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Renal II Final > AKI and CKD > Flashcards

AKI and CKD Flashcards

1
Q

AKI is defined as

A

increase in serum creatinine +/- decrease in urine output over hours to days

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2
Q

As a result of _ the following are some of the things affected electrolyte disturbances, acid-base disturbances (metabolic acidosis) inability to excrete nitrogenous waste and IV volume overload

A

AKI

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3
Q

_ can be caused by dehydration aka volume contraction or EC volume depletion, due to fluid losses from nausea and vomiting.

A

orthostatic hypotension

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4
Q

Poor tissue turgor can be due to _

A

volume deficit

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5
Q

If a patient presents to ER after passing out with no significant medical history, but history of nausea vomiting prior to this event indicating dehydration. Aside from UA, what additional labs is indicated to to determine possible causes?

A

Serum electrolytes, BUN and creatinine - need to determine Na, K, Cl levels that can be affected by dehydration. It’ll tell us if pt is retaining nitrogenous waste and retaining creatinine, indicating AKI

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6
Q

Fractional Excretion of sodium helps to sort between what two renal issues?

A

Pre-renal vs intrinsic renal issues.

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7
Q

If a patient is dehydrated, what would their specific gravity be?

A

high or on the higher end of normal. Normal is 1.003-1.040

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8
Q

how do you calculate FeNA?

A

(Una / Pna ) / (Ucr / Pcr) x 100

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9
Q

What does FeNa less than 1% indicate?

A

Tubules are intact and Na avid ie retaining sodium as would be expected in dehydration. Prerenal cause

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10
Q

Azotemia is defined as?

A

elevated BUN

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11
Q

An elevated Creatinine is implicated as

A

AKI

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12
Q

Elevated BUN plus confusion would be termed as _

A

uremia. Uremia is azotomia with symptoms.

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13
Q

Anything that compromises renal perfusion is indicated as pre-renal. What are some examples of prerenal issues?

A
  1. hypovolemia: dehydration, viral syndromes, acute pancreatitis, diuretics
  2. Low CO: CHF
  3. Altered renal/SVR ration: sepsis, cirrhosis
  4. Renal hypoperfusion with impaired autoregulation: NSAIDs
  5. Hyperviscosity syndrome (rare): myeloma
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14
Q

In many pre renal issues, such as hypovolemia due to dehydration, and even with effective volume depletion such as pancreatitis what treatment is indicated/

A
  • Fluid replacement by IV.

- treat the underlying cause

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15
Q

What are 6 methods of intrinsic renal failure?

A
  1. renovascular obstruction : renal artery obstruction e.g. embolism, dissecting aortic aneurysm (renal a. stenosis etc)
  2. Disease of glomeruli or microvasculature as seen in accelerated HTN
  3. Acute tubular necrosis: iodinate contrast dye -
  4. Interstitial nephritis: acute pyelonephritis, NSD, contrast dye etc
  5. Intratubular deposition and obstruction: myeloma
  6. Renal allograft rejection
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16
Q

what two pre renal diseases greatly increase risk of tubular damage from contrast dye?

A

HTN and DM

17
Q

if pan AKI patient is unresponsive to conservative measures, when would hemodialysis be indicated?

A

A. volume overload refractory to diuretics
B. Hyperkalemia
C. Encephalopathy otherwise unexplained
D. Pericarditis, pleuritis
E. severe metabolic acidosis compromising respiratory or circulatory function

18
Q

the 5 stages of CKD is based on what measured value?

A

GFR

19
Q

what are the 5 stages of CKD?

A
  1. kidney damage with normal or increased GFR (equal or greater than 90)
  2. Mild decrease in GFR (60-89)
  3. moderate decrease in GFR 30-59
  4. Severe decrease in GFR 15-29
  5. Kidney failure (ESRD) less than 15 or on dialysis
20
Q

If a patient comes in with stage 2 CKD, no HTN or DM what is the best mode of treatment?

A

ACE inhibitor. It poses kidney protection to delay progression of CKD even if blood pressure does not need treatment. Follow patient every 3 months

21
Q

what effects does uremic toxins have on cellular function?

A

Reduce in transmembrane voltage ( inc. Na, dec. K. Inhibit Ca influx)
- reversible with dialysis

22
Q

what effects does uremic toxins have on whole body composition?

A
  • osmoticaly induced overhyrdation of cells
  • increased EC volume
  • Malaise, anorexia, N/V/D ( protein and calorie malnutrition, negative nitrogen balance, profound loss of lean body mass and fat deposits)
23
Q

What effects does uremic toxins have on metabolism?

A
  • Hypothermia (decreased active Na transport)
  • IC deficits of K
  • Metabolic acidosis
24
Q

what effects does Uremic toxins have on Nitrogen and lipids?

A
  • Protein intolerance (increase catabolism and decrease elimination)
  • hypertriglyceridemia, decrease HDL, normal cholesterol ( decrease removal by lipoprotein lipase, increase lipogenesis, and possibly increase production by liver and intestine
25
Q

What effects does uremic toxins have on Na and Volume homeostasis?

A
  • Total body content of Na and water are increased modestly in stable CKD
  • excessive salt ingestion can lead to: CHF, HTN, ascites, edema
  • Excessive water ingestion: hyponatremia, wt gain
  • Recommended fluid intake pre-dialysis: urine output plus 500 ml/day
26
Q

What effects does K have in CKD?

A
  • it’s normal until late stages, adaptation DCT and colon sites where ALD enhance K secretion
  • increased K –> cardiac arrhythmias
  • should avoid antikaliuretic drugs like spironolactone and amloride in these pts.
27
Q

Describe how a dehydrated person would appear.

A
  • Dry mucous membrane, dizziness, syncope tachycardia, decreased JVP, orthostatis, CV collapse
28
Q

What is the most common complication of ESRD?

A

HTN. Chronic dialysis pts also have a higher incidence of accelerated atherosclerosis which contributes to the HTN

29
Q

If pt has no HTN, what other factors might be contributing to their ESRD?

A
  • Salt wasting form of renal disease causing CKD (PKD, MCD, chronic tubulointerstitial disease, papillary necrosis)
  • VOlume depletion
  • On antihypertensive therapy at the time
30
Q

Pulmonary congestion can also be a factor leading to CKD. what findings are seen in these patients?

A

Normal or mildly elevated intracardiac or pulmonary capillary wedge pressures. On chest X ray: butterfly wing distribution due to increased permeability of alvoelar capillary membranes.

31
Q

If a pt presents with pericarditis but the patient is well dialyzed, what is the likely DDX/

A

viral infection or a systemic disease. You’d see effusion often hemorrhagic

32
Q

what hematologic conditions is associated with CKD?

A

Anemia: normocytic, normochromic anemia.

  • Hemolysis - uremic pts
  • Prone to GI blood loss, chronic dialyzer blood loss
  • Hypersplenism - occasional
33
Q

With uremia, what bone change are seen?

A
  • Renal rickets - widened ostoid seams at growth margins.
  • Osteitis fibrosis cystica - due to secondary hyperparathyroidism: osteoclastic bone resorption erosions, terminal phanlages, long bones, distal clavicles
  • Osteosclerosis.
34
Q

what are some indications for dialysis?

A
  • unresponsive to conservative measures
  • Volume overload refractory to diuretics
  • Hyperkalemia
  • Encahlopahty otherwise unexplained
  • pericarditis, pleuritiss
  • Severe metabolic acidosis compromising respiratory or ciculatory funciton
  • need for fluid/drugs also a consideration
35
Q

which dialysis method is most commonly used for AKI and CDK?

A

Intermittent hemodialysis

36
Q

what complications are associated with peritoneal dialysis?

A
  • peritonitis
  • hyperglycemia
  • hypertriglyceridemia
  • obsesity
  • hypoproteinemia
  • dialysis-related amyloidosis
  • insufficient clearance due to vascular disease or other factors.

Renal II Final (4 decks)

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