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Metabolic > Kidney > Flashcards

Kidney Flashcards

1
Q

What drugs are safe in AKI

A 
Paracetamol
Warfarin
Statins
Aspirin 
Clopidogrel
BB
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2
Q

What drugs to stop in AKI

A 
NSAIDs
ACEi/ARBs
Metformin
Diuretics
Gentamicin
Amphotericin
Lithium
Digoxin
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3
Q

What is focal segmental glomerulosclerosis

A

Affects part (segmental) or some (focal) glomeruli of nephron. Foot processes of podocytes damaged, proteinuria. Proteins, lipids trapped, build up in glomeruli, hyalinosis, scar tissue > glomerulosclerosis.

Mesangial matrix expansion + capil loop collapse.

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4
Q

What is membranoproliferative/mesangio capillary GN

A

Inflam of GBM, mesangium, ↓kidney function.

IC mediated: circulating IC deposit in kidney, activate complement. Hep C, SLE, monoclonal gammopathies.

Complement mediated: less common, persistent activation of alternative complement pathway eg C3 nephritic factor.

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5
Q

What is membranous GN?

A

Inflam of GBM, subendothelium IC deposits (between podocytes + GBM), ↑permeability,
Autoantibodies target M type phospholipase A2 receptor + neural endopeptidase on GBM
Complement activated, damage to podocytes mesangial cells work to remove debris.

Light microscopy: diffuse thickening of GBM
Electron microscopy: spike + dome, GBM matrix on top of subendothelial deposits, podocyte effacement

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6
Q

Minimal change disease

A

Most common nephrotic synd in kids

Podocyte effacement > lose barrier function > albumin permeates, bigger proteins can’t get through (selective)

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7
Q

Summary of amyloidosis

A

Abnormal amyloid fibrils build up + damage tissues. AL (light chain) eg myeloma, huge no of light chain produced some misfolded + deposit in tissue. AA (serum amyloid A) normal protein that is acute phase reaction, in inflam conditions eg RA, IBD, lot of SAA in blood, accumulate in tissues.

Hepatosplenomeg
JVP distension 
Large tongue
Periorbital purpura 
Unexplained WL, N/C/D
Abdo cramps 
Fatigue 
Dyspnoea OE
Claudication 
Submandibular gland enlargement 
Light headed/ orthostatic hypotension 
Shoulder pad sign: periarticular infiltration with amyloid, pseudohypertrophy, enlarged musculature of shoulder/ hip girdles 
Diffuse muscular weakness 
Proteinuria

Tinel’s/Phalen’s sign
Serum/urine immunofixation: pos, presence of monoclonal protein
Immunoglobulin free light chain assay: abnormal kappa to lambda ratio.
Bone marrow biopsy: clonal plasma cells
Biopsy: Congo red stain, deposits pink, green birefringement under polarised light.
LM: eosinophilic deposits in mesangium, cap loops, arteriolar walls.
Serum amyloid P scintigraphy: uptake at sites of amyloid deposition
↑ALP if hepatic amyloid
↓albumin

Eprodisate: inhibits deposits in tissues
Myeloablative chemo
Dexamethasone

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8
Q

Post strep GN

A

Wks after group A β haemolytic strep
T3 hypersensitivity, IC deposition.

Rapidly progressive GN
Renal failure

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9
Q

Good pasture syndrome

A

Ant-GBM antibody disease, damage BM in lungs, kidneys

ANCA pos

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10
Q

IgA nephropathy

A

Berger’s disease.
Abnormal post translational mod of IgA, IgG binds to IgA IC deposited in mesangium. T3 hypersensitivity, alternative complement activated, cytokines released, macrophages migrate to kidney, glomerular injury, RBC leak into urine.

1-2 days after URTI

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11
Q

Rapidly progressive GN

A

Inflam of kidney’s glomeruli, crescent shaped prolif of cells in Bowman’s capsule
Crescent aggregate of macrophages + epithelial cells in Bowman’s space.

Anti GBM:Goodpasture
IC: post-step GN, SLE, IgA neph, Henoch—Schoenlein purpura.
Pauci immune: ANCA, C-ANCA > Wegener’s. PANCA > microscopic polyangiitis, Churg Strauss.

Renal failure within wks/mnths

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12
Q

Alport syndrome

A

Defect in gene coding for T4 collagen > abnormal BM of kidney glomerulus, eye, cochlea

Appear childhood/ adolescence
Renal: progressive renal insuff, HTN, GN. Microscopic/ gross haematuria, proteinuria
Eye: corneal abrasions, lens opacity, ocular pain, myopia, visual disturbance cataracts.
Ear: initial high freq/tone hearing loss, loss of normal speech, bilat
Fatigue/ breathlessness/ periph oedema: renal failure/ anaemia
Learning disability
Growth retardation
Retinitis pigmentosa

ACEi, ARB: prevent progression to kidney failure
Dialysis
Kidney transplant
Replacement of lens in ant lenticonus
Monitor renal disease
Hearing loss may benefit from hearing aids.

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13
Q

Causes of hypernatraemia

A

Extrarenal water loss: skin (sweat), GI (N/V)

Hypothalamic lesion: ↓ADH > dilute water loss as water not reabsorbed. Central DI

Renal water loss: nephrogenic DI

osmotic diuresis e.g. hyperosmolar non-ketotic diabetic coma

excess IV saline

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14
Q

Sx of hypernatraemia

A 
FRIED SALT 
F: fever
R: restless, anxious 
I: ↑fluid retention, HTN
E: oedema 
D: ↓UO, dry mouth 
S: skin flushed 
A: agitated 
L: low grade fever
T: thirst
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15
Q

Tx of hypernatraemia

A

Hypernatraemia should be corrected with great caution. Although brain tissue can lose sodium and potassium rapidly, lowering of other osmolytes (and importantly water) occurs at a slower rate, predisposing to cerebral oedema, resulting in seizures, coma and death

it is generally accepted that a rate of no greater than 0.5 mmol/hour correction is appropriate

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16
Q

Causes of hyponatraemia

A

caused by water excess or sodium depletion

pseudohyponatraemia - hyperlipidaemia (^ in serum volume) or taking blood from drip arm

need urinary sodium and osmolarity levels to make diagnosis

urinary sodium > 20 mmol/l
Sodium depletion, renal loss (patient often hypovolaemic)
diuretics: thiazides, loop diuretics
Addison's disease
diuretic stage of renal failure

Patient often euvolaemic
SIADH (urine osmolality > 500 mmol/kg)
hypothyroidism

urinary sodium <20 mmol/l
Sodium depletion, extra-renal loss
diarrhoea, vomiting, sweating
burns, adenoma of rectum

Water excess (patient often hypervolaemic and oedematous)
secondary hyperaldosteronism: heart failure, liver cirrhosis
nephrotic syndrome
IV dextrose
psychogenic polydipsia

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17
Q

Sx of hyponatraemia

A 
SALT LOSS
S: stupor/coma 
A: anorexia (N/V)
L: lethargy 
T: tendon reflex ↓
L: limp muscles (weak)
O: orthostatic hypotension
S: seizures/ headache
S: stomach cramps
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18
Q

Causes of hyperkalaemia

A 
acute kidney injury
drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin**
metabolic acidosis
Addison's disease
rhabdomyolysis
massive blood transfusion
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19
Q

Sx of hyperkalaemia

A 
M: muscle weakness
U: urine, oliguria, anuria
R: resp distress
D: ↓cardiac contractility
E: ECG changes 
R: reflexes, hyperreflexia, areflex↓K ia (flaccid)

ECG: prolonged PR, tall, peaked (tented T waves with narrow base), short QT, depressed ST, sinuisoidal

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20
Q

Management of hyperkalaemia

A

10mL 10% Ca gluconate: stabilise myocardial cells

Insulin with dextrose + β-2 agonist (salbutamol): ↑K into cells

Kayexalate: bind K, ↓K absorbed from GIT

Loop diuretics, Ca resonium (enemas more effective than oral as K is secreted by rectum), dialysis: ↑K excretion in kidneys.

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21
Q

Sx of hypokalaemia

A 
A SIC WALT 
A = alkalosis 
S = shallow resps 
I = irratibility 
C = confusion + drowsy 
W = weakness + fatigue
A = arrhythmias 
L = lethargy 
T = thready pulse

ECG: flattened/ inverted T waves, U waves, ST depression, prolonged PR, prolonged QT

22
Q

Causes of hypokalaemia

A 
Hypokalaemia with hypertension:
Cushing's syndrome
Conn's syndrome (primary hyperaldosteronism)
Liddle's syndrome
11-beta hydroxylase deficiency*
Hypokalaemia without hypertension:
diuretics
GI loss (e.g. Diarrhoea, vomiting)
renal tubular acidosis (type 1 and 2**)
Bartter's syndrome
Gitelman syndrome
23
Q

Management of hypokalaemia

A

Replenish with K supplementation
If mild oral sando-K, if severe IV K

Mg replacement, ↓K often hard to correct until Mg levels normalised.

If diuretic therapy: K sparing diuretics

24
Q

Causes of hypercalcaemia

A
  1. Primary hyperparathyroidism: commonest cause in non-hospitalised patients
  2. Malignancy: the commonest cause in hospitalised patients. This may be due to number of processes, including;
    PTHrP from the tumour e.g. squamous cell lung cancer
    bone metastases
    myeloma,: due primarily to increased osteoclastic bone resorption caused by local cytokines (e.g. IL-1, tumour necrosis factor) released by the myeloma cells
Other causes include
sarcoidosis*
vitamin D intoxication
acromegaly
thyrotoxicosis
Milk-alkali syndrome
drugs: thiazides, calcium containing antacids
dehydration
Addison's disease
Paget's disease of the bone
25
Q

Management of hypercalcaemia

A

rehydration with normal saline, typically 3-4 litres/day. Following rehydration bisphosphonates may be used. They typically take 2-3 days to work with maximal effect being seen at 7 days

Other options include:
calcitonin - quicker effect than bisphosphonates
steroids in sarcoidosis

26
Q

Sx of hypercalcaemia

A

Pyrexia
HTN

Neurological: blurred vision, slow/absent reflexes, fatigue, anxiety, confusion, hallucinations, stupor
Muscle weakness, weak bones.
Anorexia, V/C, WL

Stones: renal/biliary

Bones: bone pain, cysts + brown tumours

Groans: abdo pain/ nausea

Thrones: polyuria, nocturia

Psychiatric overtones: depression, anxiety, coma, insomnia.

ECG: shortened QT, bradycardia. Osborn wave (pos deflection as junction between QRS + ST segment)

27
Q

Causes of hypocalcaemia

A

Causes

vitamin D deficiency (osteomalacia)
chronic kidney disease
hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
pseudohypoparathyroidism (target cells insensitive to PTH)
rhabdomyolysis (initial stages)
magnesium deficiency (due to end organ PTH resistance)
massive blood transfusion
acute pancreatitis

28
Q

Sx of hypocalcaemia

A

Tetany, muscle twitching, cramps + spasm
Chvostek sign: facial muscles twitch after facial N, lightly tapped 1cm below zygomatic process
Trousseau’s sign: BP cuff occluded brachial A, nerve fire muscle spasm makes wrist + MCP joint flex.
Abdo pain
Perioral tingling/ numbness
Paraesthesia, abnormal sensation on skin eg tingling, numbness
Carpopedal spasm

ECG: prolonged QT, ST, arrhythmias, TdP, AF

29
Q

Tx of hypocalcaemia

A

Calcium gluconate 10mL of 10%

Vit D supplementation

30
Q

Causes of hyper magnesiumaemia

A

Renal failure
XS intake: Mg hydroxide, XS IV (preeclampsia)
Cell breakdown: TLS, rhabdo

31
Q

Causes of hypo magnesiumaemia

A

Loop + thiazide diuretics
↑Ca (Ca + Mg compete for transport in TAL of Henle), ↓K
Nephrotoxic: amphotericin B, cisplatin calcineurin inhib,
Channelopathies
DM: osmotic diuresis, fast flow, not enough time for Mg absorption
Malnutrition, malabsorption (chronic diarrhoea, PPIs)
Hungry bone syndrome: removal of thyroid/ parathyroid, ↑bone formation, osteoblast take Mg from blood.
Alcohol use disorder
Gitleman/ Bartter’s

32
Q

Sx of of hyper magnesiumaemia

A

Nausea
Drowsiness
Tingling sensation in face (facial paraesthesia)
Progressive loss of deep tendon reflexes (earliest sign)
Muscle paralysis
↓BP, pulse

ECG: ↑PR, widened QRS, bradyarrhythmias

33
Q

Tx of hyper magnesiumaemia

A

Ca gluconate. Ca + Mg compete for binding sites.
Furosemide, ↑urinary excretion
Stop source of XS intake
Haemodialysis if severe

34
Q

Sx of hypo magnesiumaemia

A

Ca more easily enters neurons, more excitable, tetany, Trousseau/ Chvostek sign, seizures.
Paraesthesia, ataxia, tetany

ECG: PR/QT prolongation, T wave flattening

35
Q

Tx of hypo magnesiumaemia

A

<0.4: tetany, arrhythmias, seizures: IV Mg.

>0.4: oral Mg salts. Diarrhoea can occur with oral Mg salts.

36
Q

Sx of hyperphosphataemia

A 
Mild: asymptomatic 
Severe: hypocalcaemia 
Tetany 
Chvostek’s/ Trousseau’s 
Tingling around mouth
Seizures
Bone pain 
Binds to Ca + forms bone like crystals under skin, in BV walls, joints, kidneys
37
Q

Causes of hyperphosphataemia

A

↓GFR: AKI/CKD
Hypoparathyroidism: ↑P ↓Ca reabsorption. Thyroid/parathyroid gland removal, radiation Tx, DiGeorge synd.
Pseudohypoparathyroid: kidneys don’t respond to PTH due to genetic defect in receptor.
Vit D: intoxication
↑intake: phosphate based laxative
TLS, rhabdo, crush injury, massive haemolysis.
Acidosis: ↓pH in cell, less glycolysis which normally uses lot of P
DKA

38
Q

Tx of hyperphosphataemia

A

Phosphate binders: aluminium salts, Ca carbonate.
Avoid high phosphate foods: meat, dairy, soda
Healthy kidneys: IV saline (forced diuresis), furosemide, overwhelm PCT, unable to reabsorb solutes
LT: dialysis

39
Q

Tx of hypophosphataemia

A

Oral administration: diet alone may suffice

IV for LT

40
Q

Causes of hypophosphataemia

A

1° hyperparathyroidism: phosphate lost in urine, Ca reabsorbed.
Fanconi syndrome: PCT unable to reabsorb
↓dietary P, meds (antacids with al/ca/mg impair absorption)
Alcohol use disorder
Refeeding syndrome
Insulin Tx in DKA
Resp alkalosis: ↑pH stimulates glycolysis
Sepsis

41
Q

Sx of hypophosphataemia

A

Muscle weakness
Resp/cardiac insuff
Altered mental status

42
Q

Management of UTI in pregnancy

A

Symptomatic preg: urine culture, nitrofurantoin (unless near term), 2nd: amox, cefalexin. Trimeth not in 1st trim.

Asymptomatic preg: immediate nitro, amox or cefalexin, 7 day course. Test of cure > urine culture.

43
Q

Management of UTI in men

A

Men: immediate 7 day trimeth or nitro unless prostatitis. Referral to urology not routinely required for men with 1 uncomplicated lower UTI.

44
Q

Management of UTI in paediatrics

A

<3 mnths: referred immediately to paediatrician.

> 3 mnths: 3 day, trimeth. Nitro, bring back if still unwell 24-48hrs

45
Q

Management of pyelonephritis

A

Abx: broad spec cephalopsporin or quinolone for 10-14 days. Cefalexin, co-amox, trimeth, ciprofloxacin, cefuroxime, ceftriaxone.

Chronic: correct obstruction, VUR, nephrectomy, remove damaged kidney

Transplant

Dialysis

46
Q

Cause of acute tubular necrosis

A

Tubular epithelial cell death: most common AKI cause in hospitalised pts

Ischaemic/ nephrotoxic: disruption of basolat surface, dysfunction or detachment from BM, sloughing. Obstruction of tubules, ↑pressue, ↓GFR

RF: CKD, underlying renal disease, DM, hypotension, sepsis, muscle trauma, cardiac arrest, haemolysis, mechanical ventilation.

Ischaemia: most common in prox, thick ascending tubules (most met active), vasoconstriction, ↓GFR, shock, HF, GI fluid loss, renal a stenosis, malig HTN, microangiopathies, HUS, TTP, DIC, surgical procedures esp cardiac, AAA repair, microscopic polyangiitis.

Nephrotoxins: more common PCT, myoglobin haemoglobinuria, uric acid (TLS), myeloma (light chains), aminoglycosides, cisplatin, amphotericin B, NSAIDs, lead, ethylene glycol, radiocontrast agent, organic solvents

BUN:Cr ratio: <15:1, 🡩Cr + urea

Muddy brown granular casts, sloughed off epithelial cells in tubules excreted as mass

47
Q

Tx of acute tubular necrosis

A 
Hydration: 1-2 wks for epithelial cells to regen
Blood transfusion if haem
Identify high risk indivudals 
Allopurinol for TLS 
RRT
48
Q

Prevention of kidney stones

A

Drink plenty
Ca: thiazide diuretics
Oxalate: pyridoxine, cholestyramine
Struvite: treat infection promptly
Urate: allopurinol. Urinary alkalinisation
Cystine: vigorous hydration, urinary alkalinisation, D-penicillamine to chelate cystine.
↓animal protein, low salt diet.

49
Q

Management of kidney stones

A

NSAIDS: IM diclofenac for rapid relief in severe pain

<5mm: manage expectantly most pass within 4 wks

Stones >5mm/pain not resolving: medical expulsion (nifedipine) or α-blockers (tamsulosin) promote expulsion + ↓analgesia requirements.

Magnesium citrate: inhibit crystal growth, aggregation: prevent kidney stones forming

Lithotripsy: CI in pregnancy

Uretoscopy: tube passed through ureter + into renal pelvis, pregnancy, stent left in situ for 4 wks.

Ureteric obstruction with infection: surgical emergency, decompress system, nephrostomy tube placement, ureteric catheters, ureteric stent placement.

Percut nephrolithotomy: gain access to renal collecting system, intra corporeal lithotropsy/ stone fragmentation.

50
Q

Summary of renal tubular acidosis

A

All three types of renal tubular acidosis (RTA) are associated with hyperchloraemic metabolic acidosis (normal anion gap).

Type 1 RTA (distal)
inability to generate acid urine (secrete H+) in distal tubule
causes hypokalaemia
complications include nephrocalcinosis and renal stones
causes include idiopathic, rheumatoid arthritis, SLE, Sjogren’s, amphotericin B toxicity, analgesic nephropathy

Type 2 RTA (proximal)
decreased HCO3- reabsorption in proximal tubule
causes hypokalaemia
complications include osteomalacia
causes include idiopathic, as part of Fanconi syndrome, Wilson’s disease, cystinosis, outdated tetracyclines, carbonic anhydrase inhibitors (acetazolamide, topiramate)

Type 3 RTA (mixed)
extremely rare
caused by carbonic anhydrase II deficiency
results in hypokalaemia

Type 4 RTA (hyperkalaemic)
reduction in aldosterone leads in turn to a reduction in proximal tubular ammonium excretion
causes hyperkalaemia
causes include hypoaldosteronism, diabetes

Metabolic (8 decks)

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