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Renal Path MC > Renal 1 > Flashcards

Renal 1 Flashcards

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1
Q

% of CO that goes to kidneys

A

25%

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2
Q

signifies end stage renal disease

A

GFR

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3
Q

size of particles normally filtered by kidneys

A
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4
Q

5 functional units of kidney

A

vascular supply, glomerulus, tubules, interstitium, collecting system

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5
Q

most of vasculature located within this area of kidney

A

cortex/glomeruli

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6
Q

sole blood supply of tubules

A

efferent arterioles (glomerular damage causes major problems downstream)

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7
Q

this portion of kidney is at greatest risk for ischemic and ischemic infarction

A

tubules

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8
Q

this portion of kidney is relatively avascular and has lower hematocrit

A

medulla

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9
Q

treatment for HTN caused by kidney problem

A

ACE inhibitor

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10
Q

this causes pre-renal vascular disease

A

decreased blood flow to glomeruli

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11
Q

this is result of pre-renal vascular disease

A

decreased GFR, loss ability excrete nitrogen waste, increase BUN and Cr, conservation water and Na (expanded intravascular volume and HTN)

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12
Q

this causes glomerular kidney disease

A

damage glomerular architecture (commonly immune related), vascular disease glomerular capillaries

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13
Q

result of glomerular disease (due to damage to architecture)

A

loss GFR and selective permeability (will see protein and RBC)

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14
Q

characteristic features of renal disease due to decrease in GFR

A

increase BUN and Cr, oliguria, dilution hyponatremia, increased K and phosphate, hypocalcemia, AG metabolic acidosis

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15
Q

additional problems in glomerular disease due to alteration in membrane filtration

A

proteinuria, hematuria, GN

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16
Q

this is characterized by HTN, Na conservation, azotemia W/O proteinuria or hematuria

A

pre-renal disease

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17
Q

these cells in kidney can regenerate

A

tubular epithelium

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18
Q

these are responsible for concentrating abnormal constituents of the glomerular filtrate, like toxins, lipids, proteins

A

tubular cells (epithelium sheds and tubular casts form)

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19
Q

major goal/function of tubules

A

urine concentration

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20
Q

hallmarks of tubular disease

A

loss of urine concentrating ability (end-stage), metabolic acidosis, formation tubular casts

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21
Q

this causes metabolic acidosis in tubular disease

A

loss of bicarb

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22
Q

interstitial disease is associated with this

A

loss EPO and anemia

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23
Q

interference with blood flow of this area of kidney causes production of renin and angiotensin II -> leading to HTN

A

interstitium

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24
Q

this is result of loss of prostaglandin production in interstitial disease

A

renal vasoconstriction, vascular insufficiency, HTN

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25
loss of this % of GFR signifies renal insufficiency -> azotemia, anemia, HTN
50-80%
26
this signifies renal failure
GFR
27
decrease in GFR with resulting increase in BUN and Cr
azotemia
28
this condition, with early treatment, can have reversible glomerular damage
acute post-streptococcal GN
29
loss of protein (>3.5 g/day) w/o other evidence of filtration or vascular abnormality
nephrotic syndrome
30
loss of tubular function in isolated tubular syndrome causes this to occur
increased intraglomerular pressure (secondary to tubular collapse/damage), decrease GFR
31
Henderson-Hasselbalch equation
6.1 + log (HCO3/ .03*PCO2)
32
normal pH value
7.4
33
increase in PCO2 (hypoventilation) causes this
respiratory acidosis
34
decrease in PCO2 (hyperventilation) causes this
respiratory alkalosis
35
two conditions that will lead to metabolic acidosis
retention acids renal failure, loss bicarb tubular disease
36
increase in total acids leads to this
metabolic acidosis
37
vomiting leads to this
metabolic alkalosis (lose acids)
38
diarrhea leads to this
metabolic acidosis (loss of bicarb)
39
normal value for HCO3
25 mmol
40
normal value for CO2
40 mmHg
41
metabolic or respiratory problem will cause CO2 and bicarb (very slightly) to change in same direction?
respiratory
42
condition with increased CO2, slightly increased HCO3
respiratory acidosis
43
condition with decreased CO2, slightly decreased HCO3
respiratory alkalosis
44
metabolic or respiratory problem has change in HCO3 but CO2 remains normal?
metabolic
45
condition with decreased HCO3 and normal CO2
metabolic acidosis
46
condition with increased HCO3 and normal CO2
metabolic alkalosis
47
to normalize ratio in compensation for A/B problem...will HCO3 and PCO2 change in same or opposite direction?
SAME
48
when anion gap is present, this must occur to keep anions equal to cations
Cl decreases
49
this occurs to account for decreased bicarb if no anion gap is present
Cl increases (hyperchloremic metabolic acidosis)
50
is metabolic acidosis with or without anion gap considered normochloremic?
with AG
51
does tubular or glomerular acidosis cause increase in Cl?
tubular (lose bicarb, no anion gap)
52
anion gap greater than this value signifies there is an unknown acid or acid is increased
>27 mmol
53
this condition increases K levels
acidosis (H+ exchanged for K)
54
condition with bilateral renal a genesis -> incompatible with life, many stillborn infants (head and extremity malformations)
Potter's syndrome/oligohydramnios
55
true hypoplasia is rare, but most small kidneys are due to this
scarring
56
what part of kidney is most commonly fused in horseshoe kidney?
lower poles
57
does horseshoe kidney lie anterior or posterior to great vessels?
anterior
58
this form of polycystic kidney disease is most commonly in children
autosomal recessive
59
this cystic renal disease is associated with renal cell carcinoma
acquired cysts
60
this is abnormal in multi cystic renal dysplasia (dysplasia of renal components)
metanephric differentiation
61
abnormal structures in kidney including islands of cartilage, undifferentiated mesenchyme, immature collecting ducts
multicystic renal dysplasia
62
associated conditions with multi cystic renal dysplasia
ureteropelvic obstruction, ureteral agenesis
63
hereditary disorder with multiple expanding cysts in both kidneys (ENLARGED kidneys, filled with serous/hemorrhagic fluid) -> presents in 4-5 decade
ADPKD
64
what causes renal failure in ADPKD?
expanding cysts destroy parenchyma
65
mutations associated with ADPKD
PKD1 (chromosome 16), PKD2 (chromo 4)-> polycystin (in cilia of tubular epithelial cells...secrete fluid)
66
where do cysts in ADPKD arise from?
tubular epithelium
67
morphology of ARPKD
small cysts cut surface, dilated elongated channels replacing medulla/cortex, dilation collecting tubules
68
secondary complications of medullary sponge kidney
calcification, hematuria, infection and renal calculi
69
cause of acquired cystic disease
dialysis
70
cause of renal artery stenosis (uncommon cause of HTN)
atheromatous plaque at origin of renal artery
71
stenosis of renal arteries NOT associated with atherosclerosis -> more common in women, 3rd-4th decade
fibromuscular dysplasia
72
pathology of fibromuscular dysplasia
fibrous/fibromuscular thickening intima, media, adventitia
73
hallmark of renal disease
dilutional hyponatremia with inappropriate Na loss
74
tubular disease leads to this A/B condition
non-AG metabolic acidosis
75
causes of interstitial disease
infection, drug toxicity, HS reaction, accompanying tubular or glomerular disease
76
characteristic of collection system obstruction
oliguria/anuria w/o glomerular or tubular dysfunction
77
result of longstanding obstruction of collecting system
ascending destruction tubular/interstitial, loss GFR
78
mechanism of most glomerular diseases
immunologic mechanism/deposition of substances (alters BM)
79
mechanism of most tubular or interstitial diseases
toxic mechanism, infection, or obstruction
80
signs of renal insufficiency
azotemia, anemia, HTN
81
causes of acute renal insufficiency/acute renal failure
pre-renal vascular insufficiency, ATN, acute GN
82
possible courses of slowly progressive GN
asymptomatic proteinuria/hematuria, nephrotic syndrome, GN (nephritic), crescentic GN (rapidly progressive)
83
global symptoms/indicators of renal failure
oliguria, HTN, electrolyte imbalance, metabolic acidosis
84
possible causes of pre-renal problem leading to renal insufficiency
hypotension, CHF, renal artery stenosis, arteriolosclerosis, PAN, scleroderma
85
electrolyte disturbances in acute renal syndrome
hyponatremia/calcemia, hyperkalemia/phosphatemia
86
changes in urine due to acute renal syndrome
decreased production, increased osmolality
87
non-renal systemic complication associated with renal failure and azotemia -> due to loss of normal renal function or build up of waste metabolites
uremia
88
mechanism of how nephrotic syndrome leads to HTN
hypoalbuminemia -> anasarca -> decreased intravascular volume -> RAS activation -> Na and water retention (DIURETICS to treat edema can be FATAL b/c IVV already low)
89
these are direct results of protein loss in nephrotic syndrome
reversal albumin:globulin ratio, increased infection (loss of complement/low weight globulin), hyper coagulable state, hyperlipidemia/lipiduria (loss lipoproteins)
90
lipid appears as these in urine due to loss of lipoproteins -> tubular cells that have reabsorbed the lipid and are shed (lipid casts)
oval fat bodies
91
hallmarks of chronic renal failure/uremia
interstitial fibrosis, vascular insufficiency, loss GFR, tubular dysfunction
92
systemic symptoms of chronic renal failure/uremia
anemia, bleeding diatheses, renal osteodystrophy, neurological symptoms

Renal Path MC (5 decks)

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