
Aldosterone antagnosists - spironolactone Epithelial Na channel blockers - amiloride
183
Main indications of K-sparing diuretics
K-losing tubulopathies Hypertension Heart failure
184
Method of action of K-sparing diuretics
Block epithelial Na channel | Antagonises the action of aldosterone at mineralocorticoid recptors
185
Common side effects of K-sparing diuretics
Hyperkalaemia - caution when combined with ACEi/ARBs Gynaecomastia
186
Examples of carbonic anhydrase inhibitors
Acetazolamide | Brinzolamide
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Main indications of carbonic anhydrase inhibitors
Glaucoma | Benign intracranial hypertension
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Method of action of carbonic anhydrase inhibitors
Inhibits carbonic anhydrase - causes increased renal excretion of Na, K, HCO3 and H2O Decreases production of aqueous humour
189
Common side effects of carbonic anhydrase inhibitors
Flushing Metabolic acidosis Agranulocytosis Liver failure
190
Examples of corticosteriods
Prednisolone - PO Hydrocortisone - IV, IM Dexamethasone - PO, IV Triamcinolone - IM
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Main indications of corticosteriods
Supress inflammation, allergy and immune responses
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Method of action of corticosteriods
Alters gene transcription - anti-inflammatory - immunosuppressive - increased gluconeogenesis - decreased glucose utilisation - increased liver protein catabolism
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Pharmacokinetics of corticosteriods
Metabolised - liver | Excreted - urine
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Common side effects of corticosteriods
``` Adrenal suppression - courses > 3 weeks Hyperglycaemia Psychosis Insomnia Indigestion Mood swings ```
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Long term side effects of corticosteriods
``` Diabetes Cataracts Glaucoma Peptic ulceration Susceptibility to infections Osteoporosis Muscle wasting Skin thinning Cushingoid appearance ```
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Cautions of long term corticosteriods
Long-term course should not be withdrawn abruptly Additional medication - PPI - GORD - Bisphosphonates - bone protection

Yr3 - General Medicine (9 decks)

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