Week 12: Pathophysiology of Renal Disease Flashcards

1
Q

What are the 4 main groups of renal diseases?

A
  1. Disease of the glomeruli
    - Acute or chronic
    - Often are caused by an immunologic aetiology (caused by inflammation etc.)
  2. Tubules
    - Mostly acute
    - Often have an infectious or toxic aetiology
  3. Interstitium
    - Involves the interstitium and tubules
    - Often have an infectious toxic aetiology
  4. Vascular

Changes to the nephron as a consequence of increased blood pressure or impaired blood flow through the glomerulus (which may bring in things that will damage the glomerulus. Damage can also be as a result of the high-pressure filtrate system. If there is a loss of the charge of the filtrating membrane there will also be glomerulus damage)- most commonly associated with vascular disease

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2
Q

What are the 4 main clinical presentations in patients of renal disease?

A
  1. Pain / dysuria (painful urination)
    - A patient will have painful, fever chills if a urinary tract infection / kidney stone
  2. Haematuria
    - Is blood in the urine
    - Can be caused by infections, stones and tumours
  3. Proteinuria
    - Is the presence of abnormal amounts of protein in the urine
    - This can indicate glomerular damage
  4. Azotaemia
    - Is indicative of renal failure
    - Is the abnormally high presence of urea and other nitrogen compounds in the urine
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3
Q

What are the 2 main causes for acute renal failure?

A
  1. Ageing
  2. Comorbidities (diabetes, hypertension)
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4
Q

Acute renal failure will be evident in which two obvious tests?

A

(Renal clearance) Elevation in serum creatinine and (urine output) decrease in urine output

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5
Q

What are the 3 types of acute renal failure?

A

Pre-renal, renal and post-renal

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6
Q

What is acute pre-renal failure, what is it caused by, what is it characterised by?

A
  • Caused by an issue with renal perfusion
  • There is a sudden decrease in blood flow to the nephron which could be caused by hypovolemia or heart failure
  • Vascular disease could also cause this reduced renal perfusion through atherosclerosis
  • Pre-renal acute renal failure is characterised by low GFR and oliguria
  • The kidney function will respond through the RAAS to reabsorb sodium, water and UREA
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7
Q

What is acute renal (intrarenal) failure, what is it caused by, what is it characterised by?

A
  • Caused by dysfunction within the kidneys itself
  • This is caused by issues to the blood vessels, tubules, glomeruli or interstitium
  • This type is associated with acute tubular necrosis (toxic or ischemic type), glomerular disease or acute interstitial nephritis (inflammation of kidneys)
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8
Q

What is acute post-renal failure, what is it caused by, what is it characterised by?

A
  • Caused by issues after the collecting duct of the renal, that is, post-renal is due to obstructions of the urinary tract (the cause is distal to the kidney)
  • This is usually caused by urinary obstruction, commonly kidney stones
  • This causes complete anuria, oliguria or normal urinary output
  • The clinical findings of this are based on the duration of the obstruction, how long the obstruction has been there
  • Once you remove the obstruction renal function returns to normal
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9
Q

What are the physiological effects of acute renal failure? (x7)

A
  1. Decreased GFR
  2. Retention of water and electrolytes
    - Is the effect of decreased GFR
    - This can cause hyponatremia, hyperkaliaemia, hyperphosphatemia and hypocalcaemia
  3. Metabolic acidosis
    - Acid base disturbances
  4. Edema and Hypertension
    - Fluid collecting, and volume increase may lead to hypertension (as a result of edema not cardiovascular cause)
  5. Suppressed erythropoietin secretion
    - Erythropoietin is secreted from the kidney, thus issues with the kidney cause reduced secretion
  6. Oliguria and progressive uraemia
    - A raised level of UREA and other nitrogenous waste in the blood that is normally secreted in the kidneys
  7. Anuria
    - This is a failure of the kidney to produce urine
    - This occurs in severe cases of acute renal failure

If acute renal failure not treated it will lead to chronic renal failure

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10
Q

What is chronic renal disease

A
  • Is a syndrome characterized by progressive and irreversible deterioration of renal function
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11
Q

What will be evident (tests wise) in chronic kidney disease?

A
  • Chronic kidney disease is recognised by the presence of structural kidney damage, as well as decreased GFR of less than 60mL/min, that occurs for longer than 3 months
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12
Q

What are the common causes of chronic kidney disease? (x6)

A
  1. Hypertension
  2. Diabetic kidney disease
    - Caused by diabetes mellitus
  3. Vascular disease (atherosclerosis)
  4. Urinary tract obstruction
  5. Recurrent renal stone disease
  6. Glomerular disease
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13
Q

What are the stages of chronic kidney disease and define them (x5)

A
  1. Stage 1
    - There are mild signs of kidney disease
    - Normal / increased GFR above 90% (as a result of compensatory mechanisms)
  2. Stage 2
    - There are mild signs of kidney disease
    - Reduced GFR values at 60 – 89%
  3. Stage 3
    - Signs of moderate kidney disease
    - Reduced GFR values at 30 – 59%
  4. Stage 4
    - Signs of severe chronic kidney disease
    - Reduced GFR values at 15 – 29%
  5. Stage 5
    - There is less than 15% of kidney function remaining
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14
Q

Define decreased renal reserve, renal insuffiency, renal failure and end stage kidney disease

A
  1. Decreased renal reserve
    - This is asymptomatic
    - Normal BUN and creatinine levels
    - GFR is around 50%
  2. Renal insufficiency
    - The GFR is around 20 – 50%
    - There is polyuria and nocturia
    - Elevated BUN and Creatinine values
  3. Renal Failure
    - GFR is less than 20%
    - There will be edema, metabolic acidosis and hypocalcaemia
    - There will also be symptoms of uraemia
  4. End stage kidney disease
    - There will be uremic syndrome which is abnormally high waste products in the blood
    - Patients with ESKD require dialysis
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15
Q

What are the complications that can arise due to chronic kidney disease?

A
  1. Hypertension
    - This is caused by salt and water retention (due to reduced kidney function)
    - This caused volume load and therefore hypertension
    - Can lead to heart failure, pulmonary edema
  2. Cardiovascular disease
    - Can lead to cardiac arrythmias
  3. Uremic syndrome
    - Azotaemia, electrolyte disturbances, acid-base disturbances
    - Decreased GFR
  4. Metabolic acidosis
  5. Electrolyte imbalances
  6. Bone and mineral disorders
    - Vitamin D deficiency from kidney
    - Also, hypocalcaemia
  7. Aneamia
    - Caused by decreased erythropoietin production
  8. Malnutrition
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16
Q

What type of processes cause glomerular disease?

A

immune or inflammatory processes

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17
Q

What are the 2 categories of glomerular disease?

A
  1. Primary glomerular disease
    - Is when the glomeruli is only involved in the pathology,
  2. Secondary glomerular disease
    - Is when the cause of the disease is systemic or hereditary which affects glomeruli function
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18
Q

What is glomerulonephritis?

A

Inflammatory process that involves glomerular structures

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19
Q

What are the two categories of glomerulonephritis?

A
  1. Primary glomerulonephritis
    - The glomerular damage is the only disease present (there is no other abnormality that caused the damage)
  2. Secondary glomerulonephritis
    - Is when the glomerular damage was caused by another disease (e.g. diabetes mellitus or SLE autoimmune disease)
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20
Q

What are the 2 immunological changes which lead to glomerular disease?

A
  1. Cellular changes
    - Increased inflammation
    - This causes increased proliferation of endothelial, mesangial and leukocytes as well as possible infiltration by macrophages
    - This will increase glomerular cell number
  2. Non-cellular changes
    - The glomerular basement membrane will thicken (membranous)
    - There may be changes in non-cellular glomerular components e.g. sclerosis and fibrosis
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21
Q

Explain the pathophysiology of what happens when you have glomerular injury pathology and what does it lead to?

A
  • Most glomerular diseases are immunologic in origin, that is they are caused by the deposition of immune complex or by antibodies binding to antigens in the kidney (which forms immune complexes)
  • These immune complexes clog up the filtrating membrane, initiating inflammatory response leading to glomerular damage

leads to nephritis - depending on the site of damage it will result in either nephritic or nephrotic syndrome

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22
Q

Which are the 3 cells which have increase in proliferation and deposition in the glomerular due to glomerular injury pathology?

A
  1. Mesangial (which regulates glomerular filtration)
  2. Subendothelial (which will close the foot processes)
  3. subepithelial
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23
Q

What are the two common clinical manisfestations that glomerulonephritis can lead to?

A
  • Nephritic and nephrotic syndrome
24
Q

What is nephrotic syndrome characaterised by? and what as will be present?

(Use acronym PALE)

A
  • Is a collection of features caused by glomeruli nephritis that is characterized by findings of massive proteinuria
  • As well as proteinuria, there will be hypalbuminaemia, edema, hyperlipidaemia (due to increased lipid production as a result of increased excretion) and lipiduria
25
Q

Why is their heavy proteinuria and oedema in a damaged glomerulus?

A

basement membrane damaged, therefore, lost its negative charge

  • Edema is caused by protein loss that decreases plasma oncotic pressure resulting in pulmonary edema
26
Q

What is nephritic syndrome characterised by? and what are other associated symptoms?

A

haematuria,

  • Other symptoms include hypertension, mild edema (as mild protein loss), oliguria and also some proteinuria (only mild proteinuria)
27
Q

Differentiate between the mechanism for nephrotic and nephritic syndrome

A
28
Q

Differentiate between the features for nephritic syndrome and nephrotic syndrome

A
29
Q

Explain the pathophysiology of glomerulonephritis in regards to the immune complex

A

there will be excessive inflammation caused by increased immune complex deposition in the filtrating barrier

  • These immune complexes that are formed can be either;
  • Resulting from antibodies reacting with fixed glomerular antigens
  • Resulting from circulating antigen-antibody complexes (that are then trapped at the filtration membrane)
  • Regardless of how they are formed, in glomerulonephritis, there is an increased deposition of immune complexes at the filtrating barrier of the glomerulus
30
Q

What is acute post infection glomerulonephritis and whats the pathophysiology of it?

A
  • Is glomerulonephritis that occurs shortly after infection
  • Usually, a patient will present with this form of glomerulonephritis following a throat and skin infection
  • This is caused by the attraction of immune cells to the area of inflammation resulting in lysosomal degradation of the basement membrane
31
Q

What is minimal change disease and whats it caused by?

A
  • Is another glomerulonephritis which is common in children
  • As the name suggests, there is minimal changes to the glomeruli when looked at under the light microscope (little to no structural abnormality)
  • This minimal change disease is simply caused by effacement of podocyte foot processes which will cause proteinuria
  • As well as this, anion production in the glomerular basement membrane will be reduced, which will cause the loss of filter negativity (causing increased filtration of proteins)
  • Because of these changes their will be increased permeability to albumin
32
Q

What is IgA nephropathy and what causes it?

A
  • Is another common form of glomerulonephritis that predominately occurs in males
  • IgA nephropathy presents with both nephrotic and nephritic syndrome (as both haematuria and proteinuria occur)
  • This type of glomerulonephritis is caused by deposition of immunoglobulin A in the glomerulus which causes proliferation of mesangial cells
33
Q

If glomerulonephritis is not treated, what can it lead to?

A

End stage renal disease

34
Q

What is tubulointerstitial disoders?

A
  • Are a group of disorders with prominent involvement of the renal tubules and interstitium
35
Q

What are the 3 things that cause tubulointerstitial disorders?

A
  1. Drugs and toxins
    - These cause tubulointerstitial injury by direct toxic injury
    - This causes decreased blood flow
  2. Infections
    - Infections can creep up from the bladder or come in from the blood stream
    - This can cause pyelonephritis (kidney infection)
  3. Renal tubular acidosis
    - This will damage the epithelial cells
36
Q

What are the two types of acute tubular necrosis?

A
  1. Ischemic type
    - Will have evidence of necrosis scattered all along at different parts of the nephron
    - Cellular debris will be evident as casts
  2. Toxic type
    - Will have evidence of necrosis throughout the tubule
    - Both of these will cause reduced GFR, oliguria (due to decreased function of nephron)
37
Q

Define what bartters syndrome is?

A
  • Is caused by impaired sodium-2-chloride-potassium transporter in the thick ascending limb
  • This decreases sodium reabsorption, hypocalcaemia, hypokalaemia and metabolic alkalosis
  • Autosomal recessive
38
Q

Define what gitelman’s syndrome is?

A
  • Is caused by a disorder of the DCT sodium-chloride transporter
  • This causes salt and water loss, volume depletion, hypokalaemia and hypercalciuria and hypocalcaemia
  • Same as thiazide diuretic and is autosomal recessive
39
Q

define what liddle’s syndrome is?

A
  • Is caused by mutations of ENaCs in the principal cells of the DCT and CD to increase ENaC activity
  • This causes increase sodium reabsorption, hypertension and volume overload
  • Autosomal dominant and similar to
40
Q

define what fanconi’s syndrome is

A
  • Is caused by transporter defects or renal tubular cell injury in the PCT (due to ischemia, hypoxia, toxins and drugs
  • This causes increased excretion of all those reabsorbed in PCT
  • Similar to osmotic diuretic
41
Q

What is an example of an obstructive disorder?

A

Kidney stones

  • Congenital anomalies
  • Urinary calculi
  • Pregnancy
  • Benign prostatic hyperplasia
  • Scar tissue from infection or inflammation
42
Q

What do obstructive disorder results in?

A
  • If there is obstruction to urine flow, there will be back pressure, resulting in collecting of water causing hydronephrosis
  • Hydronephrosis is the urine filled dilation of the renal pelvis and calices which can cause pain from the ureter or bladder
  • Because of this increased pressure back pressure into the collecting duct, their will be no medullary hyperosmolality meaning dilute urine cannot be formed in hydronephrosis (urine concentrating ability is lost)
43
Q

What is urolithiasis and nephrolithiasis

A
  • Nephrolithiasis are those stones formed in the kidney
  • Urolithiasis are those stones present in the ureter or urinary bladder
44
Q

How are kidney stones formed?

A
  • These are formed when urine is super saturated with the various ‘stone components’ (e.g. calcium slats, uric acid, phosphate, cystine) there will be nucleation and then a subsequent stone growth
45
Q

What are the 4 different types of kidney stones?

A
  1. Calcium stones
    - Are the most common
    - Caused by hypercalcemia, hyperparathyroidism and vitamin D intoxication
  2. Magnesium ammonium phosphate
    - Can be caused by recurrent urinary tract infection
  3. Uric acid
    - Can be caused by gout
  4. Cystine
    - Caused by defective amino acid transport
46
Q

What are some of the symptoms of kidney stones?

A
  • Severe colicky pain (radiates up the flank anteriorly)
  • Hydronephrosis
  • Infection
  • Renal damage
  • Hypertension
47
Q

What is diabetic nephropathy and what is it caused by?

A
  • Is glomerular damage that results in thickening of the basement membrane
  • This damage is caused by;
    1. High glucose levels
    2. Excessive protein reabsorption which damages the tubular cells
    3. Most importantly, in diabetic patients it is the glycated end products which produce more oxidants that cause oxidative stress (damaging the cells) that cause nephropathy
48
Q

What will diabetic nephropathy result in?

A
  • Thickening of blood vessel (occlusion)
  • Thickening of basement
  • Renal ischemia may occur
  • Enlargement of capillary pores
49
Q

Why is urine coca-colored in pephritic syndrome?

A

Myoglouria is passed through filtration barrier and appears in urine

50
Q

Why is there an increase in protein loss in nephrotic syndrome?

A

Damage to the filtration membrane - causes loss of negative charge

51
Q

Why do you get pedal edeme in nephrotic syndrome?

A

protein loss –> hypoalbuminaemia –> decrease plasma oncotic pressure (force sucking fluid into capillary) –> more fluid movement out of capallariees –> edema

52
Q

patients with nephrotic syndrome develop spontaneous arterial or venous thrombosis. Explain why there will be hypercoaguabilityin this condiition

A

Increase proteinuria –> increase antithrombin 3 loss and other anticoagulant proteins (protein c and s).

53
Q

What is obstructive uropathy? state any two causes for obstructive uropathy

A

when your urine can’t flow due to obstruction of urethra

could be from kidney stones, tumours, pregnancy

54
Q

What are teh 4 different types of kidney stones?

A

Calcium, magnesium amonium phosphate, uric acid and cystine

55
Q

what is hydronephrosis? Hydronephrosis patients may lose the urine concentrating ability, why?

A

Is when the kidney is filled with fluid due to a blockage in the urinary tract. it causes increase tubular hydrostatic pressure causing increase fluid moving to medulla of kidney –> makes it less osmotic as it moves into interstitial space where nephron is. Therefore, lose that hyperosmolarity

56
Q

What are the functional and structural changes in the kidney in diabetic nephropathy

A

Mesangial expansion, thickening of glomerular basement membrane, glomerular sclerosis.

Cuases albuminuria, decrease GFR and increase Blood pressure

57
Q

what is the pathophysiology of alports syndrome

A

affects the filtration at the glomerulus due to deficiency of type 4 collagen