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Patho 1 > Chap 20- The Kidney > Flashcards

Chap 20- The Kidney Flashcards

1
Q

where is the kidney located?

A
  • either side of vertebrae in retroperitoneal space

- positioning protects it from trauma and has a cushion of fat arround it

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2
Q

what are the layers of the kidney?

A
  • capsule- covering
  • cortex- outer layer, contains glomeruli and portions of tubules, gets the most BF -> reabsorbing function
  • medulla- inner later
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3
Q

what is the nephron?

A
  • functional unit of kidney
  • cortical nephron
  • juxtamedullary nephron
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4
Q

what is the cortical nephron?

A
  • located mostly in cortex
  • 85% of all nephrons in kidney
  • mostly help in excretory and secretory functions
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5
Q

what is the juxtamedullary nephron?

A
  • boarder between cortex and medulla
  • parts go deep into the medulla
  • helps with urine concentration
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6
Q

what is the renal hilum

A
  • opening in the kidney
  • where the renal artery and nerves enter
  • renal vein and ureter exit
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7
Q

what is the renal sinus

A
  • cavity within the kidney which is occupied by the renal pelvis
  • where all the different parts of the kidney are located
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8
Q

what are calyces (calyx)

A

tubes through which urine drains into the renal pelvis

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9
Q

parts of the nephron

A
  • glomerulus
  • proximal convoluted tubule
  • descending and ascending loops of henle
  • distal convulted tubule
  • collecting duct
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10
Q

what is the glomerulus?

A
  • cluster of capillaries

- plasma filtered from capillaries bowman’s capsule

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11
Q

what is the bowman’s capsule?

A
  • double layered, cup shaped membrane that receives plasma from glomerulus
  • filters plasma except proteins and cells
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12
Q

what is the main job of the proximal convoluted tubule?

A
  • reabsorb most of the filtered load
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13
Q

what is the main job of the loop of henle?

A

concentrate urine

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14
Q

what is the main job of the distal convoluted tubule?

A

reabsorb sodium and water

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15
Q

what is the main job of the collecting duct?

A

collect urine for excretion

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16
Q

ureter

A

transports urine from calyces to bladder

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17
Q

bladder

A

muscular structure that serves as reservoir for urine until it can be excreted

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18
Q

urethra

A

transports urine from bladder to urinary meatus

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19
Q

what is the difference in the urethra in men and women?

A
  • men have much longer urethra
  • shorter length in women is why they are more likely to get UTI
  • also more likely to get UTI due to seated position during urination
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20
Q

functions of the kindey

A
  • Excretion of metabolic wast products
  • excretion of foreign chemicals
  • hormone synthesis, metabolism and excretion
  • regulate pH
  • regulate arterial pressure
  • regulate water and electroyle imbalance
  • gluconeogenesis
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21
Q

what is gluconeogenesis?

A

new production of glucose from alternate sources like AA

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22
Q

how is urine formed?

A
  • glomerular filtration
  • tubular reabsorption
  • tubular secretion
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23
Q

what is the equation for urinary excretion rate?

A

filtration rate - reabsorption rate + secretion rate

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24
Q

filtration of urine

A
  • non selective process, filters everything except proteins and blood cells
  • helps immediately remove toxins
  • about 20% of renal plasma flow
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25
Q

reabsorption of urine

A
  • highly variable and selective
  • depends on the body’s needs
  • most electrolytes and nutritional substances are almost completely reabsorbed
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26
Q

secretion of urine

A
  • highly variable

- important for rapidly excreting some waste products, foreign substances, and toxins

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27
Q

what is normal GFR?

A

~ 125 mL/min

  • rate at which plasma is filtered
  • is directly related to perfusion pressure of glomerular capillaries maintained between 80-180 mmHg
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28
Q

where does urine formation begin?

A

large amounts of fluid flowing through glomerular capillaries into Bowman’s capsule

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29
Q

glomerular filtration barriers

A
  • endothelium of the capillary
  • basement membrane
  • layer of epithelial cells (podocytes)
  • all layers have negative charges and provide barrier to filtration of plasma proteins (proteins also neg charge)
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30
Q

endothelium of capillary

A
  • have multiple holes called fenestrae

- allows passage of fluid through them

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31
Q

basement membrane

A
  • type of ECM
  • made of collagen and proteoglycan that have large spaces through which large amounts of water and small solutes can filter
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32
Q

podocytes

A
  • epithelial cells with foot-like processes

- foot processes separated by caps called slit pores through which glomerular filtrate moves

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33
Q

determinants of GFR

A
  • glomerular hydrostatic pressure

- glomerular capillary colloid osmotic pressure

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34
Q

vasoconstrictors that control GFR

A
  • NE
  • E
  • endothelin
  • call cause a reduction in GFR
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35
Q

vasodilators that control GFR

A
  • endothelial- derived NO
  • prostaglandins
  • all cause increase in GFR
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36
Q

how does angiotensin II effect GFR?

A
  • prevents GFR from reducing
  • selectively constricts outgoing arteriole
  • constriction prevents GFR from falling
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37
Q

autoregulation of GFR

A
  • feedback mechanisms intrinsic to kidneys
  • normally keep renal BF and GFR constant despite changes in arterial blood pressure
  • types- myogenic and tubuloglomerular feedback
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38
Q

myogenic feedback

A
  • resistance to increase in arterial pressure
  • increase in arterial pressure will stretch vessel
  • stretch is opposed by contraction of vascular smooth muscle cells due to Ca
  • stretch neutralized by vascular SMC contraction
39
Q

what is the macula densa?

A
  • specialized group of endothelial cells in distal tubule
  • sodium sensor
  • secrete renin
40
Q

what is the juxtaglomerular complex?

A

macula densa and juxtaglomerular cells

41
Q

how do you calculate GFR?

A

GFR= Cinsulin = (Uin X V)/ Pin

- Cinsulin- clearance of insulin

42
Q

how to use Cinulin to determine GFR

A
  • if Cx < Cin indicates reabsorption of molecule x

- if Cx > Cin indicates secretion of molecule x

43
Q

reabsorption of different solutes

A
  • glucose and AA- completely reabsorbed
  • Ions like Na, Cl, HCO2- variable reabsorption depending on needs
  • waste products like urea and creatinine- poorly reabsorbed
44
Q

how are water and solutes transported through cell membranes?

A
  • through transceulluar route
  • through spaces between cell junctions called paracellular route
  • once moved into interstitial fluid, transported into blood
  • some substances secreted into tubules by secondary active transport with couter-transport
45
Q

what is counter tranposrt

A
  • energy greated from downhill movement of one substance enables uphill movement of second substance in opposite direction
  • i.e. hydrogen ion secretion coupled with Na reabsorption in luminal membrane
46
Q

clearance

A
  • rate at which substances are removed/ cleared from plasma
47
Q

renal clearance

A
  • volume of plasma completely cleared of substance per minute of kidneys
  • if clearance = GFR then cleared at same rate
48
Q

formation of dilute urine

A
  • continue electrolyte reabsorption
  • decrease water reabsorption
  • mechanism: decreased ADH release and reduced water permeability in distal and collecting tubules
49
Q

formation of concentrated urine

A
  • continue electrolyte reabsorption
  • increase water reabsorption
  • mechanism- increase ADH release -> increases water permeability, high osmolarity of renal medulla, countercurrent flow of tubular fluid
50
Q

what is not in normal urine?

A
  • no protein
  • no RBC
  • no heme
  • no cellular casts
  • no fat
  • no sugar
51
Q

Azotemia

A
  • biochemical manifestation of acute or chronic kidney injury
  • elevated BUN
  • elevated SCr
  • reduced GFR
52
Q

nephrotic syndrome

A
  • injury to glomerulus that causes abnormal filtration
  • excessively permeable to proteins
  • heavy proteinuria
  • hypoalbuminemia
  • edema
  • hyperlipidemia and lipiduria
53
Q

nephritic syndrome

A
  • inflammation of nephron
  • hematuria
  • azotemia
  • HTN
  • sub-nephrotic proteinuria
54
Q

what does asymptomatic hematuria or proteinuria indicate?

A
  • mild glomerular abnormablities

- can be reversible

55
Q

acute kidney injury

A
  • rapid drop in GFR
  • dysregulation of fluid and electrolyte balance
  • oligouria or anuria
56
Q

chronic kidney disease

A
  • GFR persistently <60 mL/min for at least 3 months
  • can be from any cause
  • and/or persistent albuminuria
57
Q

renal tubular defects

A
  • problem with proximal or distal tubules

- lead to nocturia, polyuria and electrolyte imbalances

58
Q

urinary tract obstruction

A
  • bateriuria

- pyuria- pus in urine

59
Q

nephrolithiasis

A
  • kidney stones
  • spasms of severe pain that spreads to inner thigh
  • often have recurrent stone formation
60
Q

what is the GFR in renal insufficiency?

A
  • 20-30% of normal GFR

- ~ 37.5 mL/min

61
Q

what is the GFR in renal failure?

A
  • 10-25% of normal GFR

- less than 37 mL/min

62
Q

what is the pathogenesis of most glomerular injury?

A
  • usually immune related
  • injury can be from antibodies in situ or deposited antigen-antibody complexes
  • other causes are viruses, drugs, toxins, systemic/ vascular diseases
63
Q

why does edema occur in nephrotic syndrome?

A
  • low serum albumin -> low oncotic pressure

- increased Na retention

64
Q

complications of nephrotic syndrome

A
  • infection and sepsis due to excessive loss of anitbodies
  • thrombosis
  • AKI
  • end state renal disease if proteinuria not controlled
65
Q

symptoms of nephrotic syndrome

A
  • fatigue
  • frothy urine
  • anorexia
  • N/V
  • abdominal pain
  • weight gain due to fluid retention
  • SOB from pleural effusion
  • signs and sx of DVT/ PE
66
Q

glomerular diseases that present as nephrotic syndrome

A
  • minimal change disease
  • focal segmental glomerulosclerosis
  • membranous nephropathy
67
Q

minimal change disease

A
  • under normal light microscope see no change
  • under electron microscope see thinning of podocytes
  • main cause of nephrotic syndrome in kids <10
  • very responsive to steroids
  • primary cause idiopathic
68
Q

focal segmental glomerulosclerosis

A
  • common cause of nephrotic syndrome in adults
  • only effects some glomeruli
  • only some of the affected glomeruli undergo sclerosis
  • primary cause is idiopathic
69
Q

membranous nephropathy

A
  • most common cause of nephrotic syndrome in elderly
  • slowly dev sx
  • basement membrane becomes thick due to immune complex deposition
  • high incidence of renal vein thrombosis, PE, and DVT
  • primary cause is idiopathic
70
Q

other causes of nephrotic syndrome

A
  • diabetes mellitus
  • amyloidosis
  • IgA nephropathy
71
Q

targets of nephritic syndrome

A
  • glomerular endothelium
  • glomerular basement membrane
  • glomerular mesangium
72
Q

post streptococcal glomerulonephritis (PSGN)

A
  • occurs a few weeks after strep infection
  • hematuria
  • serum has anti-streptolysin (ASO) titer
  • low C3
  • due to deposition of antigen-antibody complex with proteins from infection
73
Q

IgA nephropathy (berger disease)

A
  • most common primary glomerular nephritis in dev countries
  • present with dark urine 1-3 days after URT infection
  • can progress to end stage renal disease if untreated
  • dx- abnormal deposition of IgA in glomeruli that cause inflammation
74
Q

chronic glomerulonephritis

A
  • end stage glomerular disease
  • irreversible damage
  • glomerular and tubulointerstitial fibrosis
  • reduced GFR
  • uremia
75
Q

diabetic nephropathy

A
  • 2nd cause of death from diabetes
  • characterized by glomerular lesions, renal vascular lesions, and pyelophritis
  • basement membrane thickening
  • atherosclerosis
  • earliest manifestation is microalbuminuria
76
Q

acute tubular injury/necrosis (ATI/ ATN)

A
  • most common cause of AKI
  • cause- ischemia
  • can be due to endogenous or exogenous substances
77
Q

pathogenesis of ATI/ ATN

A
  • tubular injury
  • cells lining tubules die
  • release cytokines -> inflammation
  • dead cells are excreted or block lumen
  • blocked tubule will cause back flow of urine
  • causes reduced GFR
78
Q

Ischemic type ATI/ ATN

A
  • tubular necrosis is patchy

- lumen of DCT and CD contain casts

79
Q

toxic acute tubular injury

A
  • extensive necrosis is continuous

- lumens of DCT and CD contain casts

80
Q

pyelonephritis and UTI

A
  • valve between ureter and urinary bladder fails

- infectious agent colonizes in urethra, then bladder, then kidney

81
Q

why are females more likely to develope UTI?

A
  • shorter urethra
  • seated position = increased chance of urine stagnation
  • urethra can be damaged during sexual intercourse
  • don’t have prostatic secretions as protective agents
82
Q

risk factors for UTI

A
  • female sex
  • immunosuppression
  • indwelling catheters
  • diabetes mellitus
  • urinary tract obstruction
83
Q

clinical features of pyelonephritis

A
  • sudden onset of pain
  • systemic evidence of infection
  • dysuria, frequency, and urgency
  • pyuria
84
Q

complications of pyelonephritis

A
  • renal abscess
  • recurent infection -> chronic pyelonephritis
  • papillary necrosis
85
Q

chronic pyelonephritis

A
  • chronic tubulointerstital inflammation
  • scarring of calyces and pelvis
  • one of only diseases that involves renal calyx
  • most common cause- congenital lower urinary tract abnormalities
86
Q

renal artery stenosis

A
  • narrowing of renal artery
  • important cause of secondary HTN
  • HTN is due to increased production of renin from the ischemic kidney
  • clinical course similar to essential HTN
87
Q

autosomal dominant polycystic kidney disease

A
  • adult onset
  • multiple cysts in kidneys that cause destruction of parenchyma and eventual renal failure
  • due to mutation on PKD1 or PKD2 genes
88
Q

clinical course of autosomal dominant polycystic kidney disease

A
  • asymptomatic for years
  • tubular epithelial cells grow excessively and have differentiation problems
  • cysts form which can cause glomerular damage, vascular damage, inflammation and pain
  • kidneys become enlarged
89
Q

autosomal recessive polycystic kidney disease

A
  • childhood onset
  • can be either perinatal, neonatal, infantile, or juvenile
  • due to mutation in PKHD1 gene which encodes for fibrocystin
  • manifestation is same as adults
  • likely will also have congenital hepatic fibrosis
90
Q

urolithiasis

A
  • aka kidney stones

- caused by increased urinary concentration of stone constituents

91
Q

influencing factors for kidney stone formation

A
  • increased concentration of stone constituents
  • change in urinary pH
  • decreased urine volume
  • presence of bacteria
92
Q

types of kidney stones

A
  • Calcium
  • triple stones made of magnesium ammonium phosphate
  • uric acid stones
  • cysteine stones
93
Q

renal cell carinoma

A
  • most common malignant tumor of kidney

- very strongly associated with smoking, elderly, obesity

94
Q

clinical course of renal cell carcinoma

A
  • costovertebral pain
  • palpable mass
  • hematuria
  • abnormal hormone production
  • widely metastasize- lungs and bones first

Patho 1 (12 decks)

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