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Advanced Patho Exam 1 > Exam 1: Renal > Flashcards

Exam 1: Renal Flashcards

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
Q

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

A

-fever
-rash-macular blanching
-eosinophilia
only 10% will have all three

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26
Q

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

A

-removing offending agent
-provide steroids/immunosuppressin

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27
Q

Etiology of post-renal AKI

A

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
Q

what are the diagnostic considerations for post-renal AKI?

A

-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
Q

what are the treatments for post-renal AKI? (3)

A

-relieve obstruction
-re-establish urine flow
-avoid nephrotoxic agents
*goal is to remove any offending agents to prevent more or greater injury

30
Q

URINARY SEDIMENT, URINE SODIUM, URINE OSMOLALITY, FRACTIONAL EXCRETION OF SODIUM, PROTEINURIA, SPECIFIC GRAVITY, AND BUN/CREATININE RATIO (SERUM) : Pre-renal

A
  • 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
Q

URINARY SEDIMENT, URINE SODIUM, URINE OSMOLALITY, FRACTIONAL EXCRETION OF SODIUM, PROTEINURIA, SPECIFIC GRAVITY, AND BUN/CREATININE RATIO (SERUM): glomerulonephritis (intra-renal)

A
  • Urine sodium is low
  • FeNa is varied but low
  • Urine sediment is active showing RBC casts
32
Q

URINARY SEDIMENT, URINE SODIUM, URINE OSMOLALITY, FRACTIONAL EXCRETION OF SODIUM, PROTEINURIA, SPECIFIC GRAVITY, AND BUN/CREATININE RATIO (SERUM): Post-renal

A
  • Urine sodium is low
  • FeNa is low
  • BUN/Cr > 20:1
  • Urine sediment is bland
33
Q

URINARY SEDIMENT, URINE SODIUM, URINE OSMOLALITY, FRACTIONAL EXCRETION OF SODIUM, PROTEINURIA, SPECIFIC GRAVITY, AND BUN/CREATININE RATIO (SERUM): ATN (intra-renal)

A
  • Urine Sodium is >40
    o Stays in urine, sodium
  • FeNa is high >3%
  • Urine sediment is muddy showing dead tubular cells
34
Q

what labs differentiates between pre-renal and ATN?

A

FeNa (fractional excretion of sodium)
**it is what % of Na is being excreted out in urine
**only useful in oliguria

35
Q

normal values for: urinary sediment

A

0-5 hyaline casts (bland)

36
Q

normal values for: urinary sodium (spot urine)

A

20 mEq/L

37
Q

normal values for: urine osmolality (spot urine)

A

300-900 mOsm/kg

38
Q

normal values for: FeNa
helpful in oliguria <500ml/day

A

about 1%-2%

39
Q

normal values for: proteinuria (spot urine)

A

0-20 mg/dl

40
Q

normal values for: specific gravity

A

1.00-1.030

41
Q

normal values for: BUN:creat ratio

A

between 10:1-20:1

42
Q

relationship between GFR and serum creatinine

A

-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
Q

what are the major causes of chronic kidney disease?

A

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
Q

Discusses the stages of CKD: stage 1

A

kidney damage/normal or increased GFR
-usually no symptoms, high BP is common

45
Q

Discusses the stages of CKD: stage 2

A

kidney damage/mild: low GFR
progression: increasing PTH, early bone disease , increasing plasma creatinine and urea
symptoms: subtle HTN

46
Q

Discusses the stages of CKD: stage 3

A

moderate/low GFR
progression: EPO deficiency, anemia, increased plasma, creat, and urea
symptoms: mild HT

47
Q

Discusses the stages of CKD: stage 4

A

severe: low GFR
progression: Increased triglycerides, metabolic acidosis, hyperkalemia, salt/water retention, increasing plasma creatinine and urea
symptoms: moderate HTN, hyperphosphatemia, anemia

48
Q

Discusses the stages of CKD: stage 5

A

ESRD; kidney failure
progression: uremia
symptoms: severe hypertension, hyperphosphatemia, anemia

49
Q

treatments for CKD (6)

A
  • 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
Q

how is CKD related to anemia and osteodystrophy?

A
  • 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
Q

what is erythopoeitin?

A

a hormone produced by the kidney that promotes RBC production in BM

52
Q

what hormone tells the gut to hang onto Ca?

A

vitamin D

53
Q

what organ fixes Ca?

A

PTH

54
Q

Primary cause for nephrotic syndrome

A

minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy

55
Q

secondary cause for nephrotic syndrome

A

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
Q

what are the abnormal lab values for nephrotic syndrome (5)

A
  • 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
Q

what are the first signs of kidney disease (screening)

A

-hematuria/proteinuria
-decrease in GFR

58
Q

what is the actual screening test for kidney disease?

A

albuminuria

*once you have two readings with >300 mg/g= +albuminuria

59
Q

where is renin produced? and what does it do?

A

it is produced in the juxtaglomerular apparatus
- it catalyzes the formation of angiotensin from angiotensinogen

60
Q

where is erythropoeitin (Epo) produced? and what is the role?

A

-produced by the renal corticol interstitial cells
-works by stimulating the maturation of erythrocytes in the bone marrow

61
Q

what is the main difference between ADH vs aldosterone?

A

-ADH makes tubules more permeable to water absorption
-Aldosterone makes tubules more permeable to Na, thereby increasing water reabsorption by creating osmotic pressure

62
Q

Vasopressin roles (4)

A

-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
Q

where is aldosterone synthesized?

A

adrenal cortex

64
Q

what parts of the nephron does aldosterone and ADH act on? (2)

A

-distal convoluted tubules
-collecting tubules

65
Q

where is majority of K+ reabsorbed?

A

it is passively reabsorbed in the proximal tubule

Advanced Patho Exam 1 (3 decks)

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