Renal Medicine Flashcards

Question

Symptoms of hypernatraemia

Answer 1

thirst, apathy, irritability, weakness, confusion, reduced consciousness, seizures, hyperreflexia, spasticity & coma.

Answer 2

Hypovolaemic High Na  Renal free water losses (Osmotic diuresis [NG feed etc], loop diuretics, intrinsic renal disease)  Non-Renal free water losses (Excess sweating, Burns, Diarrhoea, Fistulas) Euvolaemic High Na  Renal Losses (Diabetes Insipidus, Hypodipsia)  Extra-Renal Losses (Insensible, Respiratory losses) Hypervolaemic High Na (Sodium Gains)  Primary hyperaldosteronism, Cushing’s Syndrome, Hypertonic dialysis, Hypertonic Sodium Bicarbonate, Sodium Chloride tablets

Answer 3

(differential = psychogenic polydipsia) – dilute urine (Urine osmolality <300) Can be Cranial or Nephrogenic POLYDIPSIA AND POLYURIA

Answer 4

Causes - Trauma/post-op, tumours, cerebral sarcoid/TB, infection (meningitis/encephalitis), cerebral vasculitis (SLE/Wegener’s)

Answer 5

Causes - Congenital, Drugs (lithium, amphoterecin, demeclocycline), hypokalaemia, hypercalcaemia, tubulointerstitial disease

Answer 6

Cranial = Impaired release of ADH. Nephrogenic = Resistance to ADH

Answer 7

Free Water

Answer 8

Low Na causes decreased perception and gait disturbance, yawning, nausea, reversible ataxia, headache, apathy, confusion, seizures, coma.

Answer 9

Pseudohyponatraemia – occurs with high lipids, myeloma, hyperglycaemia, uraemia etc.

Answer 10

– plasma osmolality (if normal or raised then pseudohyponatraemia), hypokalaemia/hypomagnesaemia potentiates ADH release, Urine sodium (if <20 then non-renal salt losses, if >40 then SIADH) (diuretics may confound), TSH and 9am cortisol, Calcium, albumin, glucose, LFT, CT head or chest if suspect SIADH.

Answer 11

Hypovolaemic Hyponatraemia Renal loss [Urine Na+ >20mmol/L]  Diuretics (thiazides), Osmotic diuresis (glucose, urea in recovering ATN), Addison’s disease (mineralocorticoid deficiency) Non-renal loss [Urine Na+ <20mmol/L]  Diarrhoea, Vomiting, Sweating, Third space losses (burns, bowel obstruction, pancreatitis) Treatment – give IV fluids (0.9% NaCl at 1-3ml/kg/hour) Give K if necessary Euvolaemic Hyponatraemia  Hypothyroidism, Primary polydipsia – (if urine osmolality <100), Glucocorticoid deficiency – adrenal insufficiency, SIADH Hypervolaemia Hyponatraemia  CCF, Nephrotic syndrome, Liver cirrhosis Treatment – fluid restrict and consider furosemide Risk of correcting hyponatraemia quickly Too rapid correction of chronic hyponatraemia leads to central pontine/osmotic myelinosis. Aim to correct <12 mmol/L/day

Answer 12

Low serum osmolality Inappropriately concentrated urine – Urine osmolality >100 Urine Na >20 Clinical euvolaemia Not on diuretics Diagnosis of elimination – normal renal, thyroid, adrenal function

Answer 13

Management of SIADH – Fluid restrict <800ml/day. PO sodium chloride, may give furosemide, Demeclocycline induces diabetes insipidus (reversing ADH effect), alternatively Tolvaptan

Answer 14

Acute (tends to be iatrogenic, polydipsia, colonoscopy prep, ecstasy) If acute hyponatraemia (within 48 hours) and symptomatic – Give 3% hypertonic saline IV boluses +/- Furosemide

Answer 15

Chronic If chronic (>48 hours) and symptomatic – hypertonic saline boluses if having seizures. Otherwise isotonic saline and furosemide – aim to correct 8mmol/L in 24 hours If chronic and asymptomatic – water restriction, stop offending drug, if dehydrated – restore volume, if overloaded – Na and water restriction and diuretics

Answer 16

CKD, K rich diet with CKD (dried fruit, potatoes, oranges, tomatoes, avocados, nuts)  Drugs (ACEi/ARBs/Spironolactone/Amiloride/NSAIDs/ Heparin/ LMWH/Cyclosporin or calcineurin inhibitors/High dose Trimethoprim/ Digoxin toxicity/Bblockers)  Hypoaldosteronism (T4RTA), Addison’s disease, Acidosis, DKA (insulin deficiency), Rhabdomyolysis, tumour lysis, Massive haemolysis, Succinylcholine use  Rarer – Hyperkalaemic periodic paralysis, Gordon’s syndrome  Artifact Hyperkalaemia – haemolysis, leucocytosis, thrombocytosis

Answer 17

Pseudohypokalaemia – acute leukaemia  Extra-renal losses - Inadequate PO intake, Gut losses (vomiting, NG losses, secretory Diarrhoea, laxatives, VIPoma, Zollinger-Ellison, Ileostomy, enteric fistula)  Redistribution – Delirium tremens, beta agonists, insulin, caffeine, theophylline, alpha-blockers (Doxazosin), hypokalaemic periodic paralysis (inherited or acquired from thyrotoxicosis – Asian males)  Refeeding syndrome, alkalosis, vigorous exercise, glue-sniffing (Toluene can cause Fanconi/RTA II with renal potassium wasting)  Primary hyperaldosteronism (conn’s syndrome) Cushing’s syndrome, Secondary hyperaldosteronism (liver failure, heart failure, nephritic syndrome),  Renal losses (diuretics, RTA, Tubulopathies - Bartters/Liddles/Gittelmans), liquorice, glucocorticoids, hypomagnesaemia.

Answer 18

Often hypertensive with increased extra-cellular fluid volume (renin often down-regulated by fluid overload)

Answer 19

Treatment of hyperkalaemia involves: 1. Stabilizing the myocardium to prevent arrhythmias  10mls of 10% Calcium Gluconate over 5-10 minutes 2. Shifting potassium back into the intracellular space IV fast acting insulin (actrapid)  10 units and IV glucose/dextrose 50% 50mls Sodium Bicarbonate  500mls of 1.4% Sodium Bicarbonate  Only effective at driving Potassium intracellullarly if the patient is acidotic Salbutamol  5-10mg via nebulizer 3. Eliminating Potassium From the Body: Calcium Resonium  15-45g orally or rectally, mixed with sorbitol or lactulose Frusemide  20-80mg depending on hydration status Dialysis  If resistant to medical treatment Hypo: Replace magnesium  Oral K replacement  IV K replacement (Usually in 0.9% NaCl - avoid in dextrose as induces further hypokalaemia)

Answer 20

Hyper:  Tented T waves  Prolonged QRS  Slurring of ST segment  Loss of P waves  Asystole Hypo: Small T waves  U wave (after T)  Increased PR interval

Answer 21

Diabetes  CKD  IHD/CCF/CVD  Any major medical co-morbidity  Elderly >75  Sepsis  Medications – ACEi, ARBs, NSAIDs, Antibiotics

Answer 22

gations in AKI - URINE DIPSTICK is vital (look for abnormal protein and blood) - Daily FBC, U&Es, LFTs, Bone profile, CRP – incl. serum bicarbonate (CK if rhabdomyolysis suspected) - Urine PCR, Urine MC+S, USS KUB (to rule out obstruction) - If blood and protein on urine dipstick – perform c-ANCA (PR3) + p-ANCA (MPO) too look for vasculitis, anti-GBM, ANA, C3, C4 to look for lupus nephritis, serum immunoglobulins and electrophoresis to look for myeloma - If suspected post-streptococcal GN – do Anti-Streptolysin O Titres - In case of associated thrombocytopenia consider HUS/TTP/Disseminated Intravascular Coagulopathy, request haemolysis screen - blood film, LDH, bilirubin, reticulocytes, haptoglobin, and call Renal SpR urgently. - Check cryoglobulins if unexplained rash, peripheral neuropathy, hypocomplementaemia, known hepatitis C, history of lymphoproliferative disorder, or +ve RhF.

Answer 23

Discontinue nephrotoxic agents if possible  Ensure volume status and perfusion pressure – If dehydrated give IV fluids, If overloaded give diuretics, aim for euvolaemia  Be aware of third space losses (patient may look overloaded but JVP & BP may be low indicating intravascular depletion)  Consider function haemodynamic monitoring with Central Venous Pressure (CVP) line/Arterial line  Monitor urine output and daily bloods (catheterise if necessary)  Avoid hyperglycaemia  Check for changes in drug dosing (antibiotic doses etc adjusted to renal function)  Treat underlying cause  Refer to specialist for consideration of renal replacement therapy  Consider ICU admission

Answer 24

Hyperkalaemia refractory to medical therapy  Metabolic acidosis refractory to medical therapy  Fluid overload refractory to diuretics (anuric)  Uraemic pericarditis  Uraemic encephalopathy – vomiting, confusion, drowsiness, reduced consciousness  Intoxications – ethylene glycol, methanol, salicylates, lithium

Answer 25

Oedema  Albumin <30  Urine PCR >350 (more than 3.5 grams of protein in 24 hours) o Hypercholesteraemia

Answer 26

Higher risk of Infection  Venous thromboembolism  Progression of CKD  Hypertension  Hyperlipidaemia

Answer 27

Minimal Change Disease – most common form of GN in children  Focal Segmental Glomerulosclerosis – Idiopathic or secondary to infection, malignancy, drugs etc.  Membranous Nephropathy – Idiopathic or secondary to infection, malignancy, drugs etc.  Membranoproliferative Glomerulonephritis (more commonly presents as nephritic syndrome)  Amyloidosis/Myeloma/Diabetes may have nephrotic range proteinuria but not necessarily other nephrotic features

Answer 28

Presentation can vary in a combination of some or many of the following:  AKI (sometimes GFR can drop drastically)  On urine dipstick: blood +/- and/or protein+/- Mild to moderate oedema  Proteinura <3.5g/24 hours  Hypertension  Sometimes visible haematuria

Answer 29

Supportive therapy  If suspect GN – discuss with Renal team  MDT approach depending on underlying diagnosis  ACEi/ARB for proteinuria  Control BP  Salt and water restriction if volume overloaded  Diuretics for fluid overload  If hypoalbuminaemic <20g/dl then higher risk for VTE – consider therapeutic LMWH  Statins for hypercholesterolaemia Immunosuppressive therapy:  Specific to cause of GN – decided by Renal team (+/- Respiratory / Rheumatology teams if lung or systemic involvement )  Oral Corticosteroids, IV pulsed methylprednisolone, Cyclophosphamide, Tacrolimus, Ciclosporin, Rituximab, MMF, Azathioprine Invasive therapy  Renal replacement therapy/haemodialysis for those in severe AKI or ESRF  Plasma exchange for AAV (with lung involvement), anti-GBM

Answer 30

CKD is defined as the presence of kidney damage, manifested by abnormal albumin excretion or decreased kidney function, quantified by measured or estimated GFR that persists for more than three months.

Answer 31

Diabetes * Hypertension * Glomerulonephritis * Renovascular Disease * Polycystic Kidney disease * Obstructive nephropathy – urological problems * Chronic/recurrent Pyelonephritis * Others

Answer 32

Anaemia of Chronic Kidney Disease * Chronic Kidney Disease – Mineral & Bone Disease * Secondary & Tertiary Hyperparathyroidism * Hypertension * Cardiovascular Disease – No 1 cause of Mortality * Malnutrition/sarcopenia * Dyslipidaemia * As CKD progresses * Electrolyte disturbances * Fluid overload * Metabolic acidosis * Uraemic pericarditis * Uraemic encephalopathy

Answer 33

Treat underlying disease  Treat and monitor diabetic control  Treat hypertension  Treat infections promptly  Tolvaptan if meets criteria for ADPKD

Answer 34

Start on statin  Control BP  Improve control of diabetes  Advise weight loss  Advise exercise  STOP SMOKING

Answer 35

Reduce progression of CKD  Reduce proteinuria – ACEi/ARB  Monitor blood tests  Control BP

Answer 36

Prevent or treat complications of CKD  Dietary advice regarding low phosphate/low potassium diet  Phosphate binders  IV Iron/Folate/Vit B12 replacement  EPO (Erythropoesis stimulating agent)  Replace Vitamin D deficiency  Consider Calcimimetics for tertiary hyperparathyroidism  Dietician input

Answer 37

Plan for the future  Start discussions of what options they have if they reach ESRF  Home care team input  Discuss disadvantages & advantages of types of RRT o Home therapies – APD, CAPD, Home HD o Unit-based therapies – Nocturnal HD, conventional HD o Active conservative management o Transplant  Refer for fistula o Venous mapping  Refer for PD tube insertion  Work-up for transplant o Further tests o Refer to Transplant work-up clinic

Answer 38

Diagnosis – most diabetic patients will undergo screening for diabetic nephropathy Raised Urine Albumin: Creatinine Ratio/PCR Evidence of long-standing/poorly controlled DM Evidence of other microvascular disease

Answer 39

Treatment  ACEi/ARB to reduce proteinuria  Anti-hypertensives for BP control  Cardiovascular risk modification  Continue other screens for microvascular complications – eye checks and foot checks

Answer 40

Chronic raised BP causing nephrosclerosis. Often difficult to tell if advanced renal disease at presentation whether HTN caused the renal impairment or renal impairment caused secondary HTN Investigations to identify if primary or secondary HTN (based on clinical findings and index of suspicion):  24 hour Urinary metanephrines (Phaeochromocytoma)  Aldosterone: Renin ratio (Primary aldosteronism)  Cortisol & Dexamethasone suppression test (Cushing’s syndrome)  TSH (hyperthyroidism)  MRA (Renal artery stenosis) Treated with Hypertensives

Answer 41

2 Types (both are autosomal dominant)  Type 1 (85%; PKD1 mutation on Chromosome 16)  Type 2 (15%; PKD2 mutation on Chromosome 4) Symptoms can be related to the size of the kidney, infection of the cysts (flank pain, haematuria, and fever) or can be asymptomatic Diagnosis Family history is KEY USS Treatment  Control BP  As per CKD management  Tolvaptan (Vasopression receptor-2 antagonist) is available for some patients to slow progression of CKD.  Genetic counselling and testing

Answer 42

Many factors contribute to Anaemia in CKD  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

Answer 43

Management of Anaemia of CKD * Measure haematinics – Vitamin B12, Folate, Ferritin, Iron, Transferrin Saturation, CHr * If deficient in any of above – replace this first * IV Iron may be better tolerated than PO * Discuss with renal team regarding starting ESA * Aim for Hb 100-120

Answer 44

CKD- MBD can be diagnosed if a patient with CKD has evidence of one or more of: * 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 o Low turnover states  Adynamic bone disease  Osteomalacia o High turnover states  Osteitis Fibrosa

Answer 45

CKD leads to  Increased Fibroblast Growth Factor-23  Increased Alkaline Phosphatase and PTH  Increase Phosphate  Decreased Serum Calcium  Decreased 1,25 – Vitamin D As CKD develops, disturbances in the homeostatic pathways lead to hypocalcaemia, hyperphosphataemia and Vitamin D deficiency and the development of secondary hyperparathyroidism

Answer 46

Advantages * Quality of life * It is often an excellent first choice for patients starting dialysis, particularly when they still have some residual native renal function * PD regimes are designed on a much more individualised basis than patients on HD. Disadvantages * Patients need to be able to manage technical aspects of dialysis * Unsuitable in patients with stoma/previous surgery * Risk of infection (PD peritonitis) * Complications – drainage problems, malposition, leaks, herniae, hydrothorax, long term use associated with encapsulating peritoneal sclerosis

Answer 47

Automated PD * Carried out with an automated cycler machine performed at night. * 10-12L usually exchanged, over 8-10 hours. * Lifestyle advantages – Leaves the daytime free. Continuous Ambulatory PD * Usually consisting of 4-5 dialysis exchanges per day (usually 2 litres each) * Exchanges are performed at regular intervals throughout the day, with a long overnight dwell. Assisted Automated PD Trained healthcare assistants visit the patient’s home to help with setting up APD

Answer 48

The dialysis machine pumps blood from the patient, through disposable tubing, through a dialyser, or artificial kidney, and back into the patient. Waste solute, salt and excess fluid is removed from the blood as it passes through the dialyser. Advantages * Efficient form of dialysis * Unit-based – plenty of support from staff Disadvantages/Complications * Dialysis access needs to be secured * Infection/Bacteraemia * Haemodynamic instability * Reactions to dialysers * Haematomas/risk of bleeding * Muscle cramps * Anaemia due to clotted lines/Haemolysis * AVF steal syndrome * SVCO from central lines

Answer 49

Home HD – offer training at home for more frequent HD Nocturnal HD – Overnight slow, long HD CRRT – continuous renal replacement therapy mainly used in acute setting (ITU/HDU)

Answer 50

Advantages * Near normal lifestyle * Better mortality/morbidity Disadvantages * Criteria to meet suitability to safely undergo operation * Compliance with medication lifelong * Risk of rejection * Risk of malignancies over time * Risk of infection (on immunosuppression) * Long waiting times for cadaveric organ

Answer 51

Decision made after discussion with patient and family members – often after multiple clinic visits and after patient is fully informed of risks & benefits of each mode of therapy Evidence suggests that if * Age >80 OR * WHO performance score of 3 or more …then RRT offers no survival benefit Often these patients may be unsuitable for or choose to not have invasive therapy such as PD/HD/Transplantation Active Conservative Management of ESRF * Symptom control to enhance quality of life * Respect patients preferred place of care * Advanced care plan * MDT approach * Support system for patient and family

Answer 52

Contraindications for kidney transplantation * 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

Answer 53

Living Related Donor Transplantation * This is the best possible transplant as patients have an elective procedure with a selected donor, that might have a good compatibility * Time to transplantation can happen in months Living Unrelated Donor Transplantation * 4 forms: a)live-donor paired exchange, b) livedonor/deceased-donor exchange, c)live-donor chain, d)altruistic donation * Usually have comparable outcomes to live-related donors * Time to transplantation can happen in months

Answer 54

Deceased Donor Transplantation * Approximately 60% of the transplants in the UK fall into this category * Patients receive a kidney (or two from the same donor) with little time for preparation, so transplant protocols are important to keep updated regularly * Time to transplantation happen in years * Survival of kidney allograft and patients are significantly low compared to live donor transplantation.

Answer 55

Induction treatment * At the moment of transplantation potent immunosuppressive drugs are used to create tolerance of the graft * With these therapies, hyperacute rejection is now rarely seen * These include methylprednisolone in combination with any of the following: basiliximab and thymoglobulin; less commonly used are alentuzumab and rituximab.

Answer 56

Maintenance treatment * Treatment that will be used immediately after transplantation and for long term to prevent acute or chronic rejection * Drugs commonly used are grouped as: * Steroids: prednisolone (or prednisone) Calcineurin inhibitors (CNI): tacrolimus, cyclosporine, voclosporin * Antimetabolite medications: mycophenolate, azathioprine * Rapamycin inhibitors: sirolimus and everolimus * T-cell regulation: Belatacept and belimumab

Answer 57

Long term care of the transplant patient * For the firsts months, follow up happens several times a month, after 6 months it happens less often * Monitor GFR, CNI levels, proteinuria, Ca, phosphate and PTH, lipids and glucose * Screen for infections (common and opportunistic) * Vaccination (except live or live attenuated viral vaccines) * Monitor and control cardiovascular disease, bone and mineral metabolism disease * Screen for malignancies as patients are three times more likely to have any cancer * Annual skin checks for skin cancers * Contraception is obligatory in the first year, counsel about pregnancy one year after * Mortality is related to: cardiovascular disease, infections and malignancies

Answer 58

Acute complications, within the first month are usually related to surgery or infections * When considering infections, the timeframe is important * <4 weeks: nosocomial infections or related to donor * 1 to 12 months: activation of latent infections, relapsed, residual or opportunistic infections, community * >12 months: community acquired * Important germs to consider: CMV, hepatitis B, Herpes simplex virus, Varicella zoster, EBV, BK; Aspergilllus, Pneumocystis jirovecii, Listeria, Mycobacterium tuberculosis, Toxoplasma gondii * Within the first year, some patients can develop new-onset diabetes after transplant (NODAT); important to remember personal risk factors and new factors, such as medications and a new gluconeogenic kidney. * Because of the increased risk of malignancies among transplant patients, it’s important to screen for them, such as: skin, cervix, breast, prostate, renal and urothelial, liver, colorectal, and lymphoproliferative disease. This last one in particular is common in patients with EBV.

Answer 59

Simultaneous kidney transplantation * Liver-kidney: patients with liver failure or cirrhosis and ESRF can be candidates for simultaneous transplant * Pancreas-kidney: selected patients with Type 1 diabetes mellitus. Can be done simultaneous or sequential * Patients with kidney transplant who progress into ESRF can be re-transp

Renal Medicine Flashcards

(85 cards)