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Urinary > Session 7 > Flashcards

Session 7 Flashcards

1
Q

What is CKD

A

A progressive deterioration of renal function over months to years

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2
Q

Features of CKD

A

Measured by eGFR

Usually irreversible, as renal tissue is replaced by extracellular matrix in response to damage

Deterioration can be slowed with treatment

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3
Q

How do you stage eFGR

A

Using eGFR or Albuminuria

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4
Q

stages for eGFR staging of CKD

A
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5
Q

Stages for Albuminuria staging of CKD

A
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6
Q

Treatments for proteinuria

A

Gives ace inhibitors or angiotensin receptor blockers

ACI/ARB

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7
Q

How does diabetes lead to hyper filtration

A

Diabetes = high amounts of glucose reabsorbed, coupled with sodium

Less Na+ in tubule, less Na+ delivered in macula densa, activates RAAS,

renin increases, aldosterone increases, BP increases

Over time causes damage to glomerular capillaries and capillary bed

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8
Q

First clue that diabetes is causing hyperfiltration

A

micro Albuminuria

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9
Q

How do we manage blood pressure in CKD

A

Anti-hypertensives
Diuretics
Fluid restriction

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10
Q

Blood pressure targets in CKD

A
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11
Q

Causes of primary CKD

A
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12
Q

Causes of secondary CKD

A
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13
Q

Leading causes of CKD and end stage renal failure

A

Diabetes mellitis

(Also hypertension)

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14
Q

What is the best way to monitor diabetes control in someone with poorly controlled T2DM and CKD

A

Fasting plasma glucose

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15
Q

What is HbA1c

A

Glycosylated Hb

RBC lifespan 120 days so good to assess long term control

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16
Q

When is HbA1c not a good test

A

Anaemia due to CKD due to not enough EPO

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17
Q

What do we need to correct anaemia related to CKD

A

EPO (supplements and potentially dialysis)
And Iron

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18
Q

Patient with CKD found to have bilateral crackles on lungs and pitting oedema to shins is indicative of

A

Fluid overload secondary to CKD

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19
Q

Most appropriate diuretic for fluid overload secondary to CKD

A

A loop diuretic

That inhibits the Na+ K+ 2Cl- co transporter in LoH

Use bigger doses of loop diuretics in CKD

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20
Q

How does impaired renal function impact calcium homeostasis

A

impaired mineralisation of bone , increased bone resorption, increased PTH, increased osteoclastic activity and hence bone resorption

Decreased calcium absorption, decreased plasma calcium, stimulation of parathyroid glands leading to hyperplasia

These 2 factors together lead to increased plasma phosphate and decreased phosphate excretion

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21
Q

X ray signs of impaired renal function impacting calcium homeostasis

A

Non-bone calcification

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22
Q

Ureamia symptoms

A
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23
Q

Features of RRT

A

End stage renal failure

Renal replacement therapy

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24
Q

How does haemodialysis work

A
25
Q

Haemodialysis pros and cons

A
26
Q

Peritoneal dialysis pros and cons

A
27
Q

How does peritoneal dialysis work

A
28
Q

How does renal transplant work

A
29
Q

Regulatory impacts of CKD

A

RAAS to manage fluid overload

Reabsorption of different electrolytes

Acid base balance

30
Q

Excretory impacts of CKD

A

Phosphate and potassium not well excreted

Unable to excrete fluid: become fluid overloaded

31
Q

Endocrine impacts of CKD

A

EPO, vit D activation

32
Q

What is glomerulonephritis GN

A

Inflammation of glomeruli

Often involves immune system

33
Q

4 structures in glomerulus that can be damaged

A

Capillary endothelium
Glomerular basement membrane
Mesangial cells
Podocytes

34
Q

What is nephrotic vs nephritic syndrome

A
35
Q

Main characterises of nephrotic syndrome

A

Triad of:
- Proteinuria >350mg/mmol (3.6g in 24 hrs)
- Hypoalbuminaemia
- Oedema

usually accompanied by high cholesterol

36
Q

Other features in nephrotic syndrome

A

BP often normal (can be low or high)

Creatinine may be normal

Proteinuria > 350mg/mmol alone = nephrotic range proteinuria

37
Q

Causes of primary renal disease / nephrotic syndrome e

A

Minimal change disease

membranous glomerulonephritis

Focal segmental glomerulosclerosis FSGS

38
Q

Causes of secondary renal disease / nephrotic syndrome

A

Diabetes is most common

39
Q

What is diabetes nephropathy

A

Leading cause of end stage renal disease

XS glucose in blood binds to proteins especially at efferent arteriole

Hyaline atherosclerosis obstructs blood flow

40
Q

Effect of diabetic neuropathy on GFR

A

Initially increase GFR, over time mesangial cells secrete more
structural matrix.

Thickening of basement membrane, GFR decreases

41
Q

Treatment of diabetic nephropathy

A

Control Hypertension, good glycemic control, ACE inhibitors, angiotensin receptor blockers

42
Q

What is minimal change disease

A

Most common cause of nephrotic syndrome in children under 6

Impacts podocytes, facial oedema presentation

No significant renal changes are seen under light microscope

Prognosis good in children, variables with adults

43
Q

What is membranous glomerulonephritis

A

Subepithelial deposition of immune complexes (antibody-antigen complexes)

Thickening of basement membrane

Albumin can leak out of capillaries

40% adult nephrotic syndrome

44
Q

Treatment for membranous glomerulonephritis

A

Immunosuppressants, treatment of underlying cuase

45
Q

What is Focal segmental glomerulosclerosis FSGS

A

Podocytes damaged

proteins build up in glomerulus- hyalinosis (glassy)- leading to sclerosis

46
Q

Causes of FSGS

A

Primary: idiopathic
Secondary: sickle cell disease, HIV, heroin abuse, kidney hyperperfusion

47
Q

Treatment for FSGS

A

Steroids, inconsistent results can lead to chronic renal failure

48
Q

Broad management of nephrotic syndrome

A
49
Q

Nephritic syndrome is characterised by

A

Haematuria
Reduction in GFR (renal impairment/oliguria)
Hypertension

50
Q

Other features of nephritic syndrome

A
  • Some proteinuria
  • Disruption of endothelium results in inflammatory response and damage to the glomerulus
  • Onset may be acute or rapidly progressive (RPGN)
  • Rapidly progressive. Crescentic GN - a fulminant form of nephritic syndrome
51
Q

Common causes of nephritic syndrome

A

IgA nephropathy (berger’s disease)

Rapidly progressive GN (glomerulonephritis)

Goodpasture’s (anti GMB)

Post-streptococcal GN

52
Q

Features of IGA nephropathy (Berger’s disease)

A

Most common primary glomerular disease causing recurrent haematuria

Hypertension and IgA levels raised, deposits in mesangium, sclerosis of damaged segment

53
Q

Treatment of IGA nephropathy Berger’s disease

A

Control BP, antihypertensives, steroids

20% will develop advanced CKD

54
Q

Features and treatment of rapidly progressive glomerulonephritis

A
55
Q

Features and treatment of Goodpastures syndrome

A
56
Q

Features and treatment of post-streptococcal glomerulonephritis

A
57
Q

Management of nephritic syndrome

A
58
Q

Overview of differential diagnosis of glomerular diseases

A

Urinary (20 decks)

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