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Advanced Patho Exam 1 > Exam 1: Renal > Flashcards

Exam 1: Renal Flashcards

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1
Q

what are the functions of kidneys? (3)

A

o Maintenance of fluid, electrolytes, acid-base homeostasis
o Excretion of metabolic end products and foreign substances
o Production and secretion of enzymes and hormones

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2
Q

how does the kidneys maintain fluid, electrolytes and acid-base homeostasis?

A

 RENAL POTASSIUM HANDLING PRINCIPAL CELL;
* In order for this to work you need;
o Aldosterone (hormone)
 Increases the Na/K pump activity
 If there is no aldosterone then you will not be able to get rid of K from cell= as a result HYPER K
o Sodium Delivery
 Sodium helps K get out of cell. If there is no sodium, K increases
 But if someone gets IVF saline for no reason then k is being taken out of cell, leading to HYPO K
o Urinary Flow
 Washes out K, gets rid of it in urine
 Bicarbonate is completely filtered at the glomerulus, and approximately 90% is reabsorbed in the proximal tubule – acid base balance maintained by renal excretion of daily acid load both acid, phosphate, and ammonium

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3
Q

what enzymes and hormones does the kidney produce and secrete?

A
  • renin (increase bp)
    -erythropoietin (helps with productions of RBC, hgb by BM)
    -activate Vit D hormone
    -calcium, phos, bone metabolism (low Ca levels stimulate Ca release/production, phos gets released w/ Ca since its in bone –> therefore you get hyperphos and normal Ca
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4
Q

Osmolality Control of Renal Water Excretion: Water deprivation

A

High plasma osmolality ->hypothalamus stimulation -> cause an increase in ADH release ->causes an increase in thirst and water intake, ALSO causes kidneys to retain water (antidiuresis)

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5
Q

what happens to urine osmolality if ADH is around and why?

A

-osmolality will INCREASE
-B/C there is concentration in urine

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6
Q

Osmolality Control of Renal Water Excretion: water excess

A

Low plasma osmolality -> hypothalamus is blocked in releasing ADH -> there is less ADH in blood ->therefore kidneys will excrete water (large water diuresis)

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7
Q

what is AKI defined as? (3)

A

o an increase in creatinine by >0.3mg within a 48hour -OR
o increase in creatinine to >1.5 times baseline within the prior 7days -OR
o urine volume decrease
**Basically it means there is either decrease in urine or increase in creatinine!

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8
Q

what is AKI based on?

A

-on volume of urine—» this is a prognosis not a diagnosis

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9
Q

AKI urine output for: non-oliguria

A

> 500 ml/day, but BUN:creat increases

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10
Q

AKI urine output for: oliguric

A

daily urine volume <500 ml/day

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11
Q

AKI urine output for: anuric

A

<100 ml/day

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12
Q

Describe the common etiology of: prerenal AKI

A

o Decreased renal perfusion, adaptive response to severe volume depletion (dehydration)
o hypotension w/ structurally and functionally intact nephrons
 Hypovolemic:
* Vomiting, diarrhea, blood loss, diuretics
o Treatment involves giving IVF, rehydration
 Hypervolemic:
* heart failure, cirrhosis, nephrotic syndrome (have good volume but poor perfusion)
o Treat the HF

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13
Q

in the setting of volume depletion/decreased perfusion pressure, how does the arterioles in the kidneys respond?

A

the kidneys will open afferent arterioles and close the efferent. that way the glomerulus gets the blood flow, the kidneys recover on their own to improve perfusion

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14
Q

what are affected with intra-renal AKI? (4)

A

-vascular
-glomerular
-tubular
-interstitial

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15
Q

what are the etiology of intra-renal AKI affecting: vascular

A

**affecting the renal artery/vein
etiology: embolic events leads to renal infarction
-blood clots that has traveled to the kidneys, a fib, renal vein thrombosis, plaques that have dislodged (nephrotic syndrome)

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16
Q

what are the findings of intra-renal AKI affecting: vascular (5)

A

-HTN
-gangrenous lesion in toes
-focal neuro deficits
-confusion
-eye issues
Labs: eosinophila/eosinophiluria
-low complements, C3 C4
-urine typically benign, may have hematuria

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17
Q

what are the treaments of intra-renal AKI affecting: vascular

A

-AC, if appropriate
-avoid further damage to kidneys

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18
Q

what are the etiology of intra-renal AKI affecting: glomerular

A

**actual damage to the kidneys
etiology: Glomerulonephritis
- start by checking C3/C4 and then contact nephrologist

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19
Q

what are the findings of intra-renal AKI affecting: glomerular

A
  • HTN
    -petechiae
    -purpura
    -markers of rheumatologic conditions
    -murmur
    -fever
    labs: Azotemia (elevated levels of urea)
     Active urinary sediment
     Proteinuria +
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20
Q

what are the treatments of intra-renal AKI affecting: glomerular

A

treatment varies, treat underlying cause

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21
Q

what are the etiologies of intra-renal AKI affecting: Tubular

A

typically caused by ischemia or nephrotoxic insult to the kidney
 Prolonged ischemia
* prolonged prerenal state associated w/ hypoperfusion, DON’T get better w/ IVF
 nephrotoxic
* direct damage to tubular cells
* meds, most common aminoglycosides
o cephalosporins methotrexate, NSAIDS, ct contrast
* endogenous pigments
o hgb and myoglobin- RHABDO

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22
Q

what are the findings of intra-renal AKI affecting: Tubular
FeNa:
BUN:
sediment:

A

-FeNa elevated
-BUN preserved
-muddy brown casts-sediment: that is d/t the dead tubular cells getting trapped into protein

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23
Q

what are the treatments of intra-renal AKI affecting: Tubular

A

involves supportive care, give those tubulues time to get better, you remove meds that are nephrotoxic, avoid dehydration, dialysis if needed. They can recover on own over days or weeks

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24
Q

what are the etiology of intra-renal AKI affecting: Interstitial

A

-allergy to a medication
-usually presents 3-5 days after the start of a medication

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25
what are the findings of intra-renal AKI affecting: Interstitial
-fever -rash-macular blanching -eosinophilia **only 10% will have all three**
26
what are the treatment of intra-renal AKI affecting: Interstitial
-removing offending agent -provide steroids/immunosuppressin
27
Etiology of post-renal AKI
o Obstruction anywhere in the GU tract that can cause blockage of urine flow and kidney failure ** Find obstruction and fix it (the longer the obstructions the harder to recover) etiology: could be a stone or mechanical dysfunction of the bladder where it does not contract and urine gets backed up (tumors, anticholinergics, stone, or prostate)
28
what are the diagnostic considerations for post-renal AKI?
-kidney U/S: looking for obstruction, dilatation of collecting strictures -noncontrast CT scan: prefer for locating stones or obstructions -UA: dipstick and microscopic: for protein, pH, hematura, high urea, specific gravity and microscopic sediments--looking for muddy brown case for ATN or red cell casts for glomerular hematuria
29
what are the treatments for post-renal AKI? (3)
-relieve obstruction -re-establish urine flow -avoid nephrotoxic agents *goal is to remove any offending agents to prevent more or greater injury
30
URINARY SEDIMENT, URINE SODIUM, URINE OSMOLALITY, FRACTIONAL EXCRETION OF SODIUM, PROTEINURIA, SPECIFIC GRAVITY, AND BUN/CREATININE RATIO (SERUM) : Pre-renal
* Urine sodium is low, because aldosterone causes to retain sodium water will follow that sodium. Trying to volume expand self by retaining Na/water * Urine osmolality is high **Urine concentration because of dehydration** * Specific gravity is high * Urine sediment- bland, means there is no activity of sediment
31
URINARY SEDIMENT, URINE SODIUM, URINE OSMOLALITY, FRACTIONAL EXCRETION OF SODIUM, PROTEINURIA, SPECIFIC GRAVITY, AND BUN/CREATININE RATIO (SERUM): glomerulonephritis (intra-renal)
* Urine sodium is low * FeNa is varied but low * Urine sediment is active showing RBC casts
32
URINARY SEDIMENT, URINE SODIUM, URINE OSMOLALITY, FRACTIONAL EXCRETION OF SODIUM, PROTEINURIA, SPECIFIC GRAVITY, AND BUN/CREATININE RATIO (SERUM): Post-renal
* Urine sodium is low * FeNa is low * BUN/Cr > 20:1 * Urine sediment is bland
33
URINARY SEDIMENT, URINE SODIUM, URINE OSMOLALITY, FRACTIONAL EXCRETION OF SODIUM, PROTEINURIA, SPECIFIC GRAVITY, AND BUN/CREATININE RATIO (SERUM): ATN (intra-renal)
* Urine Sodium is >40 o Stays in urine, sodium * FeNa is high >3% * Urine sediment is muddy showing dead tubular cells
34
what labs differentiates between pre-renal and ATN?
FeNa (fractional excretion of sodium) **it is what % of Na is being excreted out in urine **only useful in oliguria
35
normal values for: urinary sediment
0-5 hyaline casts (bland)
36
normal values for: urinary sodium (spot urine)
20 mEq/L
37
normal values for: urine osmolality (spot urine)
300-900 mOsm/kg
38
normal values for: FeNa helpful in oliguria <500ml/day
about 1%-2%
39
normal values for: proteinuria (spot urine)
0-20 mg/dl
40
normal values for: specific gravity
1.00-1.030
41
normal values for: BUN:creat ratio
between 10:1-20:1
42
relationship between GFR and serum creatinine
-if GFR decreases, creat will increase (this is b/c the less creat is excreted, more in blood) -the lower the creat the high the GFR
43
what are the major causes of chronic kidney disease?
definition: syndrome characterized by a slow progressive decline in GFR <60 or kidney damage that persist greater than 3 months -DM #1 -HTN -Glomerulonephritis -Cystic Kidney disease
44
Discusses the stages of CKD: stage 1
kidney damage/normal or increased GFR -usually no symptoms, high BP is common
45
Discusses the stages of CKD: stage 2
kidney damage/mild: low GFR progression: increasing PTH, early bone disease , increasing plasma creatinine and urea symptoms: subtle HTN
46
Discusses the stages of CKD: stage 3
moderate/low GFR progression: EPO deficiency, anemia, increased plasma, creat, and urea symptoms: mild HT
47
Discusses the stages of CKD: stage 4
severe: low GFR progression: Increased triglycerides, metabolic acidosis, hyperkalemia, salt/water retention, increasing plasma creatinine and urea symptoms: moderate HTN, hyperphosphatemia, anemia
48
Discusses the stages of CKD: stage 5
ESRD; kidney failure progression: uremia symptoms: severe hypertension, hyperphosphatemia, anemia
49
treatments for CKD (6)
- ACE-I -ARB -treat underlying cause/complications -adjust meds to level of GFR -avoid nephrotoxic meds -if can’t be managed then dialysis or transplant-
50
how is CKD related to anemia and osteodystrophy?
* CKD leads to uremia which leads to osteodystrophy * Hypocalcemia is accelerated by impaired renal synthesis of 1,25-dihydroxy-vitamin D3 (calcitriol) with decreased intestinal absorption of calcium o Renal phosphate excretion also decreases, and the increased serum phosphate binds calcium, further contributing to hypocalcemia. o Acidosis also contributes to a negative calcium balance. o Decreased serum calcium level stimulates parathyroid hormone secretion with mobilization of calcium from bone and may cause calcium levels to approach normal. o The combined effect of secondary hyperparathyroidism and vitamin D deficiency can result in renal osteodystrophy
51
what is erythopoeitin?
a hormone produced by the kidney that promotes RBC production in BM
52
what hormone tells the gut to hang onto Ca?
vitamin D
53
what organ fixes Ca?
PTH
54
Primary cause for nephrotic syndrome
minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy
55
secondary cause for nephrotic syndrome
o Medications, allergens, infections, neoplasm, multisystem disease, heredofamilial or metabolic disease  Most common: DM  SLE, hep B/C, NSAIDS, amyloidosis, multiple myeloma, HIV, preeclampsia
56
what are the abnormal lab values for nephrotic syndrome (5)
* Proteinuria >3g/day * Hypoalbuminemia <3.5g/dL- losing albumin * Edema- secondary to low albumin * Hypercholesterolemia- liver makes more cholesterol * Lipiduria- secondary to high cholesterol
57
what are the first signs of kidney disease (screening)
-hematuria/proteinuria -decrease in GFR
58
what is the actual screening test for kidney disease?
albuminuria *once you have two readings with >300 mg/g= +albuminuria
59
where is renin produced? and what does it do?
it is produced in the juxtaglomerular apparatus - it catalyzes the formation of angiotensin from angiotensinogen
60
where is erythropoeitin (Epo) produced? and what is the role?
-produced by the renal corticol interstitial cells -works by stimulating the maturation of erythrocytes in the bone marrow
61
what is the main difference between ADH vs aldosterone?
-ADH makes tubules more permeable to water absorption -Aldosterone makes tubules more permeable to Na, thereby increasing water reabsorption by creating osmotic pressure
62
Vasopressin roles (4)
-control of the body's osmotic balance -BP regulation -sodium homeostasis -kidney function-->this works by decreasing the water excretion by the kidney by increasing water absorption in the collecting ducts aka ADH
63
where is aldosterone synthesized?
adrenal cortex
64
what parts of the nephron does aldosterone and ADH act on? (2)
-distal convoluted tubules -collecting tubules
65
where is majority of K+ reabsorbed?
it is passively reabsorbed in the proximal tubule

Advanced Patho Exam 1 (3 decks)

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