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GU1 - Nephrology > Renal Patho > Flashcards

Renal Patho Flashcards

1
Q

prevalence of urinary system congenital malformations and why

A
  • 10% of all newborns

- because you start the process 3 different times so the chance of something going wrong increases

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2
Q

What are the potential 3 sets of kidneys?

A
  • pronphros
  • mesonephros
  • metanephros
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3
Q

pronephros

A
  • non-functional in humans
  • week 4
  • functional in lampreys and hagfishes
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4
Q

mesonephros

A
  • briefly functional in humans

- present in fish and amphibians

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5
Q

metanephros

A
  • functional human kidneys

- become functional around week 11

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6
Q

describe the human embryo at the end of week 2 of development

A
  • hollow ball of cells
  • 2 layered primordium
  • epiblast and hypoblast
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7
Q

when does the embryo progress to 3 layers?

A

at the end of week 3

  • epiblast
  • mesoderm
  • hypoblast
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8
Q

What do the 3 embryonic tissues develop into?

A
  • epiblast: skin and nervous tissue
  • hypoblast: gut lining
  • mesoderm: everything else
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9
Q

formation of the urogenital ridge

A
  • after folding (week 4-5) the mesoderm forms a buldge on posterior abdominal wall
  • it becomes the urogenital ridge / nephrogenic cord
  • reason that kidneys are retroperitoneal
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10
Q

describe the once functional mesophephros in the 5 week embryo

A
  • early mesonephros forms a duct and a vesicle

- they elongate and join to form a single nephron

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11
Q

What is the significant embryologic structure that forms off of the mesonephric duct?

A

ureteric bud

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12
Q

ureteric bud

A
  • grows out from the mesonephric duct
  • starts branching repeatedly into millions of collecting ducts
  • so: the entire collecting system of the kidney is form the ureteric bud - a branch of the mesonephric duct
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13
Q

what do the adult kidney tubules originate from?

A

metanephric mesoderm

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14
Q

kidneys develop mainly from what embryologic structures?

A
  • metanephric diverticulum off mesonephric duct

- metanephric mesoderm

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15
Q

what major change in the kidneys begins around week 9 of development?

A
  • they move from the pelvis region to adult position

- also rotate medially

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16
Q

what happens to the urine produced in the womb?

A
  • urine = amniotic fluid
  • swallowed by fetus
  • reabsorbed by gut into circulation
  • out via placenta
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17
Q

polyhydramnios and cause

A
  • too much amniotic fluid

- esophageal atresia or other obstructions that wouldn’t allow for the fetus to swallow

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18
Q

oligohydramnios and cause

A
  • not enough amniotic fluid

- anything that effects the kidneys/urinary system

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19
Q

ectopic kidney

A
  • a persistant mesonephric kidney
  • would be located above the metanephric kidney
  • always smaller and can be functional
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20
Q

kidney size vs function

A
  • 0.5% of body weight

- 25% of CO

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21
Q

general functions of the kidney

A
  • excretion
  • regulation of water and salt
  • maintain pH
  • endocrine functions
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22
Q

what is the glomerulus?

A

-anastomoses of capillaries invested by 2 layers of epithelium

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23
Q

layers of the glomerulus

A

visceral layer next to the endothelium that is continuous with a parietal layer and Bowman’s space in between

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24
Q

branching of the renal artery

A
  • renal a. enters kidney
  • branches to interlobar a. b/w the papilla
  • branches into arcuate a.
  • branches into interlobular a. in the cortex
  • branches into the afferent arteriole into the capillary tuft
  • exits as the efferent arteriole
  • vasa recta surround the nephron
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25
Q

macula densa

A
  • thick ascending limb of the LoH

- at the transition to the DCT

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26
Q

macula densa cells sense what?

A

NaCl concentration

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27
Q

decrease in NaCl causes the macula densa cells to:

A
  1. decrease resistance to blood flow in afferent arterioles
    - this raises hydrostatic pressure in glomerulus
  2. increases renin release from JG cells of afferent and efferent arterioles
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28
Q

an increase in NaCl results in what?

A

-vasoconstriction of the afferent arterioles and a decrease in JG release of renin

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29
Q

What are all of the layers of the glomerulus that make up a filter?

A
  • fenestrated endothelium
  • glomerular basement membrane
  • secondary foot processes
  • slit diaphragms
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30
Q

fenestra size

A

70-100 nm (comparison: RBCs 7000 nm)

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31
Q

glomerular basement membrane

  • secreted by
  • made of
A

-secreted by epithelial cells
-consists of Type IV collagen
and glycoproteins

32
Q

secondary foot processes

  • where
  • size
A
  • embedded in the basement membrane

- separated by 20-30 nm filtration slits

33
Q

what supports the entire glomerular tuft?

A

mesangial cells

34
Q

what do mesangial cells secrete?

A
  • mesangial matrix (BM like)

- may proliferate w/ phagocytic role

35
Q

what proteins make up the slit diaphragm between the foot process?

A

nephrin

36
Q

what happens when there is a defect in the gene for nephrin?

A
  • congenital nephrotic syndrome

- pee protein

37
Q

diagram of renal corpuscle

A

a lot of anatomical diagrams on this lecture to review!

38
Q

in summary, what is filtration based on?

A
  • size of fenestra
  • glomerular basement membrane
  • filtration slits
  • slit diaphragm
  • charge
39
Q

absorption at the proximal tubules

A

-PCT absorbs about 2/3 of glucose, K, phosphate, aa, proteins, and toxins

40
Q

why are the PCTs more prone to damage?

A

most exposure to toxins

41
Q

define acute renal failure

A
  • abrupt onset of not being able to produce urine
  • oligo/anuria w/ azotemia
  • follows rapidly progressing glomerulonephritis or ATN
  • usually reversible
42
Q

azotemia

A

elevation in BUN

43
Q

ATN

A

acute tubular necrosis

-MC cause: hypotensive shock

44
Q

oliguria

A
  • <05 ml/kg/hr of urine output

- 400-500 ml/d

45
Q

what to suspect in asymptomatic hematuria or proteinuria

A

mild glomerular disease (ex: from DM) all the way to cancer

46
Q

nephrotic syndrome

A
  • heavy proteinuria
  • > 3.5 gm/d
  • hypoalbumen
  • edema
47
Q

acute nephritic syndrome

A

gross hematuria/proteinuria and HTN secondary to post-strep glomerulaonephritis

48
Q

chronic renal failure

A

occurs over years, not reversible, and usually secondary to systemic disease

49
Q

diminished renal reserve

A
  • GFR >50%

- nl BUN/Cr

50
Q

renal insufficiency

A
  • GFR 20-50%
  • azotemia
  • anemia
  • HTN
51
Q

renal failure

A
  • GFR about 20%
  • loss of regulation of water, pH, salts
  • edematous
  • metabolic acidosis
  • hypocalcemia***
  • hyperkalemia***
52
Q

end stage renal disease

A
  • GFR about 5%

- terminal

53
Q

most causes of glomerular injury result from what?

A
  • immune mechanisms (70%)

- other 30% is from DM and toxins

54
Q

What are the two in situ types of immune mediated glomerular disease?

A
  1. anti-GBM

2. heymann model

55
Q

anti-GMB (masugi’s model) of glomerular dz

A
  • auto antibodies to type IV collagen w/i the BM
  • immune binding clogs the GBM and decreases GFR
  • less than 5% have this
56
Q

heymann model of glomerular dz

A
  • auto antibodies to glycoprotein on foot processes of visceral epithelium
  • clots filtration slits and GBM
57
Q

What is the condition called when you make auto-abs against type 4 collagen?

A

good pasture syndrome

58
Q

what are the triggers for the development of auto-antibodies?

A
  • toxins like mercuric chloride
  • “planted antigens” such as bacterial debri
  • graft vs. host dz
59
Q

in the circulating model (as opposed to the 2 in situ models) of glomerular dz, what is the process?

A
  • the antibody antigen complex is already formed and that is what clogs the system
  • there is no immunologic specificity for glomeruli
60
Q

what are the 2 types of complexes in the circulating complexes model?

A
  • endogenous

- exogenous

61
Q

endogenous complexes

A
  • think autoimmune diseases
  • SLE
  • dsDNA is worst offender
62
Q

exogenous complexes

A

complexes to bacterial/viral products

-ex: strep

63
Q

what are common viral triggers for the circulating complex model?

A
  • hep B and C
  • mumps
  • mono
  • varicella
64
Q

what are common bacterial triggers for the circulating complex model?

A
  • group A hemolytic strep
  • meningococcus
  • strep pneumo
  • syphillis
  • staph (endocarditis)
65
Q

what is the pathophys behind the circulating complexes concept?

A
  • complexes form in mesangial matrix and subendothelially
  • this activates immune system
  • infiltration of leukocytes and proliferation of mesangial cells
  • once deposited, can be cleared by phagocytosis (unless chronic like in SLE)
66
Q

Ddx when pt presents w/ fever, N/V, HTN, periorbital edema, oliguria, hematuria w/ dark-colored urine 1-2 weeks after strep

A

post-strep AGN

67
Q

pathognomonic for AGN

A

RBC casts

68
Q

labs in AGN

A

UA:

  • RBC casts
  • proteinuria

-elevated ASO titer

69
Q

prognosis of post-strep AGN

A
  • > 95% recover w/ conservative water/electrolyte management
  • hematuria and proteinuria may last weeks - months
  • about 3% will progress to acute/chronic renal failure
  • so treat strep throat!!
70
Q

puffy face, think ______

A

nephritic syndrome

71
Q

diabetic nephropathy

A

-30% of DM1 develop end-stage renal dz
-50% of DM1 and DMII have proteinuria 10-20 yrs after onset –>
signals progression of chronic renal failure w/i 4-5 yrs

72
Q

diabetic mechanisms that have a role in kidney damage

A
  • GBM thickening
  • glomerulosclerosis
  • GFR increase and subsequent decrease
  • accelerated atherosclerosis
73
Q

GBM thickening

  • when
  • process
A
  • as early as 2 yrs after onset
  • secondary to non-enzymatic glycosylation of proteins
  • glucose stimulates increase in type IV collagen
74
Q

glomerulosclerosis

A
  • associated w/ GBM thickening
  • from hemodynamic change
  • produces glomerular hypertophy secondary to increased mesangial cells and matirx
75
Q

in summary, what are the 3 main things to think about with relating DM to kidney issues?

A
  • GBM thickening
  • glomerularsclerosis
  • arteriosclerosis
76
Q

how to help DM effects on kidney

A
  • tight glucose control
  • ACE inhibits to decrease glomerular capillary pressure
  • STOP smoking!

GU1 - Nephrology (16 decks)

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