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y3 medicine > Renal > Flashcards

Renal Flashcards

1
Q

which blood tests are important to carry out when testing renal function?

A

FBC - anaemia, infection, allergic reactions
Haematinics - iron/folate/B12 deficiency
U&Es - potassium, urea, creatinine, bicarb
bone profile - calcium, phosphate, PTH, alkaline phosphatase
CRP - infection/inflammation
HbA1c - diabetic control

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2
Q

what imaging is important for looking at the kidneys?

A

US KUB - look for perinephric collection, size of kidneys, corticomedullary differentiation, hyponephrosis

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3
Q

what are the causes of metabolic alkalosis?

A
  • GI losses: D&V
  • renal losses: primary hyperaldosteronism, tubular transporter defects, duiretics
  • intracellular shifts: hypokalaemia
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4
Q

what can cause metabolic acidosis with a high anion gap? ( increased acids)

A
  1. lactic acidosis: anaerobic exercise, sepsis, organ ischaemia
  2. ketoacidosis: diabetic, alcohol abuse, starvation
  3. toxins: ethylene glycol, methanol, isoniazid, aspirin, salicylate
  4. renal failure
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5
Q

what can cause metabolic acidosis with normal anion gap? ( reduced alkali)

A
  1. GI losses of HCO3: D&V
  2. renal losses of HCO3: renal tubular acidosis, mineralocorticoid deficiency
  3. toxins: ammonium chloride, acetazolamide
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6
Q

what are the risk factors for AKI?

A
  • diabetes
  • CKD
  • IHD/CCF/CVD
  • any major medical comorbidity
  • elderly >75
  • sepsis
  • medications - ACEi, ARBs, NSAIDs, ABX
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7
Q

what are the serum creatinine levels for stage 1,2 and 3 of AKI?

A

stage 1: 1.5-1.9x baseline
stage 2: 2-2.9x baseline
stage 3: 3x baseline

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8
Q

name the pre renal causes fro AKI?

A
  • hypovolaemia: shock, dehydration
  • decreased cardiac output
  • decreased effective cirulating volume: CHF, Liver failure
  • impaired renal autoregulation: NSAIDs, ACEi/ARB, cyclosporine
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9
Q

name the renal intrinsic causes for AKI.

A
  • acute glomerulonephritis
  • ischaemia
  • sepsis/infection
  • vasculitis
  • malignant HTN
  • nephrotoxins: contrast, cisplatin, rhabdomyolysis, myeloma, aminoglycosides (gentamycin, vancomycin)
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10
Q

what are teh post renal cuases of an AKI?

A
  • bladder outlet obstruction

- bladder pelvoureteral obstruction

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11
Q

what investigations are done when diagnosing an AKI?

A
  • URINE DIPSTICK (to look for abnormal protein and blood)
  • daily FBC, U&Es, LFTs, Bone profile, CRP, CK is rhabdomyolysis
  • Urine PCR, Urine MC+S, USS KUB
  • test for vasculitis: p-ANCA and c-ANCA
  • test for lupus: ANA
  • test for myeloma: serum immunoglobulins and electrophoresis
  • test for post strep GN: anti-streptolysin O titres
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12
Q

what is the managment of AKI?

A
  • appropriate investigations
  • discontinue nephrotoxic drugs
  • if dehyrated: fluids, if overloaded: duiretics
  • monitor urine output and bloods
  • avoid hyperglycaemia
  • treat underlying cause
  • refer to specialist (+ possibly ICU) and consider renal replacemnt therapy
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13
Q

what are the indications for renal replacment therapy in AKI?

A
  • hyperkalaemia resistant to medical therapy
  • metabolic acidosis resistant to medical therapy
  • fluid overload resistant to duiretics
  • uraemic pericarditis
  • uraemic encephalopathy: vomiting, confusion , drowsiness, reduced consciousness
  • intoxications: ethylene glycol, methanol, lithium, salicyclates
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14
Q

what are the causes of hyperkalaemia?

A
  • CKD (+ rich K+ diet)
  • DRUGS (ACEi, ARBs, spironolactone, amiloride, NSAIDs, heparin, LMWH, cyclosporin, calcineurin inhibitors, high dose trimethoprim, b blockers)
  • HYPOALDOSTERONISM, ADDISONS, ACIDOSIS, DKA, RHABDOMYALYSIS, tumour lysis, massive heamolysis
  • hyperkalaemic paralysis
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15
Q

what ECG changes are shown with a patient with hyperkalaemia?

A
  • tall tented T waves
  • porlonged QRS
  • slurring of ST segment
  • loss of P waves
  • asystole
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16
Q

what is teh treatment for hyperkalaemia?

A
  • stabilising myocardium to prevent arrythmias (CALCIUM GLUCONATE)
  • shifting potassium back into intracellular space (IV FAST ACTING INSULIN, sodium bicarb, salbutamol)
  • eliminating potassium from body (FUROSEMIDE, CALCIUM RESONIUM, DIALYSIS)
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17
Q

what are the symptoms of hypokalaemia?

A

fatigue, constipation , proximal muscle weakness, paralysis, cardiac arrythmias, worsened glucose control in diabetics, HTN

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18
Q

what are the cuases of hypokalaemia?

A
  • pseudohypokalaemia
  • extra renal losses - GI losses
  • redistribution - caffeine, insulin, beta agonists
  • refeedign syndrome, alkalosis, vigorous exercise
  • primary and secondary hyperaldosteronism, cushings syndrome
  • renal losses, ( diuretics), glucocorticoids
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19
Q

what ECG chnages are seen in hypokalaemia?

A
  • smalll T waves
  • U waves ( after T)
  • increased `PR interval
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20
Q

what is the treatment for hypokalaemia?

A

replace magnesium
oral K replacment
IV k replacment (usually in 0.9% NaCl)

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21
Q

what are the symptoms of hypernatremia?

A
  • thirst
  • apathy
  • irritibility
  • weakness
  • confusion
  • reduced consiousness
  • seizures
  • hyperreflexia
  • spasticity and coma
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22
Q

what are the causes of hypernatremia?

A

hypovolemic: renal free water loss, XS sweating, burns, diarrhoea, fistulas
euvolemic: renal losses (diabetes inspidus), resp losses
hypervolemic: cushings, primary hyperaldosteronism, hypertonic dialysis

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23
Q

what is the treatment fro hypernatremia?

A

generally - free water

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24
Q

what are the symptoms

A
  • decreased perception
  • gait distuurbance
  • yawning
  • nausea
  • reversible ataxia
  • headach e
  • apathy
  • confusion
  • seizures
  • coma
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25
Q

what are the causes of hyponatremia?

A

hypovolemic hyponatremia: renal loss (diuretics, addisons) D+V, sweating, burns, bowel obstruction, pancreatitis

euvolemic hyponatremia: hypothyroidism, primary polydipsia adrenal insufficiency, SIADH

hypervolemic hyponatremia: CCF, nephrotic syndrome, liver cirrhosis

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26
Q

what is the treatment for hyponatremia?

A

acute: 3% hypertonic saline IV boludses +/- furosemide
chronic: isotonic saline and furosemide

if fluid overloaded fluid restrict and consider furosemide

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27
Q

what is teh risk of corrected hyponatremia too quickly?

A

central pontine/osmotic myelinosis

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28
Q

what are the three characteristics of nephrotic syndroee?

A
  • hypoalbuminaemia (<30)
  • oedema
  • Urine PCR >300
    (+ - hypercholesterolaemia)
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29
Q

what are the complications fo nephrotic syndrome?

A
  • higher risk of infection (excrete antibodies and immunoglobulins in urine)
  • venous thromoboembolism (excreted clotting factors in urine)
  • progression of CKD
  • HTN
  • hyperlipidaemia (liver compensates for decreased oncotic pressure and released lipids into blood)
  • risk of CVD event
  • hypocalceamia (calcium bounded to albumin is excreted)
30
Q

what are teh cuases of nephrotic syndrome?

A
  1. minimal change disease - COMMON in CHILDREN
  2. focal segmental glomerulosclerosis
  3. membranous nephropathy
  4. amyloidosis/myeloma/diabetes
31
Q

what is the gold standard of diagnosing the cause of a nephritic/nephrotic syndrome?

A

renal biopsy !!

32
Q

what are the characteristics of nephritic syndrome?

A
  • AKI
  • urine dipstick : blood +++, protein +
  • mild to moderate oedema
  • proteinuria <300mg
  • hypertension
  • sometimes visible heamaturia
33
Q

name some differentials for heamaturia that need to be excluded?

A
  • UTI
  • Malignancy
  • renal stones
34
Q

what are the cuases of nephritic syndrome?

A
  • IgA nephropathy
  • Lupus
  • mesangial proliferative glomerulonephritis
  • vasculitis (only ACUTE causes of glomerulonephritis)
35
Q

what are the TWO MAIN cuases of glomerulonephritis?

A

DIABETES AND HYPERTENSION

36
Q

what specific tests are important in diagnosing vasculitis?

A

c-ANCA and p-ANCA

37
Q

what is the treatment for vasculitis?

A

immunosupression - cyclosporin, azathioprine

or plasma exchange to get rid of antibodies

38
Q

what are the differntials for a patient with oedema?

A
  • liver failure
  • heart failure
  • renal fialure
  • clots/DVT
  • low albumin state
  • hypothryoidism
  • nephrotic syndrome
39
Q

what is teh nephrotic range for urine PCR?

A

> 300mg

40
Q

what is the treatment for glomerulonephritis?

A
  • ACEi/ARB for proteinuria
  • COntrol BP
  • salt and water restriction is overloaded
  • duiretics for fluid overload
  • statins for hyperlipidaemia
  • if hypoalbumaenia then consider thrombroprophylaxis - LWMH
  • immunosupression: steroids, ciclosporin, mycophenolate, rituximab, cyclophosphamide
  • renal repalcment therapy: HD, PD, transplant
41
Q

what is the main risk of a renal biospy?

A

BLEEDING !

42
Q

what is heamodialysis?

A

heamodialysis is a type of renal replacement therapy that removes XS fludi, salt and wastes from the blood
it involved the movement of solutes and water across a semi permeable membrane (requires going into hopsital x3 a week for 4 hrs)
fistula is made in the arm between vein and artery (alloweing vein to arterialise) and dialysis pumps blood from the patient through disposable tubing, through dialyser or artificial kidney and back into patient.
OR inserted via a PermCath into the SVC

43
Q

what are teh complications of heamodialysis?

A
  • infection/bacteraemia
  • steal syndrome
  • bleeding from fistula
  • muscle cramps
  • SVCO from central lines
  • anaemia due to clotted lines
  • fistulas need to be made and take 6 weeks to mature
  • thrombosis - at point of narrows vein (scarring due to increased venepunctures) - thrill vanishes
  • endocarditis with PermCath
44
Q

what is steal syndrome?

A

when increased blood from travles through the fistula and back up the arm instead of supplying the hand = ischaemic hand = 6P’s

45
Q

what is peritoneal dialysis?

A

home based therapy
glucose water is pumped into the peritoneum and solutes mvoe from patients blood across peritoneal mebrane into the dialysate fluid and then it is drained
can be automated (at night) OR ambulatory (multiple times a day)

46
Q

what are teh complications of peritoneal dialysis?

A
  • infections - PERITONITIS ! pain and liquid in bag is cloudy (Staph epidermis, staph aureus, pseudomonas) ABX administered via bag into peritoneum
  • leaking
  • drainage problems
  • herniae
  • dialysis failure
  • encapsulating sclerosing peritonitis
47
Q

what is importance of renal replacment therapy?

A
  • clear metabolic toxins
  • normalise serum electrolytes
  • correct volume deficit
  • prevent CKD worsening
48
Q

what si the definition of CKD?

A

presence of kidney damage manifested by abnormal albumin excretion or decreased kidney function, quantifies by measured or estimated GFR that persists for more than three months

49
Q

what are the cuases fo CKD

A
  • HTN
  • diabetes
  • glomerulonephritis
  • renovascular disease
  • polycystic kidney disease
  • obstructive nephropathy (urological problems)
  • chronic/recurrent pyelonephritis
50
Q

what are the main complications of CKD?

A
  • aneamia of chronic disease
  • mineral and bone disease (CKD-MBD)
  • secondary and tertiary hyperparathyroidism
  • hypertension
  • CVD - MAIN CAUSE OF DEATH
    -malnurtition/sarcopenia
  • dyslipidaemia
    as CKD progresses: electrolytes disturbances, fluid overload, metabolic acidosis, uraemic pericarditis, uraemic encephalopathy
51
Q

what are the stages of CKD?

A

stage 1 >90 GFR - mild kidney disease w normal GFR
stage 2 60-89 GFR - mild damage with lower GFR
stage 3 30-59 GFR - moderately damaged
stage 4 15-29 GFR - severe kidney disease
stage 5 > 15 GFR - failed/closed to failed kidneys

52
Q

management of CKD?

A
  1. treat underlying diseases: diabetes, HTN, infections, ADPKD = tolvaptan, GN = immunosupression
  2. reduce CVD risk: statins, control BP, control diabetes, weight loss, exericise, stop smoking !!!
  3. reduce progression: reduced proteinuria = ACEi/ARB, monitor blood tests, control BP
  4. prevent/treat complications: low phosphate/K+ diet, phosphate binders, IV iron/folate/B12 replacement, EPO, vit D, calicmimetics, dietician input
  5. plan for future: discuss RRT, refer for fistula/PD tube insertion, transplant list
53
Q

what is diabetic nephropathy? how is it screened for? what is the treatment?

A
  • diabetic nephropathy is decline is kidney function due to T1DM or T2DM (associated with retinopathy and peirpheral neuropathy)

undergo screening for:

  • raised ACR/PCR
  • evidence of long standing/poorly controlled DM
  • evidence of other microvascualr disease

treatment:
- ACEi/ARB to reduce proteinuria
- anti-hypertensives
- CVD risk modification
- continue screens for microvascular complications

54
Q

what is hypertensive nephropathy? what investigations need to take palce to diagnose it? how is it treated?

A

chronic raised BP causing nephrosclerosis

investigations:
- 24 hr urinary metanephrines (phaeochromocytoma)
- aldosterone:renin ratio (primary aldosteronism)
- cortisol and dexamethasone supression test (cushings)
- TSH (hyperparathyroidism)
- MRA (renal artery stenosis)

treatment: antihypertensives

55
Q

what is adult polycystic kidney disease?

A

APCKD is a autosomal dominant disease - there are two different types
characterised by multiple cysts bilateralyl in both kidneys

56
Q

what are teh symptoms of APCKD?

A

related to the size of the kidney, infection of the cysts (flank pain, haematuria, fever) or can be asymptomatic

57
Q

how is APCKD diagnosed/

A
  • family history !!

- USS KUB

58
Q

what is the treatment of APCKD?

A
  • control BP
  • as per CKD managment
  • tolvaptan (vasopressin receptor-2 antagonist)
  • genetic counselling and testing
59
Q

what are the complications of APCKD?

A
  • infection
  • bleeding
  • renal failure
  • pain
  • hypertension
    (extra renal involvment - cerebral aneurysms)
60
Q

what factors contribute to aneamia in chronic kidney disease?

A
  • decreased EPO production in kidneys
  • absolute iron deficiency (poor absoprtion and malnutrition)
  • functional iron deficiency ( inflammation, infection)
  • blood loss
  • shortened RBC survival
  • bone marrow suppression from uraemia
  • medication induced
  • Vit b12/folate deficiency
61
Q

what is the manangement of anaemia of CKD?

A
  • meausre heamatinics - vit B12, folate, ferritin, iron, transferrin saturation, CHd AND REPLACE any deficits
  • IV iron over PO
  • aim for Hb 100-120
62
Q

how does CKD-MBD occur?

A
  1. decreased phosphate excretion due to kidney failure
  2. increased calcium excretion as bound to albumin
  3. decreased calcitriol produced by kidney = hypocalcaemia

therefore PTH levels increased to increase serum calcium = increased bone resorption and osteopenia

= hypocalcaemia, hyperphosphataemia, vit D deficiency and secondary hyperparathyroidism

63
Q

what is the treatment for CKD-MBD?

A
  1. phosphate binders
  2. vit D
  3. calcimimetics
  4. parathyroidectomy
64
Q

hwo can CKD-MBD be diagnosed?

A
  • abnormalities of calcium, phosphate, alkaline phosphatase, PTD or vit D metabolism
  • vascular and/or soft tissue calcification
  • abnormalities in bone turnover, metabolism, volume, lineal growth and strenght
65
Q

what is tertiary hyperparathyroidism?

A

occurs when PTH release continues despite raised serum calcium levels (independently)

  • as a result of parathyroid gland nodular hyperplasia
  • consequence of advanced CKD
66
Q

what are some indications and contraindications for kidney transplant?

A

indications:

  • to be fit enough
  • need advanced CKD or ESRD
  • malignancy

contraindications:
- acitve 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 adherance
- short life expectancy

67
Q

what are the different type of donor tranplants and which are the best?

A
  1. living related donor - best
  2. living unrelated donor - usually comparable outcomes to live-related donors
  3. deceased donor - 60% of donors, survival of kidney allograft significantly lower
68
Q

what treatment is given prior to transplant surgery to prevent hyperacute rejection?

A

methylprednisolone in combo with any of: basiliximab, thymoglobulin

69
Q

what treatment is given to transplant patients post surgery?

A

prevent aucte/chronic rejection:

steroids: prednisolone
calcineurin inhibitors: tacrolimus, cyclosporine, voclosporin
antimetabolite meds: mycophenolate, azathioprine
rapamycin inhibitors: sirolimus and everolimus
T cell regulation: belatacept and belimumab

70
Q

what long term care is given to a transplant patients (not including medications)

A
  • monitor GFR, CNI levels, proteinuria, Ca, phosphate and PTH, lipids and glucose
  • screen for infections
  • vaccination
  • monitor and control CVD, bone and mineral metabolism disease
  • screen for malignancies as immunosuppressed
  • contraception in first yr

HIGHEST MORTALITY related to: CVD death, infection and malignancies

71
Q

what are the main complications of a kidney transplant?

A
  • rejection
  • infection (if <4 weeks post surgery then related to donor)
  • drug toxicity
  • cancer
  • diabetes (new onset diabetes after transplant (NODAT))
  • CVS disease
72
Q

name some of the common atypical infections that cna be acquired post transplant?

A
  • CMV 1-6 months , marrow supression, ocular, GI, liver, lung => decreased immunosupression +/- antivirals
  • EBV - related to PTLD => antivirals
  • BK nephropathy - diagnosed on biopsy - haematuria and rising Cr => decreased immunosupression +/- antivirals
  • pneumocystic - very bad yeast like fungus = SOB and desaturation on walking => Co-trimoxazole given

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