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Internal Medicine > Kidney > Flashcards

Kidney Flashcards

1
Q

Define CKD

A

Severe reduction in nephron mass over time (at least 3 months, other wise AKI) resulting in uraemia

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2
Q

Name 8 causes of CKD

A
  1. Glomerulonephritis
  2. DM (cause glomerulosclerosis over time) !!! (Most common)
  3. Toxic nephropathies:tobacco, traditional medicine alcohol
  4. Polycystic kidney disease
  5. Systemic vascular disease
  6. Hypertensive nephrosclerosis !!!
  7. Autoimmune disorders: SLE, rheum arthritis, HIV
  8. Analgesic nephropathy: NSAIDs

HAT PAD: Hypertensive, autoimmune, toxins, analgesic, poly cystic kidneys, diabetes

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3
Q

Common symptoms CKD (4)

A

Confusion - coma/ death (encephalopathy)
Muscle cramps
Bleeding
Loss appetite, nausea

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4
Q

Skin signs CKD (3)

A

Subcut nodules: Calcium phosphate deposits
Scratch marks (pruritis)
Pallor (anaemia)

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5
Q

Hand signs CKD (3)

A

Leuconychia
Asterixis
Uraemic frost

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6
Q

Heart signs CKD(2)

A
  • Pericarditis due to uraemia
  • Arrhythmia due to hyperk
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7
Q

Vital sign CKD

A

Increased BP

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8
Q

Definition of nephrotic syndrome (4 points)

A
  1. Proteinuria >3,5 g per 24h (other features caused by this )
  2. hypoalbuminaemia <25-30g/L
  3. Edema
  4. Hyperlipidaemia

Other: urine protein:creatinine >0.2g/mmol

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9
Q

Causes of nephrotic syndrome (5)

A

Primary
Glomerulonephritis (minimal change gn in children, membranous gn most common in adults, mesangiocapillary , proliferative) or glomerulosclerosis (focal segmental) = 80 %

Secondary
• drugs: penicillamine, lithium, ampicillin, bisphosphonates, NSAIDs, allergies
• systemic disease!: SLE,DM, amyloidosis
• malignancy
• infections: hepatitis, ie, malaria, HIV

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10
Q

Definition of nephritic syndrome (4)

A

PHAROH

  • Haematuria
  • only mild to moderate Proteinuria <3.5g per 24h
  • Azotemia (increased urea and creatinine)
  • Oliguria
  • red cell casts
  • HT
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11
Q

Name 7 complications of CKD

A

A WET BED

  • acidosis (metabolic): inability kidneys to excrete acid
  • water: pulmonary oedema
  • erythropoiesis: anaemia of chronic disease; bleeding due to uraemic coagulopathy
  • toxins: uraemic encephalopathy
  • bp: cardiovascular disease (due to combination of bp, salt + water over load,accelerated atherosclerosis)
  • electrolytes: hyperkalaemia, hyper P, hypo Ca
  • D vitamin: ckd-bmd (due to increased secretion PTH [ 2° hyperparathyroid ] due to impaired renal hydroxylation of vit D and renal P retention )
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12
Q

Name 3 complications nephrotic syndrome

A
  • Infections: loss immunoglobulins in urine. Prone to cellulitis, strep, spontaneous bacterial cellulitis
  • thromboembolism: eg DVT /pe, renal vein thrombosis. Due to increased clotting factors and platelet abnormalities
  • hyperlipidaemia: due to hepatic lipoprotein synthesis in response to low oncotic pressure
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13
Q

Treatment nephrotic syndrome? (5)

A
  • Monitor UCE, bp, fluid balance, weight regularly. Treat underlying cause.
  • restrict salt. Take in protein normally
  • diuretics: furosemide with or without spironolactore. Aim 1 kg/day loss
  • chronic nephrotic: ace -I renoprotective - reduce proteinuria and slow progression of renal impairment. Some also advocate A2A (adenosine A2A R agonist - decrease inflammation and prevent fibrosis)
  • treat infections promptly (pneumococcal vaccines recommended) , prophylactic heparin if immobile, treat HPT , persisting hyperlipid and other risk factors.
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14
Q

Name 5 indications for acute dialysis

A

Aeiou

  • Acidosis severe metabolic: ph < 7,2 or base excess <10
  • electrolytes: persistent hyper k >7
  • intoxication: istumbled ( INH, salicylates, theophylline, uraemia, methanol, barbiturates, lithium, ethylene glycol aka antifreeze, dabigatran )
  • overload: refractory pulmonary oedema,,
  • uraemia: encephalopathy, uraemic pericarditis
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15
Q

Approach to causes acute kidney injury? (10)

A

Prerenal = hypoperfusion

  • hypovolaemia
  • sepsis
  • drugs
  • hyper calcaemia

Renal

  • vascular
  • glomerular
  • interstitial
  • tubular
  • hepatorenal syndrome

Postrenal (especially if solitary kidney)

  • neurogenic
  • anatomic
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16
Q

Name 4 causes prerenal AKI

A

Due to kidney Hypoperfusion

  • Hypovolaemia
    → absolute: haemorrhage, gi loss, skin loss, renal loss, renal artery stenosis
    → effective: low cardiac output (cardiac failure), cirrhosis, sepsis, 3rd space loss
  • Sepsis → systemic vasodilation
  • Drugs: NSAIDs (constrict Afferent arteriole ), ace - I /arbs (inhibits vasoconstriction of efferent arteriole), calcineurin inhibitors (cyclosporine)
  • Hypercalcaemia
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17
Q

Name 10 renal causes AKI

A

Tubular

  • acute tubular necrosis (50% mortality)
    → ischaemiA (due to prerenal causes)
    → nephrotoxins: drugs (aminoglycosides, amphotericin b, tetracyclines), contrast, uric acid crystals, haemoglobinura in rhabdomyolysis, myeloma

Vascular

  • vasculitis
  • malignant hypertension
  • cholesterol emboli
  • haemolytic uraemiC syndrome
  • thrombotic thrombocytopeniC purpura TTP

Glomerular

  • glomerulonephritis

Interstitial

  • acute interstitial nephritis

Hepatorenal syndrome

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18
Q

Name 6 postrenal causes AKI

A

Neurogenic urinary tract obstruction

  • multiple sclerosis
  • spinal cord lesion
  • peripheral neuropathy

Anatomic

  • ureter: stones
  • bladder: tumour
  • urethra: posterior urethral valve, BPH
19
Q

Name 4 clues to prerenal etiology of AKI

A
  • Clinical: decreased bp, high hr, orthostatic hr /bp changes
  • urea x 20 = more than the creatinine (urea increase more than creat)
  • hyaline casts
  • urine Na < 10-20 , fractional excretion of Na <1 %
  • urine osmolality > 500

Why? Urine is concentrated and sodium is reabsorbed by working tubular cells.

20
Q

Name 5 clues to renal etiology of AKI

A
  • Urinalysis positive for casts (tubular = pigmented granular, interstitial = WBC, glomerular = rbc)
  • systemic features, anaemia , ht, mild-moderate ECF volume overload
  • thrombocytopenia
  • urine Na > 40 , fractional Na excretion > 2% in ATN
  • urine osmolality < 350 in ATN

Why? Urine not concentrated and sodium not reabsorbed by sick tubules

21
Q

Name 5 clues to postrenal aetiology of AKI

A
  • Known solitary kidney
  • older man (bph)
  • recent retroperitoneal surgery
  • signs urinary tract obstruction: anuria, palpable bladder
  • ultrasound shows hydronephrosis
22
Q

Name the 4 phases AKI

A
  • Initiating event ( hours to days)
  • oliguric/anuric phase (1-3 weeks) (fluid retention, hyperk)
  • polyuric/ diuretic phase (2 weeks) (dehydration, hypo Na, hypok)
  • recovery phase (months years)
23
Q

Name complications renal failure

A

Mad hunger

  • metabolic acidosis
  • dyslipidaemiA
  • high potassium
  • uraemia
  • Na/H2O retention
  • growth retardation
  • erythropoietin failure (anaemia)
  • renal osteodystrophy
24
Q

Diagnostic criteria AKI? (3)

A

Akin/kdigo criteria

Urine output < 0,5 ml /kg/hour for > 6h
Or
Increase serum creatinine 0,3 mg/ dL or more within 48 hours
Or
Increase serum creatinine 50% or more within 7 days

25
Q

Staging criteria AKI? (5)

A

Rifle criteria

  • Risk (stage 1): increase serum creat 1,5 x baseline or urine output < 0,5 ml/kg/hour for 6-12h
  • injury (stage 2 ): increase serum creat 2 x baseline or urine output < 0,5 ml/kg/hour for 12-24 h
  • failure (stage 3 ): increase serum creat 3 x baseline or urine output < 0, 3 ml/kg/hour for > 24h or anuria >12h or increase serum creat by > 0,5 - > 4.0 mg/dl or initiation renal replacement therapy
  • loss: RRT > 4 weeks
  • end stage: > 3 months
26
Q

Treatment AKI? (6)

A

General

  • Treat underlying cause and stop nephrotoxic drugs
  • correct volume depletion with normal saline
  • diet: normal calorie intake, protein 0,5 kg/day

Treat complications

  • hyperkalaemia: iv calcium gluconate (cardioprotective), iv insulin and glucose to promote uptake, salbutamol nebuliser, calcium resonium to bind K in gut.
  • pulmonary oedema: sit up, high flow oxygen. Venous vasodilator eg morphine. Furosemide.
  • bleeding: FFP and platelets as needed
  • Acute dialysis if indicated
27
Q

Define ckd

A

Abnormality of kidney structure/function for at least 3 months with GFR < 60 or markers of kidney damage (proteinuria, haematuria, raised creat, small kidneys on u/s, biopsy abnorms)

28
Q

CKD staging? (5)

A

Kdigo staging

  • stage 1: GFR 90 or more (normal) with other evidence kidney damage
  • 2: GFR 60 - 89 + other evidence kidney damage
  • 3: GFR 30 - 59 + or - other evidence kidney damage
    → 3a: GFR 45 - 59
    → 36: 30 -44
  • 4: GFR 15 - 29 + or - other evidence kidney damage
  • 5: < 15. End stage renal disease.
29
Q

Causes CKD? (8)

A

Prenenal

  • dm!
  • ht!
  • SLE, hepatitis b/c

Renal

  • glomerulonephritis!
  • renovascular disease!
  • pyelonephritis!
  • polycystic kidneys!
  • interstitial nephritis!
  • nephrocalcinosis (ageing)
  • Analgesic nephropathy
30
Q

How manage CkD complications? (10)

A

Nephron

  • Nitrogen: low nitrogen diet. Na restriction.
  • Electrolytes: monitor K. Restrict in diet. If hyper K, kexelate (polystyrene sulfonate) 15g 6-24hrly
  • ph: metabolic acidosis
  • hypertension: ace-i or A2A can decrease rate of loss of renal function even if bp normal.; Hyperlipid: Statins
  • RBCs: manage anaemia with erythropoietin; Restless legs: clonazepam /Gabapentin
  • osteodystrophy: give Ca between meals to increase ca, and Ca with meals to bind and decrease PO4. Restrict dietary PO4 (milk, cheese, eggs). Supplement Vit D; Oedema: loop diuretics
  • nephrotoxins: avoid eg ASA, gentamicin and adjust doses of renally excreted medications.

All must get pneumococcal vaccine every 5 years, influenza annually, hep B to susceptible

31
Q

Name 3 causes nephritic syndrome

A

Infections

  • post-streptococcal glomerulonephritis (type 3 hypersensitivity reaction, + anti-aso, anti - DNase, decrease C3)

Immune complex mediated

  • IgA nephropathy/Berger’s disease
  • rapidly progressing glomerulonephritis (causes = goodpasture syndrome, SLE nephritis)
  • membranoproliferative glomerulonephritis (type 1 = ig mediated; 2 = C3 )

Vascular

  • small vessel vasculitis (henoch schonlein purport, Churgg Strauss syndrome )
32
Q

Calcium, phosphate, vitamin d, PTH levels in renal osteodystrophy?

A

Calcium + vitamin D low
Phosphate, PTH high

33
Q

Investigation for nephritic and nephrotic syndrome?

A

Biopsy

34
Q

What is the hallmark of glomerular injury/disease?

A

Proteinuria

35
Q

Name 4 causes acute interstitial nephritis

A

Characterised by electrolyte abnormalities, moderate proteinuria, renal impairment

  • drug allergic: penicillins, NSAIDs, PPI, mesalizine ( aminosalicylate used for IBD )
  • immune
  • infection: TB, acute bacterial pyelonephritis
  • toxic: mushrooms
36
Q

Name 6 common clinical features polycystic kidney disease

A
  • Vague discomfort in loin/abdomen
  • acute loin pain/ renal colic due to haemorrhage into cyst
  • ht
  • haematuria,, with little/no proteinuria
  • UTI
  • renal failure
37
Q

Name 6 presentations and clinical features renal artery stenosis

A
  • Severe, recent onset, refractory ht
  • kidneys asymmetrical
  • flash pulmonary oedema occurs repeatedly, especially if bilateral
  • peripheral vascular disease
  • renal impairment, especially if bilateral
  • renal function deterioration on ace -i/ arb
38
Q

Define haemolytic uraemic syndrome

A

Type of thrombotic microangiopathy that predominantly affects renal microcirculation, with involvement of other organs (including brain ) in severe cases

39
Q

Name 3 thrombotic microangiopathies associated with acute renal damage

A
  • Haemolytic uraemic syndrome
  • TTP
  • Dic
40
Q

Cause haemolytic uraemic syndrome

A

Infections with organisms that produce enterotoxins : E. coli, shigella dysenteriae

41
Q

Complication untreated pre renal AKI?

A

Acute tubular necrosis

42
Q

Name 5 options renal replacement therapy

A
  • Haemodialysis
  • haemofiltration
  • haemodiafiltration
  • peritoneal dialysis
  • renal transplant
43
Q

Most common type renal stone?

A

Calcium oxalate

Internal Medicine (20 decks)

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