232 acute care Flashcards
progressive alterations to kidney function
risk level catergory serum creatinine, GFR and urine output
Increased Creatinine x 1.5
Decrease in GFR >25%
urine output
<0.5mL/Kg/hr
>6 hours
progressive alterations to kidney function
injury level catergory serum creatinine, GFR and urine output
Increased Creatinine x 2
Decrease in GFR >50%
urine output
<0.5mL/Kg/hr
>12 hours
progressive alterations to kidney function
faiure level catergory of serum creatinine, GFR and urine output
Increased Creatinine x 3
Decrease in GFR >75%
urine output
<0.3mL/Kg/hr
>24 hours or
Anuria >12 hours
progressive alterations to kidney function
loss level catergory serum creatinine, GFR and urine output
Complete loss of kidney function >4 weeks
progressive alterations to kidney function
end stage level catergory serum creatinine, GFR and urine output
End-stage kidney disease >3 months
classifications of acute kidney injury
prerenal
intrareal
post renal
Prerenal Acute Kidney Injury
Caused by impaired renal blood flow Renal vasoconstriction Hypotension Hypovolaemia Haemorrhage Inadequate cardiac output GFR declines because of a decrease in filtration pressure Failure to restore blood volume or flow will cause irreversible cell injury
Intrarenal acute kidney injury
Intrarenal causes
Acute Tubular necrosis r/t prerenal kidney injury
Nephrotoxic acute tubular necrosis
Acute glomerulonephritis
Vascular disease – malignant hypertension, disseminated intravascular coagulation, renal vasculitis
Allograft rejection
Interstitial disease – drug allergy, infection, tumour growth
Acute Tubular necrosis
Caused by ischaemia
After surgery
Sepsis
Obstetric complications
Severe trauma including burns
Nephrotoxins (radiocontrast media, antibiotics)
Hypotension assoc. with hypovolaemia
Ischaemia generates free radicals that cause cell swelling, injury and necrosis
Reversible – depends on recovery of injured cells, removal of necrotic cells and intratubular casts, regeneration of tubular cells
Manifestations of ATN
Initiation Phase
Hours or days
Onset of causative event to tubular injury
Maintenance phase
Oliguric or non-oliguric Phase
Transition to oliguric – Decrease in GFR, retention of metabolic wastes (creatinine, urea and sulfate).
Urine output at lowest
Fluid retention – oedema, water intoxication and pulmonary congestion or oedema
Recovery phase
Repair of renal tissue takes place
Gradual increase in urine output, creatinine levels Fall
Postrenal acute kidney injury
Caused by urinary tract obstruction that places pressure on the kidney
Gradual decrease in GFR
Oliguria in AKI
Tubular obstruction theory
Necrosis of the tubules leads to sloughing cells and ischaemic oedema that obstructs the tubules. Backpressure leads to a reduction In GFR
Back-leak theory
GFR constant, tubular reabsorption of filtrate accelerated through alteration in permeability
Alterations to renal blood flow
Arteriolar vasoconstriction caused by release of angiotensin II, or blood moving from the cortex to the medulla. Autoregulation of blood flow impaired decreased GFR.
kidney injury management principles
Correct fluid and electrolyte imbalances Treat infections Maintain nutrition Monitor impact on medication regime May require renal replacement therapy (haemodialysis)
what are the islets of langerhan
small clusters of endocrine tissue
Account for 2% of weight of pancreas
endocrine functions
Produce hormones secreted into bloodstream
Involved in nutrient balance (blood glucose levels) and gastrointestinal functions
what are the cells of the pancreas and what do they produce
Insulin produced by beta cells
Glucagon produced by alpha cells
Somatostatin by delta cells
Gluconeogenesis ?
– the formation of glucose, especially by the liver from carbohydrate sources such as amino acids and the glycerol portion of fats
Glycogenolysis ?
– breakdown of stored glucose to increase the blood glucose levels
Glucagon ?
– hormone produced by the alpha cells, stimulating the breakdown of glycogen in the liver, the formation of carbohydrates in the liver and the breakdown of lipids in both the liver and adipose tissue
main categorises for diabetes
Three main categories
Type 1 Diabetes Mellitus
Characterised by an absolute insulin deficiency
Type 2 Diabetes Mellitus
Insulin resistance with an accompanying deficiency in insulin production
Gestational Diabetes
describe type 1 diabetes
Autoimmune Destruction of the Beta (β) cells in the Islets of Langerhans
Severe or absolute lack of insulin caused by the loss of β cells
Slowly progressive autoimmune T-cell mediated disease that destroys the β cells
Concurrent abnormal production by alpha (α) cells with an increase production of glucagon.
Hyperglycaemia and ketonaemia can result from insulin deficiency however the excess of glucagon facilitates the other metabolic alterations seen in diabetes.
type 1 diabetes clinical maifestations
Classical Presentation Polyphagia (increased hunger) Polydipsia (increased thirst) Polyuria (increased urine production) Weight Loss Ketoacidosis Sweet Smelling Breath
type 1 diabetes assessment and management
Urinalysis Presence of classic signs and symptoms Management Aim Avoid swings in insulin and glucose levels Mimic body’s natural patterns Monitoring Blood Glucose Levels Long Term – Glycolated haemoglobin A1c The future Islet cell transplantation
describe type 2 diabetes mellitus
Currently around 1.7 millions Australians have diabetes (of which 85% have Type 2 diabetes)
280 Australian develop diabetes every day (1 every 5 minutes)
Total annual cost in Australia is approx. $14.6 billion
Fastest growing chronic disease in Australia
describe type 2 diabetes
Fasting hyperglycaemia occurs despite insulin being available
Cellular Insulin resistance
No ketoacidosis
Gradual increase in hyperglycaemia
Metabolic Abnormalities
Insulin resistance
Increased glucose production by the liver
Impaired secretion of insulin by β cells
type 2 diabetes risk factors
History of diabetes in parents or siblings
Obesity
Physical inactivity
Race/ethnicity
