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M202 > W26 Pathophysiology of AKI and CKD (SM) > Flashcards

W26 Pathophysiology of AKI and CKD (SM) Flashcards

1
Q

What is renal failure?
What are the 2 types of renal failure?

A
  • A reduction in the kidneys ability to sufficiently filter waste products from the blood
  • Acute Kidney Injury: A rapid loss of renal/kidney function
  • Chronic Kidney Disease: A progressive deterioration of renal/kidney function

Also: Polycystic Kidney Disease: An inherited condition (Kidney are larger than usual due to the gradual growth of masses of cysts in both kidneys)

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2
Q

What is an Acute Kidney Injury?
Features? (6)
What is the diagnosis and staging based upon?

A
  • A rapid loss of renal/kidney functions
    -reduced urine output
    -large abdomen due to urine retention in the bladder
    -fluid overload-raised jugular venous pressure, peripheral and pulmonary oedema
  • hypertension
  • nausea and vomiting or diarrhoea, indicate dehydration (postural hypotension)
  • confusion, fatigue and drowsiness
  • AKIs diagnosis and staging are based on serum creatinine or urine output (RIFLE, AKIN, KDIGO guidelines)
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3
Q

AKI Incidences and Risk factors:
What are the types of AKI incidences?
Risk factors?

A
  1. Community-acquired:
    * Poor fluid intake
    * Dehydration
    * Drugs (ACEIs, ARBs, diuretics, NSAIDs)
    * Infection
    * Trauma
    * Rhabdomyolysis
  2. Hospital-acquired:
    * Volume depletion
    * Hypotension
    * Low cardiac output
    * Nephrotoxic drugs
  3. ICU-acquired:
    * Sepsis/septic shock
    * Major surgery,
    * Multiorgan failure,
    * Hypotension,
    * Low cardiac output,
    * Nephrotoxic drugs
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4
Q

What are the 3 categories of AKI causes?

A
  • Prerenal- Impairment in the blood supply to the kidney
  • Intrinsic/Intrarenal- Impairments within the kidney’s blood vessels, glomeruli and tubules
  • Postrenal- Obstruction of the urinary collecting system
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5
Q

What are the prerenal causes of AKI?

A

Reduced renal perfusion (blood supply to the kidney) :
- Volume depletion (diarrhoea, vomiting, burns, haemorrhage)
- Decreased effective circulatory blood volume (heart failure, sepsis, anaphylactic shock)
- Altered renal haemodynamic (artery stenosis/ embolism/ thrombosis
- Drugs, such as NSAIDs, ACEis, ARBs

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6
Q

What are the Intrinsic (or intrarenal) causes of AKI?

A

Pathological damage to glomerular, tubular or interstitial regions
* Glomerulonephritis (due to abnormal immune reaction)
* Nephrotoxic damage/ tubular necrosis (ischaemic or toxic) e.g. heavy metals, ethylene glycol, antibiotics, myoglobin
* Pyelonephritis (assoc with infection)

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7
Q

What are the postrenal causes of AKI?

A

Obstruction to urine flow-back pressure inhibits filtration:
* Swelling compresses blood vessels leading to ischaemia
* Obstructions (in ureter, bladder, prostate, urethra)
-Urinary tract stones, precipitation of calcium, urates or cystine
-Tumour either within the wall of the tract or outside the wall

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8
Q

What 3 things need to be managed in AKI?

A

Fluid overload
Metabolic acidosis
Hyperkalemia (clinical emergency)

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9
Q

What is fluid overload in AKI?

A

Excess fluid accumulation in the body,
including arms and legs (peripheral oedema)
and in lungs (pulmonary oedema)
-swollen ankles, feet and legs

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10
Q

What is metabolic acidosis?

A
  • Decreased Na+ delivery to late DCT & CD is associated with decreased H+ secretion/ loss in the urine (urinary pH becomes alkali and blood pH becomes acidic)
  • Nausea, vomiting, drowsiness and breathlessness
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11
Q

What is hyperkalaemia? (clinical emergency)

A
  • Due to impaired potassium homeostasis (excretion/secretion), the level of potassium in
    the blood raise.
  • Cardiac arrythmia (ventricular fibrillation or asystole) and arrest, paralysis and muscle weakness
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12
Q

AKI- Management
What are the underlying causes?

A

Identify the cause and eliminate the stressors:
infection- antibiotics
obstruction- remove or catheter to empty bladder
toxic drugs- stop taking

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13
Q

How to manage the symptoms of an AKI?
Dehydration/volume depletion

A

Dehydration/volume depletion: Crystalloids/colloids ? Hartmann’s solution
Fluid resuscitation: To optimise intravascular circulating volume and to decrease cardiac
output and prefusion pressure (improve renal blood flow and filtration)

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14
Q

How to manage the symptoms of an AKI?
Oedema?

A

Oedema: Loop diuretics (furosemide, only for the management/no proven benefit to prevent
AKI or lower risk of RRTs), direct acting vasodilator infusions (GTN). Restrict salt and fluids intake

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15
Q

How to manage the symptoms of an AKI?
Metabolic acidosis?

A

Sodium bicarbonate (cautioned for patients with hyperkalaemia or infused under supervision

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16
Q

What is Hyperkalemia defined as?
What are the ECG changes resulting from Progressive hyperkalaemia? (5)

A

Hyperkalaemia: (at >7mmol/L; clinical emergency, If ECG changes are present)

  • peaked T wave
  • prolonged PR interval
  • prolonged QRS duration
  • flattened P wave
  • ST depression
17
Q

AKI Management of Hyperkalemia:

A
  1. Stabilise myocardium and cardiac rhythms:
    -Calcium gluconate antagonise the membrane excitability.
    -It raises the cell depolarization threshold and reduces myocardial irritability by excess potassium (CG has no effect on potassium level)
  2. Redirect the potassium from blood to cells.
    -Insulin & glucose: Insulin stimulates the sodium-potassium (Na-K) adenosine
    triphosphatase (ATP) pump resulting in intracellular uptake of K (this effect is independent of hypoglycaemic action). Glucose administered to maintain the glycaemia.
    -Salbutamol (β2 agonist): Salbutamol binds to β2 receptors in liver and muscle cells stimulates the Na-K ATP pump resulting in intracellular K uptake.
    -Sodium bicarbonate: Used to manage metabolic acidosis. But it has no effect on
    potassium level and therefore not recommended)
  3. Removal of the potassium from the body.
    Haemodialysis: most effective, but it is an invasive method.
18
Q

Summary:
What are the differences between AKI and CKD?
Onset?
Duration?
Causes?
Pathophysiology?

A

Onset: Rapid (hours to days)
Duration: Usually short-term, potentially reversible
Causes of AKI can result from renal, intrarenal and postrenal causes
Pathophysiology: Immediate response to injury with potential for recovery if underlying cause is treated

Onset: Gradual/Progressive (months to years)
Causes of CKD results from long-term damage to the kidneys due to various chronic conditions e.g. DM, HTN, Glomerulonephritis, Polycystic Kidney Disease
Pathophysiology: Progressive loss of nephrons, glomerular hyperfiltration, fibrosis, and chronic inflammation leading to decreased kidney function over time.

19
Q

What is Chronic kidney disease?
What are the symptoms in the progressive stages?

A

-A progressive, irreversible loss of nephrons
(due to disease/injury or ageing)
-Asymptomatic in early stages (due to adoptive mechanisms)

Symptoms in the progressive stages:
* Weight loss and poor appetite
* Peripheral oedema
* Dyspnoea
* Haematuria
* Nocturnal polyuria
* Insomnia
* Uraemia (itchy skin, muscle cramps, headache, feeling sick and erectile dysfunction in men)

20
Q

What are the aims in CKD Assessment? (3)

A
  • Assess the severity and course of the kidney disease
  • Determine the approximate percentage of kidney function
  • Determine the drug and dosing regime
21
Q

What are the tools used in CKD Assessment?

A

Efficiency of Renal Function: Glomerular Filtration Rate

  • eGFR is used (serum creatinine level), BUT is only an estimate! Used to stage CKD.
  • Modification of Diet in Renal Disease (MDRD) accounts for serum creatinine levels, gender, age, ethnic origin, serum nitrogen urea and albumin
  • Estimated creatinine clearance Cockcroft and Gault formula is preferred for children, malnourished patients, in pregnancy, in acute renal injury or oedema, & extremes of muscle mass (e.g. amputee, body builder, muscle-wasting disease)
22
Q

What are the cause/risk factors of CKD? (6)

A
  • Hypertension (excessive strain to tiny renal arteries)
  • Hyperglycaemia (high glucose damages the GFR)
  • Hyperlipidaemia (fat deposit-narrowing of renal arteries)
  • Renal infections/inflammation (similar to AKI)
  • Post-renal obstructions (similar to AKI)
  • Drugs (NSAID’s and Lithium)
23
Q

Renal failure- what are the mechanisms and markers for:

  1. Altered glomerular integrity
  2. Decreased excretion
  3. Decreased hormonal synthesis
A
  1. Altered glomerular integrity:
    * Proteinuria, Haematuria
  2. Decreased excretion
    * creatinine, uraemic toxins (uraemia), sodium and water (hypertension and oedema), potassium (hyperkalaemia) and phosphates (hyperphosphatemia), Hydrogen ion (metabolic acidosis)
  3. Decreased hormonal synthesis
    * Erythropoietin (anaemia)
    * Activation of vitamin D (hypocalcaemia and osteodystrophy)
24
Q

Renoprotection- SGLT-2 inhibitors:
What is an example?
moa?

A

Dapagliflozin (new drugs introduced recently)
* Inhibit renal glucose reabsorption
- reversibly inhibit SGLT-2 in renal PCT to reduce glucose reabsorption
- increase urinary glucose excretion

Adding dapagliflozin to current standard care
has been shown to significantly reduce the risk of having declining kidney function, end-stage kidney disease, or dying from causes related to the kidneys or cardiovascular system.

Side effects: diabetic ketoacidosis, urinary tract infections

25
Q

Summary:

A

AKI:
Onset: Sudden
Cause: Volume depletion, infection/inflammation, nephrotoxic drugs, injury
Hypertension, Diabetes,
Infection/inflammation,
nephrotoxins and genetic (polycystic
kidney disease
Reversibility Usually reversible Irreversible, progressive

CKD:
Gradual:
Symptoms: oedema, dehydration,
metabolic acidosis and hyperkalaemia
Same as listed in AKI
Renal anaemia
Renal bone disease
Hypocalcaemia, Hyperphosphatemia
Management Treat reversible causes
Treat fluid overload,
hyperkalaemia and acidaemia
Treat primary cause
Electrolyte balance
Treat renal anaemia and osteopathy

M202 (72 decks)

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