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year 2 s2 pathology > Kidney diseases > Flashcards

Kidney diseases Flashcards

1
Q

what are the principle functions of the kidney

A
  • eliminate waste materials ]
  • regulate fluid and electrolyte balance and acid-base balance
  • endocrine function (prostaglandins (inflammtion), erythropoietin (growth hormone for RBC), 1,25-(OH)2-D3 (activated vit d3 is formed in kidney), renin)
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2
Q

which part of the kidney do most kidney diseases affect

A
  • most are associated with abnormalities of the GLOMERULAR CAPILLARY or RENAL TUBULE system
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3
Q

which symptoms can suggest renal tract disease

A
  • dysuria
  • haematuria
  • urinary retention
  • alteration of urine volume (either polyuria or oliguria)
  • pain along the renal tract
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4
Q

what is the kidney highly sensitive to

A
  • immune reactions
  • this is due to IMMUNE COMPLEXES either forming/ being deposited on glomerular epithelial capillary walls
  • this can damage the kidney
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5
Q

what is the cause of kidney diseases affecting the glomeruli

A
  • IMMUNOLOGICALLY MEDIATED disease
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6
Q

what is the cause of kidney diseases affecting the tubules

A
  • TOXIC/INFECTIOUS agents
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7
Q

what is the cause of kidney diseases affecting the INTERSTITIUM (intertubular, extraglomerular, extravascular space of the kidney)

A
  • TOXIC/INFECTIOUS agents
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8
Q

what is the cause of kidney diseases affecting the blood vessels

A
  • DECREASED BLOOD SUPPLY which leads to damage
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9
Q

what causes progression to renal failure

A
  • severe damage to all 4 structures (glomeruli, tubules, interstitium and blood vessels) causes CHRONIC RENAL DISEASES which leads to RENAL FAILURE
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10
Q

what is nephritis

A

inflammation of any part of the kidney

1) glomerulonephritis (GN)
2) interestitial nephritis
3) pyeloneophritis

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11
Q

describe glomerulonephritis

A
  • general term for a GROUP OF DISORDERS: (bilateral, symmetrical (affects both kidneys) immunologically mediated injury to the glomerulus)
  • accounts for 1/3 of cases of TERMINAL RENAL FAILURE
  • PRIMARY: kidney is the predominant organ involved (e.g. post-streptococcal glomerulonephritis)
  • SECONDARY: systemic diseases with glomerular involvement (eg SLE)
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12
Q

what is the pathogenesis of glomerulonephritis

A

1) in situ fomation of IMMUNE COMPLEX (antibody-antigen complex forms on the glomerulus)
2) or deposition of circulating immune compex (antibody-antigen binding complex is deposited)
3) or the GLOMERULAR basal membrane acts as ANTIGEN O the antibody binds directly to it causing damage
4) OR cell mediated glomerular damage

  • these all cause INFLAMMATION which triggers the SECONDARY MECHANISMS
  • secondary mechanisms:there is HYPERCEULLULAROTY (inc proliferation of cells), BASEMENT MEMBRANE THICKENING (can cause dysfunciton of kidney), SCLEROSIS and HYALINISATION (loss of structure)
  • these can cause: protein leakage O plasma volume is reduced O cardiac output is DECREASES, leads to HYPOVOLAEMIA. This can cause activation on renin-angiotensin-aldosterone system, which causes Na+ sodium and WATER RETENTION and OEDEMA and HIGH BLOOD PRESSURE (hypertension)
    MANIFESTS AS:
    1) ACUTE NEPHROTIC SYNDROME (classic kidney inflammation)
    2) NEPHROTIC SYNDROME ( characterised by increased renal failure)
    3) RENAL FAILURE, ACUTE AND CHRONIC
    4) ASYMPTOMATIC PROTEINURIA (milder disease, proteins present in urine)
    5) MICROSCOPIC HAEMATURIA (blood in urine)
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13
Q

describe the pathogenesis of acute nephritic syndrome
clinical features
management

A
  • exogenous antigen (eg infetcive agents- group A beta-haemolytic Strep.) or endogenous antigen (eg SLE)
  • they cause acute nephritic syndrome
    Pathology: diffuse (throughout the entire glomerulus) proliferative glomerulonephritis
  • hypercellular glomeruli

Clinical features:

  • Haematuria (due to damage to glomerulus, blood enters urine)
  • Proteinuria (protein in urine due to permeability of glomerulus being increased O proteins leak to urine)
  • Hypertension (due to sodium and water retention)
  • Oedema (periorbital) (due to retention)
  • Oliguria (reduced urine due to filtration is damaged O not enough) & uraemia (kidney clearance is reduced)

Management:

  • Supportive measures until spontaneous recovery
  • Hypertension: salt restriction, diuretics, vasodilators
  • Fluid balance monitoring
  • In oliguric with fluid overload, fluid restriction
  • Management of life-threatening complications
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14
Q

what is nephrotic syndrome

A

a different type of GN (Glomerulonephritis)

  • damage to the BASAL MEMBRANE can cause nephrotic syndrome
  • O there is loss of ELECTROSTATIC BARRIER (which repels ions and proteins) and PHYSICAL BARRIERS (due to tissue damage)
  • passage of large molecular weight proteins which should be retained into the glomerular filtrate leads to PROTEINURIA
  • due to HIGH PROTEIN LOSS, the plasma lacks protien
  • O we have HYPOALBUMINAEMIA
  • this causes REDUCED ONCOTIC PRESSUE and thus HYPOVOLAEMIA
  • O renin-angiotensin-aldosterone is activated and causes Na sodium and water retention which leads to OEDEMA
  • hypoalbumibaemia causes INC SYNTHESIS OF PROTEIN in the liver and abnormal transport of circulating lipid and DECREASED CATABOLISM
  • excess lipid causes HYPERLIPIDAEMIA
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15
Q

what is classed as proteinuria

A

> 3.5g/24 h in adults

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16
Q

what is classed as hypoalbuminaemia

A

serum albumin <30g/L)

17
Q

how is proteinuria managed/treated

A
  • Steroids, e.g. prednisolone

- Immunosuppressors e.g. cyclophosphamide

18
Q

how is hyperlipidaemia managed/treated

A

if oedema:

  • bed rest
  • dietary salt restriction
  • thiazide diuretic
19
Q

what is renal failure

A

Failure of renal excretory function due to depression of GFR (Glomerular filtration rate)

  • accompanied to a variable extent by failure of:
    • Erythropoietin (EPO) production
    • Vit D hydroxylation
    • Regulation of acid-base balance
    • Regulation of salt & water balance, and blood pressure
20
Q

what is acute renal failure
aetiology
pathogenesis

A
  • Abrupt deterioration in parenchymal renal function;usually (not invariably) reversible over days or wks

causes:
- Pre-renal (~70%): shock, hypovolemia etc
- Intrinsic renal (~25%): acute tubular necrosis etc.
- Post-renal (~5%): obstruction etc

pathogenesis:
Reduced excretion of nitrogenous waste products (urea) causes →uraemia which leads to INC creatinine

21
Q

what are the clinical features of acute renal failure

A
  • Early stages often asymptomatic
  • Symptomatic when plasma urea> 40mmol/L:
    −Oliguria, oedema
    −Plasma creatinine rises (by ~ 100mol/day)−Hyperkalaemia & metabolic acidosis
    −Uraemic syndrome: anorexia, nausea, vomiting, irritability, seizures, coma
22
Q

what is the treatment for acute renal failure

A
  • Correct reversible underlying factors eg. volume depletion, nephrotoxic drugs
  • Treat hyperkalaemia
  • Dialysis - Indications: Hyperkalaemia (> 6.5 mmol/L )
    Severe metabolic acidosis (pH<7.2)
    Pulmonary oedema
    Complications of uraemia: encephalopathy, pericarditis, seizures
23
Q

what s chronic renal failure

A

long standing and ususally progressive impairment in renal function

causes:
- diabetes
- hypertension
- glomerulonephritis
- pyelonephritis
- cystic (polysystic) renal disease
- nephrotoxins (eg,NSAIDs, esp phenacetin; heavy metals)

24
Q

what are the clinical features of chronic renal failure

A
  • insidious
  • Often asymptomatic until GFR < 15ml/min
  • Symptoms common when serum urea > 40mmol/L
    • Uraemic syndrome:
    • -> Nervous system (malaise, loss of energy, loss of appetite, insomnia)
  • -> Gastrointestinal (nausea, vomiting, and diarrhea)
  • -> Dermatological (itching)–
    • Nocturia and polyuria
    • Oedema
25
Q

what are the heamatological and metabolic complications of chronic renal failure

A
  • Anaemia
    • Largely due to EPO deficiency
    • Normochromic, normocytic
    • Typical “anaemia of chronic disease”
    • Responds to EPO
  • Renal osteodystrophy (due to decreased activation of vitamin D in kidney, there is loss of calcium)
  • Electrolyte/acid-base disorders
    • Hyperkalaemia; Na retention (usually)
    • Hypo~ (early) & hyper~ (late) -calcaemia
    • Metabolic acidosis

year 2 s2 pathology (22 decks)

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