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PBL SEM 4 > diabetic kidney disease > Flashcards

diabetic kidney disease Flashcards

1
Q

where do the kidneys sit in relation to the peritoneum?

A

they are retroperitoneal

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2
Q

what are the 3 stages of mammalian kidney development?

A

pronephros, mesonephros, metanephros

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3
Q

what is the functioning unit of the kidney?

A

nephron

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4
Q

what happens at the proximal end of the nephron?

A

filtration

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5
Q

how many nephrons roughly in each kidney? relevance?

A

about 1 million

having too little is relevant in kidney disease

loose functioning nephrons as we age

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6
Q

what is actually the filtration barrier in the glomerulus?

A

the wall of the capillaries in the glomerulus

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7
Q

a 70kg adult will filter how many L through the nephrons each day?

A

180L

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8
Q

what cells line the capillaries of the glomerulus?

A

endothelial cells

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9
Q

what are podocytes?

A
  • sit on outside of the glomerular capillaries
  • specialised epithelial cells
  • essential for filtration
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10
Q

what are the 2 main components of matrix?

A

basement membrane
- glomerular
- tubular
- bowman’s capsule

intestitial matrix (looser)
- mesangium
- tubulointerstitium

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11
Q

what early changes occur due to a variety of diseases to the glomerulus (cellular and matrix defects)?

A

loss of filtration function
- thickening of basement membrane
- flattening of foot processes of podocytes

reversible however dont present with clinical symptoms!

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12
Q

what can be one of the earliest signs of kidney disease and requires investigation?

A

persistent leakage of proteins that can be detected in the urine — this is ABNORMAL

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13
Q

what later changes occur due to a variety of diseases to the glomerulus (cellular and matrix defects)?

A
  • podocyte detachment — fall into urine
  • accumulation of matrix — thickening of basement membrane
  • sclerosis
  • infiltration of cells that shouldn’t be there

leads to irreversible loss of function

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14
Q

what is Anti-GBM disease?

A

get antibodies to the basement membranes in the glomerulus — fairly aggressive disease, not much in the way of proteinuria, but get a rapidly progressive destructive glomerulonephritis

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15
Q

what is IgA nephropathy?

A

get IgA deposited in the kidneys — assoicated with a range of presentations (range of proteinuria)

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16
Q

what are the 3 characteristic features of nephrotic syndrome?

A

clinical presentation - not a condition by itself

  1. massive proteinuria
  2. low serum albumin (cut off is 25g/L)
  3. oedema — accumulation of fluid in tissues
17
Q

what are the different types of proteinuria?

A
  • glomerular = most common (up to 90%)
  • tubular
  • overflow
  • post-exercise
  • post-prandial
  • infection-associated
18
Q

what are characteristics of tubular proteinuria?

A

may be genetic

low molecular weight proteins, such as B2-microglobulin

19
Q

what is overflow proteinuria?

A

increased production, that is, light chains in multiple myeloma

20
Q

characteristics of post-prandial proteinuria

A
  • transient physiological proteinuria
  • poss through insulin action in podocytes
21
Q

what are normal vs nephrotic range values for protein:creatinine ratio (PCR) ?

A

normal = <20mg/mmol
nephrotic range = 200mg/mmol

22
Q

what are normal vs nephrotic range values for albumin:creatinine ratio (ACR) ?

A

microalbuminuria = >3mg/mmol

albuminuria = >30mg/mmol

23
Q

what % of diabetics develop nephropathy?

A

40%

24
Q

what are the stages of injury in diabetic kidney disease?

A
  1. hyperfiltration
  2. microalbuminuria
  3. macroalbuminuria
  4. proteinuria
  5. declining renal function
25
Q

diabetic mechanism of glomerular hyperfiltration

A

whole kidney level:

  • increase in renal blood flow
  • increase in filtration fraction
  • vasodilation of afferent arteriole
  • proximal tubular sodium reabsorption
  • glomerular hypertension
  • increase in RAAS

SHE DIDNT GO THROGUH THIS

26
Q

pathology in the glomerulus

A
  • GMB thickening
  • mesangial expansion — proliferate and expansion of matrix
  • nodular sclerosis
  • advanced sclerosis
27
Q

how is diabetic nephropathy classified (flow chart)?

A
28
Q

treatment goals for DN

A
  • glycaemic control
  • BP control
  • RAAS blockage ACEi/ARB (RENAAL T2DM Losartan, also in normotensive T1DM, Aliskiren renin inhibitor)
  • lipid lowering
  • reduce other CV risks
29
Q

when would diuretics be used?

A

if there is fluid accumulation or oedema associated with significant proteinuria

30
Q

what are the 2 main types of diuretics used in clinical practise?

A

thiazide and loop diuretics

31
Q

what do diuretics do?

A
  • reduce the ECF volume
  • lower BP
  • augment effects of RAAS inhibitors
32
Q

SGLT2 inhibitors can be used for kidney disease and what?

A

diabetes, heart failure

33
Q

why are SGLT2 inhibitors not yet approved for T1DM?

A

there is a risk of ketoacidosis

34
Q

what is peritoneal dialysis?

A
  • tube is surgically placed into the abdomen = peritoneal dialysis catheter which is connected to a hypotonic fluid bag
  • immediate use reduces fluid overload
  • no anticoagulation
  • cheapest - global application
  • continuous
  • least likely to cause fluid shifts and hypotension
35
Q

describe haemodialysis and haemofiltration

A
  • need to access circulation via central venous catheter, surgically if permanent, arteriovenous fistula etc
  • specialist nursing care
  • tertiary units
  • need for good central venous access
  • high and efficient solute clearance
  • anticoagulation
  • intermittent : not tolerated when haemodynamically unstable
  • continuous : haemofiltration used in less stable patients eg in ICU, not as aggressive in terms of fluid removal aspect

dialysis - diffusion
filtration - convection

36
Q

in peritoneal dialysis, where is the hypotonic fluid put in the body?

A

peritoneal space — pulls out water and waste products from circulation via tissues

37
Q

what kind of transplants can you get?

A
  • kidney
  • combined kidney and pancreas
  • islet cell

PBL SEM 4 (50 decks)

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