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6-11 ENDOCRINE RENAL > Anatomical pathology > Flashcards

Anatomical pathology Flashcards

1
Q

General approach to endocrine and metabolism disorders

A

Recognise/think of possibility of endocrine disorder

Confirm quantitatively with testing

Investigate cause

Manage

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2
Q

Functions of endocrine organs

A

Growth, reproduction, energy metabolism, stress responses, electrolyte and water handling, mineral metabolism

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3
Q

Common symptoms in endocrine disorders

A
  • weight change
  • lethargy
  • BP high or low
  • fractures
  • electrolyte/mineral changes
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4
Q

Clinical consequences of pituitary pathology

A

Mechanical:

  • raised ICP
  • bony erosion
  • local pressure

Altered hormonal secretion:

  • hyperpituitarism
  • hypopituitarism
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5
Q

Hypopituitarism

A

Inadequate functional tissue
• Absence or destruction of pituitary Bssue
e.g. injury, ischaemia, infec/on, pressure from adjacent tumour,
Rathke’s cleA cyst, trauma, previous surgery or radiotherapy
• Sheehan’s syndrome: post partum hypopituitarism (enlarged ant pit during pregnancy, intra or post partum haemorrhage leads to ischaemia of pituitary)
• Simmond’s syndrome: hypopituitarism due to other causes

Lack of stimulus driving secreBon (e.g. hypothalamic disease)
Hyperfunc/on of one product may be associated with Hypofunc/on of others (as a result of ‘pressure’ atrophy), and pituitary hypofuncBon leads to secondary hypofuncBon of pituitary dependent endocrine glands (through feedback inhibiBon).

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6
Q

Hyperpituitarism

A 
•  Excess secretion of trophic hormones
•  Can be caused by:
– Pituitary adenoma
– Secondary hyperplasia
– Pituitary carcinoma (rare)
– Secretion of hormones by non-pituitary tumours – Hypothalamic disorders
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7
Q

Posterior pituitary syndromes

A

(1) Diabetes insipidus: passage of large volumes of dilute urine
2 main forms:
- central - decreased ADH secretion
- nephrogenic - ADH resistance in the kidney

(2) Syndrome of inappropriate ADH secretion
- resorption of XS amounts of water
- usually caused by ectopic ADH secretion

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8
Q

Clinical consequences of thyroid disease

A

Mechanical
• Thyroid enlargement = ‘goitre’ (unilateral, bilateral, localised, diffuse), usually not painful
• Compression effects (airway, oesophagus, large vessels, nerves)

Functional
• Hyperthyroidism
• Hypothyroidism
• Euthyroid

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9
Q

Examples of hyper plastic, neoplastic and inflammatory thyroid pathologies

A

Hyperplasia
– Diffuse / Graves (Autoimmune)
– Mul2nodular goitre / Nodular colloid goitre

Neoplasia
– Adenomas
• Follicular/HurthleCell/Other – Carcinomas
• Papillary/Follicular/Anaplastic/Medullary

Inflammatory
– Hashimoto (Autoimmune)
– Lymphocytic, Granulomatous (De Queryvain)

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10
Q

Cause of hypothyroidism

A

Defect anywhere in the hypothalamic-pituitary-thyroid axis

  • iodine deficiency
  • thyroiditis (hashimoto’s, lymphocytic)

Children: cretinism (iodine deficiency usually)
Adults: myxoedema (TSH raised if normal feedback inhibition is lost)

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11
Q

Hashimoto’s thyroiditis

A

Autoimmune disease - anti-TPO found

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12
Q

Symptoms and signs of hyperthyroidism

A

Symptoms:
– Nervousness, Anxiety, Increasedperspiration, – Heat intolerance, Hyperactivity,
– Palpitations

Signs
– Tachycardia or atrial arrhythmia
– Systolic hypertension with wide pulse pressure
– Warm, moist, smooth skin
– Lid lag
– Stare
– Hand tremor
– Muscle weakness
– Weight loss despite increased appetite (although a few patients may gain weight, if excessive intake outstrips weight loss)
– Reduction in menstrual flow or oligomenorrhea

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13
Q

Most common causes of hyperthyroidism

A
  • Grave’s disease
  • Multi nodular goitre (hyper functional)
  • thyroid adenoma (hyper functional)
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14
Q

Grave’s disease antibodies and diagnosis

A

Auto-antibodies against TSH receptor and other thyroid antibodies

  • presence of these antibodies indicates Grave’s
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15
Q

Actions of PTH

A

Bone resorption
Renal tubular resorption of calcium
Increases conversion of Vit D to active (hydroxy) form in kidney
With Vitamin D, promotes calcium resorption from small intestine
Increases urinary phosphate excretion causing phosphaturia
Net effect is to increase serum calcium

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16
Q

Common cause of chronic hypocalcaemia

A

Usually due to chronic renal failure, vitamin D deficiency, drugs or intestinal malabsorption of calcium

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17
Q

Signs/symptoms of hypocalcaemia

A

Convulsions, arrhythmias, tetany, numbness and parasthesia, cramps, fatigue, depression, altered cognition

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18
Q

Most common causes of hypercalcaemia and clinical manifestations

A
  • hyperparathyroidism
  • hypercalcaemia of malignancy - adenoma

Clinical - renal stones, bones (pain, arthritis), groans (confusions, lethargy, weakness) and moans (nausea, vomiting, weight gain or anorexia, pain)

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19
Q

4 Classifications of hyperparathyroidism

A

Primary HP: XS PTH production

Secondary HP: other disease process drives increased PTH levels

Tertiary HP: autonomous PTH secretion, caused by longstanding secondary HP

Ectopic secretion - paraneoplastic from other malignancies

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20
Q

MEN syndromes in endocrine disorders

A

MEN-1 - loss of tumour suppressor gene, primary hyperparathyroidism (adenoma or hyperplasia)

MEN-2 - medullary thyroid carcinoma is main manifestation, usually due to RET protocol-oncogene mutation

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21
Q

6 types of cells in the Islet’s of Langherans and their function

A
  • β – Insulin (regulates glucose in tissues, reduces blood glucose)
  • α - Glucagon (stimulates glycogenolysis in the liver, increases blood sugar)

• δ – Somatostatin (suppresses both insulin and glucagon release)

• PP – secretes pancreatic polypeptide (stimulates gastric and intestinal enzymes and inhibits intestinal motility)
– Also
• D1 – Vasoactive intestinal polypeptide (VIP), induces glycogenolysis and hyperglycaemia

• Enterochromaffin cells – Serotonin

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22
Q

Diagnosis criteria for Diabetes

A
  1. Fasting plasma glucose ≥ 126 mg/dL,
  2. Random plasma glucose ≥ 200 mg/dL (in a patient with classic hyperglycemic signs),
  3. 2-hour plasma glucose ≥ 200 mg/dL during an oral glucose tolerance test (OGTT) with a loading dose of 75 gm
  4. Glycated hemoglobin (HbA1C) level ≥ 6.5%
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23
Q

Clinical presentation of T2DM vs T1

A

T1: indolent onset (years) but sudden presentation (decompensation)
Polyuria, polydipsia, polyphagia, subsequently DKA
T2: unexplained fatigue, dizziness, blurred vision, often asymptomatic and may become hyperosmolar non-ketotic state

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24
Q

Pathogenesis of T1DM

A

¥ Develops in childhood, manifests at puberty, progresses with age

¥ Without exogenous insulin patients become ketotic → coma → death

¥ Interplay of genetics (esp HLA-DR3 or HLA-DR4) and environment (still unclear)

¥ β cell destruction follows loss of self tolerance for T cells specific islet antigens (insulin receptor, GAD, others)
o Autoreactive T cells are not removed
o Are able to attack islets

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25
Q

Pathogenesis of T2DM

A

¥ Interplay of genetics (multiple loci, all small to moderate increase in risk) and environment (central/visceral obesity, sedentary lifestyle)

¥ Develops in adulthood, slow progression, initially high insulin but peripheral insulin resistance, later low insulin due to β cell dysfunction

¥ Insulin sensitivity decreases due to

o Free fatty acids

o Adipokines (secreted by adipocytes)

o Inflammation (pro-inflammatory cytokines secreted in response to nutrient excess)

¥ This results in β cell dysfunction develops later as cells exhaust their capacity to increase secretion

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26
Q

Two scenarios of gestational diabetes

A

o Patients with pre-existing DM may become pregnant

o Pregnancy may result in impaired glucose tolerance

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27
Q

Acute consequence more common in T1DM

A

DKA - insufficient insulin

Causes hyperglycaemia, osmotic diuresis and dehydration
Activates ketogenic pathway
Fatigue, nausea, vomiting, abdo pain, ketotic breath, laboured breathing, coma

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28
Q

Acute consequence more common in T2DM

A

Hyperosmolar hyperosmotic state: severe dehydration due to severe osmotic diuresis due to hyperglycaemia

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29
Q

Chronic conséquences of diabetes

A

Microvascular complications
Macrovascular complications
Predisposition to infection
Diabetic nephropathy

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30
Q

Macroangiopathy associated with diabetes

A
  • accelerated atherosclerosis involving aorta + medium sized vessels
  • widespread hyaline atherosclerosis
  • MI most common cause of death
  • gangrene of legs 100x more common in diabetics
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31
Q

Microangiopathy associated with diabetes

A
  • diffuse thickening of basement membrane of capillaries
  • in skin, muscles, retina, glomerulus
  • poor wound healing
  • underlies complications including diabetic nephropathy, retinopathy and some neuropathies
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32
Q

Aetiology of bladder cancer

A
  1. Cigarette smoking
  2. Occupational exposure; eg: aniline dyes
  3. Phenacetin
  4. Drugs such as cyclophosphamide, exposure to radiation
  5. Chronic infections
    b. Schistosoma Haematobium - Squamous cell carcinoma. Recurrent UTI, Calculi etc.
  6. Arsenic
  7. Genetic alterations: chromosome 9 monosomy or deletions of 9p and 9 q as well as deletions of 17p, 13q, 11p and 14q. Second pathway – p53 mutations.
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33
Q

Clinical features of bladder cancer

A
  • Painless gross haematuria.
  • Clotting and painful micturition
  • Dysuria, urgency and frequency.
  • Hydronephrosis
  • Palpable pelvic mass, lower extremity oedema
  • Weight loss, abdominal or bone pain.
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34
Q

Imaging used to diagnose bladder cancer

A

US, IVU, CT, MRI; used for detection and staging

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35
Q

TNM classification

A

¥ Ta – non invasive papillary carcinoma

¥ Tis – carcinoma in situ

¥ T1- invades subepithelial connective tissue

¥ T2- invades muscle; T2a- superficial muscle, T2b- deep muscle

¥ T3 – invades perivesical tissue T3a – microscopically
T3b – macroscopically

¥ T4 – invades prostate, uterus, vagina (T4a), pelvic wall, abdominal wall (T4b).

¥ N – Regional lymph nodes.

¥ N1- metastasis in I LN 2cm or less in greatest dimension.

¥ N2 - >2cm but <5cm in one or multiple LNs.

¥ N3 - >5cm.

¥ M – Distant metastasis.

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36
Q

Grading of urothelial tumours

A

¥ Urothelial papilloma
¥ Urothelial neoplasm of low malignat potential
¥ Papillary carcinoma, low grade
¥ Papillary carcinoma, high grade

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37
Q

Treatment for localised papillary low grade tumour

A

Transurethral resection

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38
Q

Treatment for high grade papillary tumours, multifocal, rapid recurrence

A

Intravesical BCG therapy

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39
Q

Treatment for tumour invading muscularis propria, extending to prostatic urethra/ducts

A

Radical cystectomy

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40
Q

Difference between invasive and non invasive urothelial tumours

A

Invasive - invades the lamina propria/muscularis propria

Non-invasive is limited to the epithelium

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41
Q

Grading of urothelial tumours - 4

A

¥ Urothelial papilloma
¥ Urothelial neoplasm of low malignant potential
¥ Papillary carcinoma, low grade
¥ Papillary carcinoma, high grade

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42
Q

Benign tumours of the kidney

A

¥ Renal papillary adenoma

¥ Renal fibroma or Hamartoma

¥ Juxtaglomerular cell tumour

¥ Angiomyolipoma

¥ Oncocytoma

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43
Q

Malignant tumours of the kidney

A

¥ Renal cell carcinoma: Clear cell renal cell carcinoma, papillary carcinoma, Chromophobe renal carcinoma, Collecting duct carcinoma, renal medullary carcinoma, Xp11translocation carcinoma, mucinous tubular and spindle cell carcinoma, multilocular clear cell renal cell carcinoma.

¥ Nephroblastoma

¥ Mesenchymal tumours – children and adults.

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44
Q

Clinical features for kidney tumours

A

¥ Haematuria

¥ Pain

¥ Flank mass

¥ Paraneoplastic syndromes: polycythemia, hypercalcemia etc

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45
Q

Most common renal tumour in childhood

A

Nephroblastoma

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46
Q

Which tumours arise from the renal tubular epithelium?

A

Renal papillary adenoma and renal cell carcinoma

47
Q

TNM staging of renal cell carcinoma

A

TNM staging:
T1- 7cm or less confined to kidney,
T2 - >7cm limited to kidney, T3 – extends into major veins, directly invades adrenal gland or perinephric tissue,
T4- invades beyond Gerota fascia.

48
Q

Classification of renal disease (3)

A
  1. Glomerulonephritis
  2. Tubulointerstitial diseases
  3. Vascular diseases of the kidney
49
Q

Clinical presentation of renal disease

A 
¥	Acute renal failure 
¥	Chronic renal failure 
¥	Nephritic syndrome – rapidly progressive glomerulonephritis 
¥	Nephrotic syndrome 
¥	Asymptomatic urinary abnormalities
50
Q

What is acute renal failure characterised by?

A

¥ Azotaemia/uraemia
o Rapid rise in serum urea/creatinine
o Over days to week
o Renal function more reliably assessed by estimated GFR

Often with oligonuria/anuria
It may resolve or progress to chronic renal failure

51
Q

Characteristics of chronic renal failure

A

¥ Gradual persistent and progressive rise in serum urea/creatinine for months to years
¥ Accompanied by symptoms and signs of renal dysfunction
¥ Eventual progression to end stage renal failure requiring dialysis/transplantation

52
Q

Clinical manifestations of renal dysfunction

A 
¥	Lethargy 
¥	Anorexia 
¥	SOB
¥	Peripheral neuropathy 
¥	Oedema
53
Q

What is nephritic syndrome?

A 
¥	Azotaemia/uraemia – elevated serum urea and creatinine
¥	Oliguria 
¥	Haematuria 
¥	Mild to moderate proteinuria
¥	Hypertension 
¥	Usually due to glomerulonephritis
54
Q

What might urinalysis show for asymptomatic urine abnormalities

A 
¥	Microscopic proteinuria
¥	Microscopic haematuria
¥	Leucocytes 
¥	Glucosuria 
¥	Nitrites
55
Q

Classification of glomerulonephritis

A

Primary - no identifiable cause

Secondary - drugs, infections, AI, malignancy

56
Q

What is benign nephrosclerosis?

A

Chronic hypertension
BP >140/90
Primary essential HTN
Secondary HTN

57
Q

What is malignant nephrosclerosis

A

Accelerated HTN
Malignant HTN
- BP >180/110
- Acute end organ damage

58
Q

Pathogenesis of benign hypertensive nephrosclerosis?

A

Thickening of small arteries and arterioles. Ischaemic damage to glomeruli and tubules

59
Q

Pathogenesis of malignant hypertensive nephrosclerosis

A

Severe damage to small arteries and arterioles, ischaemic injury to glomeruli and tubules

Medical emergency - urgent but controlled reduction in BP

60
Q

What is renal artery stenosis?

A

Usually unilateral critical narrowing of main renal artery due to atheromatous disease in elderly
Results in ischaemic damage to glomeruli and tubules
Can be a cause of secondary hypertension

61
Q

What is thrombotic microangiopathy?

A

Uncommon condition characterised by widespread thrombosis or arterioles and capillaries due endothelial damage or platelet activation

3 main types:

  1. haemolytic uraemia syndrome
  2. Atypical haemolytic uraemia syndrome
  3. Thrombotic thrombocytopenia purpura
62
Q

3 phases of acute tubular necrosis

A
  1. initiation phase: mild oliguria with mild increase in serum creatinine
  2. Maintenance phase: sustained oliguria, rising serum creatinine with uraemia
  3. Recovery phase: massive diuresis with electrolyte disturbance
63
Q

What is chronic pyelonephritis?

A

Chronic inflammation and scarring centred on renal calyces, pelvis and tubulointerstitium

64
Q

Renal complications of myeloma kidney

A
  • cast nephropathy
  • amyloidosis
  • light chain deposition disease
  • acute tubular necrosis
  • renal vein thrombosis
65
Q

Clinical syndromes associated with hypo and hyper function of ACTH

A

Cushings disease and hyoadrenalism

66
Q

Clinical syndromes associated with hypo and hyper function of FSH and LH

A

Hyper - often silent, maybe testicular enlargement or menstrual abnormalities, infertility

Hypo - hypogonadism

67
Q

Clinical syndromes associated with hypo and hyper function of growth hormone

A

Hyper - acromegaly

Hypo - mild can have decreased muscle mass, severe may show dwarfism

68
Q

Clinical syndromes associated with hypo and hyper function of thyroid stimulating hormone

A

Hyperthyroidism (rare)

Hypothyroidism

69
Q

Clinical syndromes associated with hypo and hyper function of PRL

A

Hyperprolactinaemia

Hypo - amenorrhoea, impotence

70
Q

Clinical syndromes associated with hypo and hyper function of ADH

A

Hyper - SIADH

Hypo - diabetes insipidus

71
Q

What is diabetes insidious?

A

Passage of large volumes of dilute urine. The kidney is unable to resorb water from the urine. Thirst and polydipsia present and risk of dehydration. Due to reduced ADH secretion (central) or ADH resistance (nephrogenic).

72
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion: resorption of XS amounts of water resulting in hyponatremia, cerebral edema.

Usually caused by ectopic ADH secretion from small cell lung carcinoma

73
Q

3 most common causes of hyperthyroidism

A

Graves - diffuse hyperplasia
Hyperfunctional MNG
Hyperfunctional thyroid adenoma

74
Q

How might older and younger patients present with hyperthyroidism?

A

Younger - sympathetic activation

Older - more cardiovascular symptoms - dyspnea, AF, weight loss

75
Q

What commonly causes nodular colloid goitre (early stages)?

A

Iodine deficiency

76
Q

What cells release which hormone in response to low calcium serum levels?

A

Chief cells in the parathyroid hormone release parathyroid hormone

77
Q

Actions of PTH

A

¥ Bone resorption
¥ Renal tubular resorption of calcium
¥ Increases conversion of Vit D to active (hydroxy) form in kidney
¥ With Vitamin D, promotes calcium resorption from small intestine
¥ Increases urinary phosphate excretion causing phosphaturia
¥ Net effect is to increase serum calcium

78
Q

Organs affected in MEN-1 (Wermer’s syndrome)

A

Parathyroid: primary hyperparathyroidism
Pancreas: NET
Pituitary: prolactinomas

79
Q

Main manifestation in MEN-2 syndrome

A

Thyroid medullary carcinoma

80
Q

Microvascular and microvascular complications of diabetes

A

Macro: atherosclerosis, ischaemic heart disease, cerebrovascular disease, peripheral vascular disease

Micro: retinopathy, nephropathy, neuropathy

81
Q

What is crescentic glomerulonephritis and its importance?

A

Medical emergency

Filling of the Bowmans’s space by proliferation of parietal epithelial cells

82
Q

What might be seen on LM, IF and EM in membraneous nephropathy? and how might the patient present?

A

LM: thickened BM with spikes
IF: capillary loop IgG + C3
EM: Subendothelial deposits with spikes
Present: nephrotic syndrome

83
Q

What might be seen on LM, IF and EM in IgA nephropathy? and how might the patient present?

A

LM: Mesangiopathic
IF: IgA mesangial deposition
EM: mesangial immune deposits
Present: nephritic syndrome

84
Q

What might be seen on LM in acute tubular necrosis? and how might the patient present?

A

Dehydration leading to acute renal failure

LM: tubular injury/necrosis

85
Q

What might be seen on histology in benign hypertensive nephrosclerosis? and how might the patient present?

A
  • Arteriosclerosis of intima
  • hyperplasia of media
  • hyalinosis of arteriole due to leakage of plasma proteins due to HTN
  • Tubular atrophy and interstitial scarring

Present: chronic renal failure and hypertension

86
Q

What types of glomerulonephritis might nephrotic syndrome be associated with?

A

Minimal change disease
Focal segmental glomerulosclerosis
Membraneous nephropathy

87
Q

What types of glomerulonephritis is nephritic syndrome associated with?

A

Membrano proliferative/mesangiocapillary
Post infectious glomerulonephritis
IgA nephropathy

88
Q

What is benign hypertensive nephrosclerosis?

A

BP > 140/90
Thickening/sclerosis of small arteries and arterioles
Resulting in ischaemic damage to glomeruli and tubules
Presentation: chronic renal failure

89
Q

What is malignant hypertensive nephrosclerosis?

A

BP > 180/110
Severe damage to small arteries and arterioles requiring urgent but controlled reduction in blood pressure
Results in ischaemic injury to glomeruli and tubules
Presentation: acute renal failure

90
Q

3 main types of thrombotic microangiopathy

A
  1. haemolytic uraemic syndrome - E coli
  2. thrombocytopenic purpura - autoantibodies to ADAMTS-3
  3. atypical haemolytic uraemic syndrome
91
Q

What is thrombotic microangiopathy?

A

Widespread thrombosis of arterioles and capillaries due to endothelial damage or platelet activation

92
Q

Most common cause of acute renal failure

A

Acute tubular necrosis: tubular injury/necrosis due to ischaemia or toxins

93
Q

What is tubulointerstitial nephritis?

A

Tubulointerstitial inflammation due to various causes

  1. Acute - interstitial edema, neutrophilic infiltrate
  2. Chronic - lymphocyte infiltrate with tubular atrophy and fibrosis

Immune mediated

94
Q

What is chronic pyelonephritis?

A

Chronic inflammation and scarring centred on renal calyces, pelvis and tubulointerstitium
2 Main clinical settings:
1. reflux nephropathy
2. obstructive nephropathy

95
Q

What is myeloma kidney?

A

Medical emergency

Widespread tubular obstruction by intraluminal light chain casts causing acute renal failure

96
Q

Causes of hyperprolactinaemia

A

Prolactinoma, hyperplasia, head trauma or mass effect

Stalk compression - due to reduced dopamine from hypothalamus

97
Q

Cause of hypothyroidism in infancy/childhood

A

Cretinism: endemic iodine deficiency

98
Q

Pathology of T1DM vs T2DM

A

1: insulitis infiltrate of T cells and macrophages, beta cell depletion and islet atrophy
2: no insulitis, amyloid deposition in islets, mild beta cell depletion

99
Q

What are the following functional syndromes:

  1. Hyperinsulinism
  2. Zolligner Ellison syndrome
A
  1. Hyperinsulinism
    Usually benign, result in episodic hypoglycaemia
  2. Zolligner Ellison syndrome
    Results in XS gastrin secretion leading to severe peptic ulceration with possible diarrhoea
100
Q

Which renal stones are likely to form after infection with urea-splitting bacteria - klebsiella or proteus?

A

Struvite stones - magnesium ammonium phosphate

101
Q 
What do these terms mean in relation to glomerulonephritis: 
Focal
Diffuse
Segmental
Global
A

Focal: <50% of ALL glomeruli
Diffuse: >50% of ALL glomeruli
Segmental: <50% of individual glomerulus
Global: >50% of individual glomerulus

102
Q

Acute consequences of T1 and T2DM

A

Type 1
DKA: insufficient insulin leads to hyperglycaemia which causes osmotic diuresis and dehydration. This activates the ketogenic pathway whereby there is increased fat breakdown and ketone bodies as a by product. If urinary excretion is compromised = systemic ketoacidosis

Type 2
Hyperosmolar, hyperosmotic state
Severe dehydration due to severe osmotic diuresis as a result of hyperglycaemia (absence of ketosis)

103
Q

Zolinger Ellison syndrome

A

XS gastrin secretion by gastrinoma of pancreas, duodenum, stomach
= severe peptic ulceration and diarrhoea
- half malignant
- 25% associated with MEN1 syndrome

104
Q

Hyperinsulinism

A

Episodic hypoglycaemia may be precipitated by exercise or fasting, relived by glucose

105
Q

Types of crescentic glomerulonephritis

A
  1. antiglomerular membrane disease - A/B to a3 chain of type 4 collagen in GBM
  2. Immune complex mediated GM (SLE) -ANA
  3. Paul glomeruloneprhitis - ANCA
106
Q

Vasculitis associated with Pauci glomerulonephritis

A
  1. Wegener’s granulomatosis: tried of necrotising granulomatous inflammation of upper + lower resp tract and kidney
  2. Churg-Strauss syndrome: similar to Wegener with asthma and peripheral eosinophilia
  3. Microscopic polyangitis: widespread small vessel vasculitis in multiple organs
107
Q

Acute tubular necrosis

A

Most common cause of acute renal failure
Due to: ischaemia or toxins
Causes tubular injury/necrosis - dead cells plug the tubule and raise pressure = reduced GFR and present with brown casts

108
Q

Clinical course/3 phases of acute tubular necrosis

A
  1. initiation - mild oliguria with mild increase in serum creatinine
  2. maintenance - sustained oliguria, rising serum creatinine with uraemia
  3. recovery phase - massive diuresis with electrolyte disturbances
109
Q

Acute vs chronic tubulointerstitial nephritis

A

Acute: interstitial deem with neutrophilic/eosinophilic infiltrate
Chronic: lymphocytic infiltrate with tubular atrophy and interstitial fibrosis

110
Q

Aetiology of tubulointerstitial nephritis

A 
Drugs - NSAIDS, PPI, a/b
Infections
Metabolic - urate, calcium, oxalate
Vascular diseases 
Malignancy
111
Q

Clinical presentation of tubulointerstitial nephritis

A

Fever, peripheral eosinophilia, rash, mild proteinuria, eosinophils in urine and acute renal failure

112
Q

Two main clinical settings of chronic pyelonephritis

A
  1. Reflux nephropathy

2. obstructive nephropathy

113
Q

Renal complications of myeloma kidney (malignant clinical proliferation of plasma cells)

A 
Cast nephropathy 
Amyloidosis
Light chain deposition 
Acute tubular necrosis 
Renal vein thrombosis

6-11 ENDOCRINE RENAL (7 decks)

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