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year 2 > Nephritic And Nephrotic Syndrome/ PBL B10 W1 > Flashcards

Nephritic And Nephrotic Syndrome/ PBL B10 W1 Flashcards

1
Q

Normal kidney GFR

A

180L of plasma, where 1.5L leaves as urine

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2
Q

How do kidneys affect prostaglandin synthesis?

A

When there is renal hypoperfusion (low kidney blood flow), increased prostaglandin synthesis to increase vasodilation of vessels.

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3
Q

How does increased sympathetic tone of kidneys occur?

A

Activation of renal B1 receptors

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4
Q

What is the HCO3-/CL- antiporter channels?

A

AE2 channels

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5
Q

What is the HCO3-/Na+ symporter channels?

A

NBC1 channel

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6
Q

Where does urea reabsorption occur?

A

Half is absorbed in the PCT and the rest is excreted out in the urine.

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7
Q

When is Na+ secreted into the filtrated?

A

Never

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8
Q

Where does majority of K+ reabsorption occur?

A

PCT

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9
Q

Where does water reabsorption occur?

A

1) PCT
2) Loop of Henle
The rest is reabsorbed in the collecting duct

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10
Q

Nephrogenic diabetes insipidus

A

Excessive urination mistaken for diabetes mellitus- occurs due to ADH deficiency because of lesion in posterior pituitary gland. Or, Mutation in aquaporin channels that leads to excess water loss in urine

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11
Q

When are ANP levels elevated?

A

Released by atrial myocytes in response to atrial distention. Pathologically, increased levels related to heart failure.

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12
Q

When are BNP levels elevated?

A

Released by heart ventricles and brain. Pathologically, increased levels are related to heart failure.

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13
Q

How does ADH affect the kidney?

A

Insertion of aquaporin channels into collecting duct via V2 receptors and permeability of urea. Acts on V1 receptors to cause smooth muscle contraction of blood vessels.

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14
Q

What are the types of primary nephrotic syndromes?

A

Minimal change disease
Focal seggmental glomerulitis
Membranous nephropathy/ Membranoproliferative glomerulonephritis

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15
Q

Effect of ACE

A

Induces arteriole constriction and causes elevation of bradykinin levels

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16
Q

Indication of ACE inhibitor

A

Hypertension
Myocardial infarction
Congestive heart failure
Diabetic nephropathy

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17
Q

Diabetic nephropathy

A

High levels of glucose of blood entering kidneys causes glycation of type 4 collagen in kidney basement membrane in efferent arteriole, causing damage so increased deposition of type 4 collagen occurs. This leads to vasoconstriction of efferent arteriole and increases the GFR, leading to hyperfiltration which results in renal vessel damage. To relieve this, ACE inhibitors induce vasodilation.

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18
Q

Congestive heart failure

A

Failure of the heart in systole that cannot pump hard enough or diastole where the pre-load is low, so ventricles do not fill enough. This may cause blood to back up into the pulmonary arteries and cause dyspnoea, systemic congestion, and higher BP.

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19
Q

Cause of L sided congestive heart failure

A

L sided is caused by ischaemia due to atherosclerosis, hypertension that causes cardiac hypertrophy and narrowing of the arterioles. In response to diastole HF, heart chamber may grow and cause muscles to weaken. L sided causes blood to flow backwards and affect the source in the lungs primarily

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20
Q

Cause of R sided congestive heart failure

A

Right sided heart failure is generally a byproduct of left sided heart failure. It is also caused by chronic lung disease that causes the pulmonary arteries to constrict and create high BP. This leads to systemic congestion in the body, creating pitting oedema and enlarged JVP.

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21
Q

Contraindication of ACE inhibitor

A

Foetal toxicity and co-administering with NSAIDS which will result in decreased GFR

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22
Q

Types of acute kidney injury

A

Pre-renal
Intrarenal
Post renal

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23
Q

Pre-renal AKI

A

Decreased blood flow entering kidneys.
Lower blood volume caused by hypovolemia (blood loss) and haemorrhage or fluid loss via vomiting or skin burns.

Issue with the heart like congestive heart failure means not enough blood is pumped to the kidney.

The vessel itself may be affected such as stenosis or embolism.

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24
Q

What is pre-renal AKI linked to?

A

Generally linked to lower BP, so aldosterone is released to increase H20 and Na+ reabsorption in blood for increasing BP, but this also increases urea uptake, worsening azotaemia.

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25
Q

Intrarenal AKI

A

Issue within the glomerulus
such as:
Acute tubular necrosis
Glomerulonephritis
Vascular diseases
Acute interstitial nephritis

This affects the glomerular integrity and allows large proteins and fluids to leak, reducing GFR and causing oedema, oliguria

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26
Q

Acute tubular necrosis

A

Intrarenal AKI where epithelial cells of tubular cells of nephrons die due to ischaemia caused by pre-renal injury, affecting mainly the PCT and ascending limb. The dead cells build up and create high pressure area, disrupting filtration down pressure gradient, reducing GFR for removing toxic waste like urea and creatinine and generating urine causing oliguria.

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27
Q

Causes of acute tubular necrosis

A

Damage from external factors like contrast dyes for X-rays, aminoglycosides, heavy metal, myoglobin (from damaged muscles) and uric acid. Uric acid is a waste product of cancer cell death in treatment.

28
Q

Acute interstitial necrosis

A

Type 1 or Type 4 hypersensitivity affecting connective tissue of interstitium. Caused by NSAIDS, diuretics or penicillin.

29
Q

Post renal AKI

A

Caused by obstruction to the ureter. Congenital malformations and neurogenic bladder that leads to multiple sclerosis

30
Q

Features of AKI

A

Urea retention as azotemia resulting in uremic frost, neurological symptoms and GI issues. Urea and creatinine levels in the blood are measured in a ratio called BUN. Most of creatinine is excreted in the body but urea levels undergo more regulation in increase and decrease, because it is reabsorbed passively via Na+ and H20 uptake. Urea levels in the blood are higher than creatinine.

31
Q

What happens in post renal AKI?

A

Backflow of fluid and urine, increasing pressure and disrupts the pressure gradient. This reduces GFR and causes retention of urea in the blood because it can’t enter nephron.

32
Q

Nephron categories

A

Short cortical nephrons: majority of all kidney nephrons located in cortex

Juxtamedullary nephrons: located mainly in medulla and have a greater effect at concentrating urine

33
Q

Vasopressin/ADH

A

Produced from the posterior hypophysis and released into circulation in response to low Na+ and H20 levels and increases polypsia. It causes insertion of aquaporin channels in the DCT and collecting duct. Causes vasoconstriction and increase in peripheral resistance.

34
Q

Aldosterone

A

Released via action of angiotensin 2 on adrenal medulla. It acts on the DCT and the principal cells of the collecting duct to increase expression of the Na+/K+ ATPase pump. Also increases expression of Na+ channels.

35
Q

Nephrotic syndrome

A

Damage to the podocytes of the glomerulus which results in the loss of proteins into the urine which becomes frothy. Proteins leak into urine filtrate causing hypoalbumeniemia. This induces increased liver production of proteins which increases lipid levels as a byproduct, causing hypercholesterolemia. The loss of albumin disrupts oncotic pressure and leads to peripheral oedema.

36
Q

Cause of nephrotic syndrome

A

Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy
Diabetes mellitus
Amyloidosis

37
Q

Common cause of nephrotic syndrome in children

A

Minimal change disease: commonly occurs after viral infection, with cytokine mediated damage of podocyte foot processes, disrupting protein retention. There is sudden onset and sudden offset and this disease is responsive to steroids.

38
Q

Most common cause of primary nephrotic syndrome in adults

A

Focal segmental glomerulosclerosis which is when there is gradual scar tissue formation on glomerular capillary membrane due to external factors such as infection or drug use leads to IgG mediated loss of podocyte foot processes. Primary cause is idiopathic with secondary cause related to

39
Q

Membranous nephropathy

A

Autoimmune condition where there is subepithelial immune complex deposition between podocytes and basement membrane, involving IgG antibody. In idiopathic, the target is the phospholipase A2 receptor within the podocytes. This can result in renal vein thrombosis due to the loss of anti-thrombin which would be bound to heparin.

40
Q

What is a risk of membranous nephropathy?

A

Renal vein thrombosis- this occurs due to hypoalbuminemia because albumin binds to heparin. There is also loss of anti-thrombin.

41
Q

Why is albumin important in clotting?

A

Albumin is a carrier for anti-thrombin and heparin cofactor which regulate clotting. This leads to excess clotting in blood and thrombosis.

42
Q

Membranoproliferative glomerulitis

A

Membranous nephropathy caused by immune complex deposition; It can manifest as nephrotic or nephritic syndrome. It is typically caused by lupus or chronic inflammation.

43
Q

What is type 1 membranoproliferative glomerularitis?

A

Immune complex deposition occurs in the subendothelium, between the podocytes and glomerular basement membrane. It is associated with hepatitis B and C and is a Nephrotic and nephritic condition.

44
Q

What is type 2 membranous membranoproliferative glomerulitis?

A

Immune complex deposition within the glomerular basement membrane and there is over activation of the complement cascade via C3 convertase. Nephrotic and nephritic condition.

45
Q

No proteinuria in membranoproliferative glomerulitis

A

Nephritic membranoproliferative glomerulitis

46
Q

Proteinuria in membranoproliferative glomerulitis

A

Nephritic- nephrotic membranoproliferative glomerulitis

47
Q

What is the secondary cause of nephropathy?

A

Diabetic nephropathy
Sytemic lupus
Amyloid nephropathy

48
Q

Most common primary nephropathy in elderly patients

A

Amyloid nephropathy: deposition of abnormal proteins called amyloid in the kidney interstitium arteries, arterioles and mesangium. Multiple myeloma which is cancer of the bone marrow can lead to amylodosis due to mutation of light chains of antibodies.

49
Q

Primary amyloid nephropathy

A

Inability to degrade antibodies which is idiopathic

50
Q

Secondary amyloid nephropathy

A

Caused by chronic inflammatory conditions

51
Q

Presentation of glomerulonephritis

A

Loss of proteins in urine such as antithrombin, protein C and S which increases hypercoagubility so increased thrombosis and embolus
Hypertension
Loss of immunogoblins
Hypercholesterolemia
Sytemic oedema

52
Q

What is nephritic syndrome?

A

Inflammation of the glomerulus which becomes hypercellular, characterised by haematuria, lesser proteinuria and anaemia. As kidney worsens over time, leads to hypertension, azotemia and oliguria

53
Q

Nephritic syndrome

A

Post streptococcal glomerunephritis
IgA nephropathy
Small vessel vasculitis
Goodpasture syndrome
Alport syndrome
Membranoproliferative glomerulonephritis

54
Q

Post-streptococcal glomerulonephritis

A

Occurs after infection with streptococcus pyogenes with subepithelial immune complex deposition in the glomerulus.

55
Q

Nephritic syndrome-presentation

A

Oliguria with haematuria,
Lesser Proteinuria associated with oedema.
Kidney function deteriorates causing hypertension: due to Na+ and H20 retention
azotemia
oliguria

56
Q

What is IgA nephropathy?

A

Deposits of IgA in the kidney which can occur a few days post-infection and result in alveoli bleeding and glomeruli bleeding. It is a nephritic syndrome and the most common chronic glomerulonephritis in children

57
Q

When does H+ secretion stop?

A

Urine pH falls below 4.5

58
Q

Where is the majority of buffering capacity in the body?

A

1) Cells perform 52%
2) EC space 43%
3) RBC

59
Q

What are the features of chronic kidney disease?

A

Hypertension, peripheral oedema, uraemia and loss of mineral bone density.

60
Q

What are the features of uraemia?

A

Fatigue, loss of appetite, anaemia, GI symptoms, increased infection risk and encephelopathy.

61
Q

Polycystic kidney disease

A

Genetic disease charactersied by the formation of cysts in the tubular epithelia which causes dysfunction and reduces GFR.

62
Q

How does polycystic kidney disease present?

A

Begins as asymptomatic but may progress and cause
Hypertension
Hameaturia
Fullness in abdomen
Polyuria

63
Q

Goodpasture syndrome

A

Type 2 hypersensitivity that is IgG mediated against the glomerular basement membrane which causes bleeding. It is a nephritic syndrome and also presents with haemoptysis because it targets the type 2 collagen in alveoli.

64
Q
A
65
Q

What is diffuse proliferative glomerulonephritis?

A

Subendothelial immune complex deposition which results in thickening of capillary wall and presents with symptoms of nephrotic AND nephritic syndrome.

66
Q

What is Alport syndrome?

A

Nephritic syndrome where there is mutation of type 4 collagen in the glomerular basement membrane which also presents with damage to the eyes with cataracts and sensineural deafness.

67
Q

What is the lining of the kidney?

A

Epithelium of fenestrated endothelium
Connective tissue of the glomerular basement membrane which is negatively charged to repel proteins
Podocytes which have foot processes

year 2 (247 decks)

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