Renal pathology Flashcards

1
Q

Describe the pathological features of acute pyelonephritis

3

A

Infection travels up from Lower UTI ->Upper UTI = BACTERIAL INFECTION OF KIDNEY
- Bacteria travels upwards from urethera –> into the bladder

Causes :

  • sex
  • bacteria from faeces
  • Bacterila infection = E.coli, proteus, enterobacter
  • Vesicoureteral reflux (VUR), where urine flows back up ureter ( normally a valve stops it )

Pathogenisis :
1- UNILATERAL = only effects one kidney

1) Pathogen adheres to renal capillary
2) Chemokines bring neutrophils to renal epithelium , intersititum
- You can see this under the microscope = lobulated nucleus
3) Neutrophils infiltrate and die off , to make their way to the uring = increasing WBC levels in urine , also can cause WBC cell casts ,

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2
Q

Explain how glomerulopathies cause nephrotic and nephritic syndrome

A

-Immunological disturbance not due to infection with numerous sub types
2 main categories :
1) Dysfunction in glomelular filtration barrier (problems in basement membrane , no inflammatory cell infiltrate, oedema) = massive loss of protein in URINE = NEPHROTIC syndrome

2)Inflammation in the glomeruli , which causes haematuria, proteinuria, HT, = Nephritic Syndrome

You can also get mixed both nephrotic and nephritic …

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3
Q

Compare and contrast simple renal cysts and inherited polycystic kidney disease

A

Cyst =closed cavity or sac lined by epithelium , containing liquid or semi solid material

Simple cyst = harmless

Autosomal recessive polycystic kidney disease = more serious , presents in first few days of life , very fatal

Autosomal dominant polycystic kidney disease = presents later in life: kidney failure , 50% require treatment for kidney failure ,

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4
Q

Describe the pathological features of renal calculi

CSUC

A

1) calcium oxalate
2) Struvite
3) Uric acid
4) Cystein

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5
Q

Describe the pathological features of renal cell carcinoma

A

1) Angiomyolipoma: triad = blood vessel, clear fat cells, spindley smooth muscle cells = benign
2) Benign = Oncocytoma

Malignant tumour :
1- Renal caricinoma ( well rounded edges, clear cytoplasm and are arranged in nests with intervening blood vessels)
2-Wilms tumour in children

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6
Q

causes of respiratory alkalosis

A

1) Salicyate ingestion = ventillation = respiratory alkalosis
2) Hyperventilation = hypocapnia ( over breathing not enough CO2 )= alkalosis
3) Hypoxia
4) Liver diseases
5) Heart failure
6) 1) Asthma = irregular bronchoconstrictions , ventilation /perfusion mismatch = hypoxia, hypocapnia = alkalosis

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7
Q

Outline the main causes of acute renal failure

A

-Decrease in eGFR detected in hours or weeks
3 types :
1)Pre-renal AKI = disordered perfusion of kidney which is structurally normal due to :
-shock
-sepsis
-loss of blood
-MI ,arrhythmia
-heart failure , pulmonary emobolism
causes small volume of concentrated URINE

2) Renal AKI = nephrons have been damaged after prolonger pre renal insults
- ischaemic, hypoxic renal injury
- nephrotoxins
- Transporters in the walls don’t work , Na left in tubule , hence water left in tubule = less reabsorption
- increased urine
- osmolality decreases
- H+ transport doenst work so H+ cant be secreted , HCO3- production decreases too = metabolic acidosis
- hyperkalaemia
- risk of fluid overload as eGFR decreases

3) Post renal AKI
- Urinary drainage is obstructed : due to stones, benign or malignant cancer

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8
Q

Chronic renal failure

  • symptoms ( funny boys like noodles in bread)
  • signs
A

Decrease in eGFR over months or years which is irreversible !
Caused by diabetes and HT
- measure: U&E Serum creatine , eGFR

Symptoms :

Fatigue due to anemia 
Breathlessness
Leg swelling
Nausea, anorexia, weight loss due to toxins
Itch
Bone pain

SIGNS:

  • pallour
  • Oedema
  • HT
  • Proteinuria
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9
Q

Causes of chronic kidney disease

A

1) Diabetic Kidney disease leads to glomelular basemenr membrane thickening , mesangial expansion ,glomeluar sclerosis
2) Hypertensive , athersclerotic vascular disease
3) Glomerulonephritis
4) Polycystic kidney disease

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10
Q

consequences of low eGFR
(2)
Consequence of reduced renal tubular function

A

-Fluid retention (Heart failure,oedema)
-Reduced metabolite excretion
(Uraemia, increased creatine in serum , serum urate increases, increased drug levels )

Redcued renal function :
1-Reduced fluid reabsoprtion
2-Reduced K+ excretion
3-Reduced acid secretion and bicarbonate formation

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11
Q

Explain the body’s response in diabetic chronic kidney disease

A

Glomerulus Hypertension in Diabetes :

1) Thick but leak glomerulus basement membrane ( meaning albumin gets into the urine ), but the vessel is narrow = low grr
2) RAAS released –> Angiotensin 2 acts on efferent arteriole to cause vasoconstriction = EVEN higher pressure
3) Basement membrane = damages , glucose deposits
4) Thickening of renal mesangium , support system = diabetic glomerulus, HT ,

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12
Q

Chronic renal failure treatment

A

-Treat HT
-ACE, and Angiotensin receptor blockers
-Reduce CV risk (statins)
TREAT THE COMPLICATIONS:
-anaemia with erythopoetin injection (normally kidney will make EPO to make more RBC)
-Renal bone disease ( give activated VIT D)
-Hyperphosphataemia ( phosphate binding drugs)
-Hyperkalemia (restrict the dietary intake)

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13
Q

Acute Renal Kidney disease

renal

A

2) Renal AKI = nephrons have been damaged after prolonger pre renal insults
- ischaemic, hypoxic renal injury
- nephrotoxins
- Transporters in the walls don’t work , Na left in tubule , hence water left in tubule = less reabsorption
- increased urine
- osmolality decreases ( less solutes)
- Specific gravity decreases ( less solid matter)
- H+ transport doesn’t work so H+ can’t be secreted , HCO3- production decreases too = metabolic acidosis
- hyperkalaemia
- risk of fluid overload as eGFR decreases

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14
Q

pre renal kidney disease

A

1) Pre-renal AKI = disordered perfusion of kidney which is structurally normal due to :
- shock
- sepsis
- loss of blood
- MI ,arrhythmia
- heart failure , pulmonary emobolism

Causes small volume of concentrated URINE

  • osmolality of urine is increased (meaning it has more particles in it )
  • specific gravity increases ( more solid matters , ions)
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15
Q

Acute Post renal Kidney disease

A

3) Post renal AKI
- Urinary drainage is obstructed : due to stones, benign or malignant cancer

to treat this you must :

1) Exclude obstruction
2) prevent UTI
3) treat underlying causes

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16
Q

Explain the physiological basis of the main symptoms and signs of acute renal failure

  • symptoms
  • signs
  • investigations
  • Treatment
A

Symptoms

  • pulmonary oedema
  • Hyperkalemia
  • Metabolic acidosis
  • sepsis

SIGNS :
-thirts , nephroxins , pulse , BP ,O2 saturation,urine output

Investigate:

  • dipstick ,ECG
  • Arterial blood gas
  • Chest X-ray
Action:
1-O2
2-Adequate fluid resuscitation 
3-STOP drugs
4-treatment of sepsis
17
Q

Explain the body’s response in acute kidney disease

A

less volume of urine , very concentrated

  • reduced perfusion leads to RAAS, ADH secretion
  • Renal causes = acute tubular necrosis = hypoxia due to poor blood flow
18
Q

Tests for renal function (3)

A

1) Urine volume
2) Serum creatinine
3) eGFR

19
Q

Causes of respiratory acidosis

A

1) Hypoventilation
2) Asthma
3) COPD = impaired ventilation , ventillation perfusion mismatch leads to hypoxia and hypercapnia = respiratory acidosis
4) Respiratory depressants such as morphine or barbiturates

20
Q

Causes of metabolic alkalosis

4

A

1) Vomiting = loss of stomach acid = alkalosis
2) Hyperaldosteronism =Na+ kept in DCT , collecting duct , H+ secreted = alkalosis
3) Hypovolemia
4) increased antacids
5) Diuretics

10)Hepatocellular dysfucntion = toxins cause metabolic alkalosis

21
Q

causes of metabolic acidosis

4

A

1) Renal tubular acidosis
2) Chronic Kidney disease = failure to secrete acid , and reabsorb HCO3. Hyperkalaemia means K+ increases and H+ is secreted from cells = more acidic = metabolic acidosis treated with bicarbonates

3) Renal tubular acidosis = H+ is not secreted in DCT ,failure to secrete K+ = metabolic acidosis
- TYPE 2: PCT HCO3- is not reabsorbed in the PCT = acidosis

4) Diarrhoea = loss os fluids , loss of bicarbonate = metabollic acidosis
5) Indigestion
6) Hypoaldosteronism = less H+ secretion , more Na+LEAVES = metabolic acidosis ( Na+ /H+ pump function decreases)
7) Diabetic Ketoacidosis
8) Ingestion of acid
9) Intravenous saline (7.0pH) = dilutes bicarbonate , increasing chloride concentration = leads to metabolic acidosis