Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Urinary System > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

Definition of AKI

A

(AKA) Acute Renal Failure, Sudden decrease in kidney function over hours or days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Clinical Manifestations of AKI

A
  • Oliguria (Decrease in Urine Output)
  • Acute Increase in Serum Creatinine and Blood Urea Nitrogen levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What do the CMs lead to?

A
  1. Disturbance of extracellular fluid (ECF) volume
  2. Electrolyte Imbalances (e.g. Hyperkalemia - High Calcium levels)
  3. Acid-Base Abnormalities (e.g. Metabolic Acidosis)
  4. Retention of Nitrogenous Waste Products
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pathophysiology of AKI

A

Due to a sudden disruption in Kidney function, leading to reduced glomerular filtration, tubular damage, and impaired waste elimination.

Ischemic injury to renal cells (Decreased renal profusion, toxic inflammatory damage or UT obstruction), causes inflammatory and vascular response, which leads to tubular cell death, leading to decreased renal function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Underlying mechanisms (Pre-, Renal, Post-)

A

Pre: Hypo-perfusion causes ischemic damage resulting in tubular necrosis

Renal: Damage by Nephrotoxins or Glomerular/Intestinal inflammation, leads to necrosis (death) of tubular cells, causing sloughing (removing) of cells into lumen, which leads to tubular obstruction. Causing rise in intraluminal pressure, leading to deceased glomerular filtration rate (GFR).

Post: Obstruction to the urine outflow, increases the intra-tubular pressure and back flow, leading to damage to the tubular cells -> Acute Tubular Necrosis (ATN), and decreased glomerular filtration rate (GFR).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Functions of Kidney

A
  1. Regulate blood volume (Na, Water)
  2. Regulates electrolytes (Na, K, Ca, PO4)
  3. Regulates pH levels
  4. Removes wastes, toxins
  5. Produces hormones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pre-renal causes of AKI

A

Decreased renal blood flow or perfusion to nephrons that can be improved / resolved with fluid resuscitation without causing permanent damange to renal cells.

  1. Volume depletion (e.g. Haemorrhage, Diarrhoea, Vomiting, Burns)
  2. Reduced effective circulating volume (e.g. Heart Failure, Cariogenic Shock, Sepsis, Liver Cirrhosis)
  3. Renal Hypoperfusion (e.g. Renal Artery Stenosis, Embolism/Thrombosis or Renal Artery/Vein)
  4. Drugs altering Renal Auto-regulation (e.g. NSAIDs, ACE Inhibitors, Angiotensin II Receptor Blockers (ARBs))
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Renal causes of AKI

A

Acute damage to the renal tissue / direct damage to Kidney. Divided by location, Glomeruli (e.g. Glomerulonephritis), Tubules (e.g. Acute Tubular Necrosis, caused by Nephrotoxicity / Ischemia), Blood Vessels, and Interstitium.

  1. Ischemic Injury (e.g. Any cause reducing renal perfusion)
  2. Nephrotoxicity (e.g. Endogenous toxins, Exogenous toxins)
  3. Immune-mediated Injury (e.g. Antibodies and Immune complexes, Systemic Lupus Erythematosus)
  4. Vascular Disease (e.g. Vasculitis, Atheroemboli to the Kidney)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Post-renal causes of AKI

A

Obstruction to lower Urinary Tract and cause Post-renal Injury. Anuria (Lack of Urine) in Incomplete Obstruction. Obstruction of Urine Outflow increases pressure in Bowman’s Capsule, which opposes glomerular filtration.

Examples of Obstructions:
- Kidney Stones (Renal Calculi)
- Enlarged Prostate
- Tumours compressing Urinary Structures
4. Blood Clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Phases of AKI

A
  1. Initiation Phase
  2. Maintenance (Oliguric) Phase
  3. Recovery (Polyuric) Phase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Initiation Phase of AKI

A
  • Period of decreased perfusion, toxicity / obstruction
  • Prevention of AKI is still possible at this point
  • Usually lasts 1-3 weeks
  • Oliguria, as a result of decreased filtration in glomerulus, tubular obstruction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Maintenance (Oliguric) Phase of AKI

A
  • May last up to a few weeks to months
  • Oliguria continues as Urine Output is at its lowest (Due to Vasoconstriction, Tubular Injury)
  • Increased Creatinine, Blood Urea Nitrogen (BUN)
  • Clinical Manifestations:
    1. Fluid Overload (e.g. Peripheral oedema, CCF, Pulmonary Oedema, Ascites, Pleural Effusion)
    2. Electrolyte Disturbance (e.g. Hyperkalemia, Hyponatremia)
    3. Metabolic Acidosis
    4. Accumulation of Toxins (Anorexia, Nausea, Vomiting, Encephalopathy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Recovery (Polyuric) Phase of AKI

A
  • Occurs as Renal Function improves, progressive increase in Urine Output, due to to recovery of glomeruli with increased Glomerular Filtration Rate (GFR).
  • Diuresis (Increased amount of Urine) occurs initially as tubules are still damaged.
  • Polyuria (Excessive Urination) with loss of Na & K
  • Fluid and Electrolyte must be carefully monitored
  • Serial Creatinine levels provides index of kidney function
  • Tubular recovery occurs over 3-12 months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Definition of Renal Auto-regulation

A

Maintains constant blood flow to the glomerulus despite changes in blood pressure, which ensures Glomerular Filtration Rate (GFR).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mechanism of Renal Auto-regulation

A
  1. Afferent (Toward) Arteriole Constriction:
    - Decreases glomerular pressure
    - Decreases GFR
  2. Efferent (Away) Arteriole Constriction:
    - Increases glomerular pressure
    - Increases GFR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Drugs that affect auto-regulation

A
  1. NSAIDs - Inhibits prostaglandins:
    - Decreases afferent arteriole dilation
    - Decreases renal blood flow
    - Worsens kidney perfusion
  2. ACE Inhibitors/ARBs - Block Angiotensin II:
    - Prevents efferent arteriole constriction
    - Decreases glomerular pressure
    - Causes/Worsens AKI in at-risk patients
17
Q

Pharmacological Management of AKI

A
  1. Fluid Management
  2. Drug Adjustments
  3. Renal Replacement Therapy (Dialysis)
18
Q

Fluid Management of AKI

A
  • Replace fluid for hypovolemia (e.g. IV Fluids)
  • Blood Transfusion, if due to haemorrhage
  • Loop Diuretic (e.g. Furosemide) for when Kidney fails to excrete fluids and the body is overloaded with fluid, leading to Oedema

Side effects: Hypokalemia (Low potassium), Dehydration, Hypotension

19
Q

Drug Adjustments for AKI

A
  • Avoid nephrotoxic drugs (e.g. NSAIDs, Amino-glycosides)
  • Adjust doses of renally excreted drugs (e.g. Opioids, Antibiotics)
20
Q

Renal Replacement Therapy (Dialysis) for AKI

A
  • Indicated for:
    1. Life-threatening hyperkalemia / fluid overload
    2. Acidosis not responding to treatment
  • Dialysis includes hemodialysis to remove waste, correct electrolyte, and manage acid-base imbalances

Urinary System (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions