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pathophysiology 4802 > Kidney Disease (Final Exam) > Flashcards

Kidney Disease (Final Exam) Flashcards

1
Q

what are the basic functions of the kidney

A
  • cleansing of the extracellular fluid (ECF)
  • maintenance of ECF
  • acid-base balance
  • excretion of metabolic wastes and foreign substances
  • eyrthropoiesis (making RBCs)
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2
Q

what are some ways the RAAS is activated to result in increased cardiac pumping and O2 demand

A

decreased blood volume, decreased BP, decreased renal perfusion, beta1 stimulation

renin release -> angiotensin I -> angiotensin II -> aldosterone (increases sodium and water retention and increases potassium excretion -> vasoconstriction

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3
Q

this is a syndrome characterized by rapid deterioration of renal function; it is reversible

A

acute kidney injury (AKI)

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4
Q

a ___________ (decrease/increase) in serum creatinine (SCr) concentration often associated with a reduction in urine volume in AKI

A

increase

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5
Q

true or false: BUN rapidly rises in AKI

A

true

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6
Q

true or false: oliguria (decreased urine output) is always present in AKI

A

false - not always present

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7
Q

what are some causes of AKI

A
  • aging
  • comorbidities
  • trauma to kidney
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8
Q

this is the most common form of AKI. it is retention of metabolic wastes, and is monitored by BUN.It is the designation for a rise in SCr or BUN concentration due to inadequate renal plasma flow and intraglomerular hydrostatic pressure to support normal glomerular filtration. can produce widespread systemic affects.

A

pre renal azotemia

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9
Q

what are some causes of pre-renal AKI that cause an absolute decrease in circulating blood volume

A
  • dehydration
  • burns
  • hemorrhage
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10
Q

what are some causes of pre-renal AKI that cause a relative decrease in circulating blood volume

A
  • distributive shock (sepsis, anaphylactic)
  • heart failure, MI
  • decrease cardiac output
  • third-spacing and edema
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11
Q

what are some primary renal hemodynamic abnormalities that cause pre-renal AKI

A
  • occlusion or stenosis of renal artery
  • drug induced impairment of renal auto-regulation in susceptive persons
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12
Q

what are some causes of intra renal AKI

A
  • prolonged pre renal failure
  • sepsis
  • transfusion reactions
  • rhabdomylosis
  • antimicrobials
  • cytotoxic chemotherapy agents
  • snake and insect venom
  • acute glomerulonephritis
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13
Q

what are some causes of acute post-renal AKI

A
  • benign prostatic hyperplasia
  • kinked or obstructed catheters
  • intra-abdominal tumors
  • calculi (kidney stones)
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14
Q

this is one of the theories related to the pathogenesis of AKI. accumulation of cellular debris. occlusion of tubules leads to decreased GFR

A

tubular theory

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15
Q

this is one of the theories related to the pathogenesis of AKI. afferent arterioles obstruction combined with efferent arteriole dilation (sepsis) leads to decreased GFR

A

vascular theory

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16
Q

true or false: under a normal situation, are arteriolar resistances the same or different in afferent and efferent arterioles

A

same!!

17
Q

what happens intranrenally if there is decreased perfusion pressure in order to maintain a normal GFR

A

less resistance in afferent, more resistance in efferent to maintain a normal GFR

18
Q

explain what happens intrarenally if someone is taking NSAIDs

A

afferent resistance increases because there are less vasodilatory prostaglandins (because NSAIDs inhibit these) therefore we get a low GFR

19
Q

explain what happens intrarenally if someone is taking an ACE-I or an ARB

A

efferent resistance is reduced therefore more being filtered out than coming in which leads to low GFR

20
Q

how may inflammation/injury lead to oliguria in AKI

A

inflammation/injury -> tubular obstruction -> increased tubular intraluminal pressure -> decreased GFR -> oliguria

21
Q

what are some clinical manifestations of AKI

A
  • fatigue/malaise
  • dyspnea, orthopnea, rales, third hard sounds
  • peripheral edema
  • altered mental status
  • elevated BUN
    very vague
22
Q

this is characterized by low GFR, oliguria, high urine specific gravity and osmolality and low urine sodium. S/S of fluid overload are present. if this is prolonged, it can lead to intra-renal injury

A

pre-renal AKI

23
Q

this is caused by primary dysfunction of the nephrons. most often a problem within the renal tubules resulting in acute tubular necrosis.

A

intra-renal AKI

24
Q

this is caused by obstruction within the urinary collecting system distal to the kidney; elevated pressure in the Bowman’s capsule; impedes glomerular filtration. if this is prolonged, can lead to intra-renal AKI

A

post-renal AKI

25
Q

what are the three stages of acute tubular necrosis

A

oliguric stage, diuretic stage and recovery stage

26
Q

this stage of ATN is characterized by oliguria and progressive uraemia, decreased GFR and hypovolemia. may last 1-2 weeks and dialysis may be required

A

oliguric stage

27
Q

in this stage of ATN, urine volume increases, but tubular function remains impaired and azotemia continues. may last 2-10 days

A

diuretic stage

28
Q

this stage of ATN is characterized by gradual normalization of SCr and BUN. may last up to 12 months. there is often a degree of renal insufficiency that persists

A

recovery stage

29
Q

what are some comorbidities associated with chronic kidney disease

A

hypertension
DM
infection
obsruction
polycystic kidney disease
glomerulonephritis

30
Q

this is defined as a decreased kidney function or kidney damage of 3 months duration based on blood tests, urinalysis, and imaging studies. GFR < 60 for 3 months with or without indication of damage to the kidney

A

chronic kidney disease

31
Q

the pathogenesis of this disease is progressive and irrevocable loss of nephrons
- greater burden placed on raining nephrons
- fibrosis and scarring occur

A

chronic kidney disease

32
Q

what are some differences between a normal glomerulus and a hyperfiltering glomerulus

A

hyperfiltering as damaged endothelium and sclerosis along with enlarged arterioles

33
Q

how is uraemia in chronic kidney disease caused

A
  1. retained products normally excreted by the kidney (nitrogen wastes)
  2. accumulation of normal products (hormones)
  3. loss of normal products (EPO)
  4. increased intracellular sodium and water
  5. decreased intracellular potassium
34
Q

what are some clinical manifestations of uremic syndrome

A
  • disorientation/lethargy
  • weakness/numbing
  • microcytic hypochromic anemia
  • infections
  • anorexia/n/v/uremic frost (can see uremic crystals on skin when u sweat)
  • metabolic acidosis
35
Q

what are some further complications of chronic kidney disease

A

HTN and CVD
uremic syndrome -> metabolic acidosis
electrolyte imbalance
renal osteodystrphy (weakened bones, kidneys unable to resorb calcium and elevated PTH therefore can make vitamin D)
malnutrition
anemia

36
Q

what are the two ways CKD are monitored

A

nephron loss and reduction in GFR
(GFR reduction occurs with nephron loss)

pathophysiology 4802 (16 decks)

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