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Session 7 Flashcards

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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

25
Haemodialysis pros and cons
26
Peritoneal dialysis pros and cons
27
How does peritoneal dialysis work
28
How does renal transplant work
29
Regulatory impacts of CKD
RAAS to manage fluid overload Reabsorption of different electrolytes Acid base balance
30
Excretory impacts of CKD
Phosphate and potassium not well excreted Unable to excrete fluid: become fluid overloaded
31
Endocrine impacts of CKD
EPO, vit D activation
32
What is glomerulonephritis GN
Inflammation of glomeruli Often involves immune system
33
4 structures in glomerulus that can be damaged
Capillary endothelium Glomerular basement membrane Mesangial cells Podocytes
34
What is nephrotic vs nephritic syndrome
35
Main characterises of nephrotic syndrome
Triad of: - Proteinuria >350mg/mmol (3.6g in 24 hrs) - Hypoalbuminaemia - Oedema usually accompanied by high cholesterol
36
Other features in nephrotic syndrome
BP often normal (can be low or high) Creatinine may be normal Proteinuria > 350mg/mmol alone = nephrotic range proteinuria
37
Causes of primary renal disease / nephrotic syndrome e
Minimal change disease membranous glomerulonephritis Focal segmental glomerulosclerosis FSGS
38
Causes of secondary renal disease / nephrotic syndrome
Diabetes is most common
39
What is diabetes nephropathy
Leading cause of end stage renal disease XS glucose in blood binds to proteins especially at efferent arteriole Hyaline atherosclerosis obstructs blood flow
40
Effect of diabetic neuropathy on GFR
Initially increase GFR, over time mesangial cells secrete more structural matrix. Thickening of basement membrane, GFR decreases
41
Treatment of diabetic nephropathy
Control Hypertension, good glycemic control, ACE inhibitors, angiotensin receptor blockers
42
What is minimal change disease
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
What is membranous glomerulonephritis
Subepithelial deposition of immune complexes (antibody-antigen complexes) Thickening of basement membrane Albumin can leak out of capillaries 40% adult nephrotic syndrome
44
Treatment for membranous glomerulonephritis
Immunosuppressants, treatment of underlying cuase
45
What is Focal segmental glomerulosclerosis FSGS
Podocytes damaged proteins build up in glomerulus- hyalinosis (glassy)- leading to sclerosis
46
Causes of FSGS
Primary: idiopathic Secondary: sickle cell disease, HIV, heroin abuse, kidney hyperperfusion
47
Treatment for FSGS
Steroids, inconsistent results can lead to chronic renal failure
48
Broad management of nephrotic syndrome
49
Nephritic syndrome is characterised by
Haematuria Reduction in GFR (renal impairment/oliguria) Hypertension
50
Other features of nephritic syndrome
- 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
Common causes of nephritic syndrome
IgA nephropathy (berger’s disease) Rapidly progressive GN (glomerulonephritis) Goodpasture’s (anti GMB) Post-streptococcal GN
52
Features of IGA nephropathy (Berger’s disease)
Most common primary glomerular disease causing recurrent haematuria Hypertension and IgA levels raised, deposits in mesangium, sclerosis of damaged segment
53
Treatment of IGA nephropathy Berger’s disease
Control BP, antihypertensives, steroids 20% will develop advanced CKD
54
Features and treatment of rapidly progressive glomerulonephritis
55
Features and treatment of Goodpastures syndrome
56
Features and treatment of post-streptococcal glomerulonephritis
57
Management of nephritic syndrome
58
Overview of differential diagnosis of glomerular diseases

Urinary (20 decks)

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