Unit 1: Chapter 34 Flashcards

(25 cards)

1
Q

Acute Kidney Injury

A

Represents a rapid decline in kidney function that happens without a few hours or within a day.
Decreased blood flow to kidney
Buildup of nitrogenous waste (azotemia) products and impairs fluid and electrolyte balance.
Decrease in GFR
Reversible if can be corrected

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2
Q

GFR

A

Glomerular filtration rate
With a decrease in this rate excretion of nitro go us waste is reduced and fluid and electrolytes cannot be maintained

GFR is used as a guide for stages of CKD
Beginning with kidney damage with normal or elevated GFR, progressing to CKD and potentially failure

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3
Q

AKI Classifications

A
  1. Prerenal
  2. Intrinsic Or Intrarenal
  3. Postrenal
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4
Q

Prerenal AKI

A

Caused by decreased blood flow to the kidneys

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5
Q

Intrarenal or Intrarenal AKI

A

Caused by disorders in the kidney itself

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6
Q

Postrenal AKI

A

Caused by obstruction to urine output

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7
Q

Main Cause of AKI

A

Is ischemia, sepsis or nephrotoxic agents

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8
Q

Four Phases of AKI

A
  1. Onset phase: (hrs/days)which is the time fromt he onset of the precipitating event until tubal injury occurs
  2. Oliguria/anuric phase: (8-14 days) during which there is marked decreased int he GFR causeing sudden retention of endogenous metabolites. Urine is at its lowest.
  3. Diuretic Phase: in which the kidney try to heal and urine output increased but tubule scarring and damage occur
  4. Recovery phase: during which the GFR, urine output and blood levels of nitrogenous waster return to normal
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9
Q

Chronic Kidney Disease

A

GFR best measure of function
Either kidney damage or a GFR less than 60 mL/min/1.73 for 3 months or longer
Most common: hypertension and DM
Progressive decline in fucntion because of permanent loss of nephrons

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10
Q

CKD Guidelines

A
  1. A GFR < 15mL/min/1.73 usually accompanied by most of the s&s of uremia
  2. A need to start renal replacement therapy (dialysis or transplantation)
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11
Q

Disorders of Calcium, Phosphorus Metabolism and Bone Disease

A

Abnormalities of these occur early in the course of CKD.
Phosphate excretion is impaired with deteriorating renal function causeing and increase thus decrease of Calcium.
Decreased calcium causes PTH release with a result of increase Ca resorption from bone.

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12
Q

Vitamin D and CKD

A

Vit D synthesis is impaired with CKD.
Kidneys regulate Vit D activity by converting the inactive form to calcitriol.
Calcitriol have direct suppressive effect on PTH production
So reduced levels of calcitriol causes elevation of PTH.

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13
Q

Acute Tubular Injury or Necrosis (ATN)

A

Characteriezed by the destruction of the tubular epithelial cells with acute supression of renal function
Occurs in people with extensive surgery, sever Hypovolemic or overwhelming sepsis, trauma or burns

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14
Q

ATN Causes

A

Acute tubular damage because of ischemia, sepsis, nephrontoix effect of drugs, tubular obstruction and toxins form a massive infection
Tubular cells are sensitive to ischemia and vulnerable to toxins.
Damage can be reversible.

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15
Q

Uremia

A

Urine in the blood
Clinical manifestation of kidney failure
Onset s&S: weakness, fatigued nausea and apathy are subtle. Extreme weakness, vomiting, lethargy and confusion
Include s&s of altered fluid, electrolytes, and acid base balance, alternations in regulatory functions.

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16
Q

Anemia

A

Chronic anemia (13.0 g/dlmen, ,12g/dl women)
Is the most profound hematology alteration that accompanies CKD.
Assessment: measure of hemoglobin, hematocrit and iron studies
Due to chronic blood loss, hemolysis, bone marrow suppression and decreaed red cell production because of production of erythropoietin and iron deficiency.

17
Q

Erythropoietin

A

Kidneys are primary site for this hormones production
Controls red blood cell production

18
Q

Anemia s&S

A

Weakness
Fatigue
Hea he
Irritability
Depression
Insomnia
Decreaed cognitive function

19
Q

Hypertension

A

Common and early manifestation of CKD
Multifactorial: increased vascular volume, elevation of peripheral vascular resistance, decreased levels of renal vasodilator prostaglandins and increased activity of renin angiotensin system

20
Q

Heart Disease

A

Spectrum of CVD because CKD includes left ventricular hypertrophy and ischemic heart disease
People with CKD have increaed prevlacen of left ventricular dysfunction with both depressed left ventricular ejection fraction
CHF and PE tend to occur in late staged of kidney failure

21
Q

Pericarditis

A

Occurs with people ion stage 5 CKD due to uremia and prolonged dialysis
Manifestations: cardiac tamponade, mild to sever CP with resp accentuation and a pericardial friction rub.

22
Q

Elimination of Drugs

A

Main organ: kidneys
CKD can interfere with the absorption, distribution and elimination of drugs
Drugs bind to plasma proteins: albumin
A decreased of plasma proteins as seen in CKD means less protein bound drugs and more free drugs.

23
Q

Hydrolysis

A

Pathway of drug metabolism
Slowed with uremia

24
Q

Hemoglobinlobinuria

A

Presen of hemoglobin in urine from excessive blood cell breakdown.
Significantly impacts the kidneys, leading to potential damage like AKI or CKD through tubular obstruction, heme, toxicity, and vascoconstruction.

25
ATN Recovery Phases
1. Initiation phase: initial stage, lasts hours to days. Onset of ischemia or toxin. Rapid decreased in GFR 2. Maintenance Phase: 1-3 weeks. Low ursine output (Oliguria), kidney Dysfuntion, high creat/BUN, lytes emblances 3. Recovery phase: 10-14 days. tubular cell repair and regeneration. Increase in urine output(diureses or poly uria. 3-5 L/day