265 - renal disorders Flashcards
what is the vasa recta?
network or blood vessels surrounding the nephron tubules which allow the urine to become concentrated
describe the blood vessel structure of the glomerulus
about 50 capillaries, with arterioles on either side of the capillaries (smooth muscle of arteriole allows for vasoconstriction to regulate glomerular blood pressure
which ion concentrations do the kidneys regulate?
Na+ Cl- K+ Ca2+ HPO4(2-) (hydrogen phosphate)
how do the kidneys regulate blood pH?
excrete H+ in urine and retain HCO3- to reduce acidosis
excrete HCO3- and retain H+ to reduce alkalosis
what is venous blood pH?
7.32 - 7.42
how do the kidneys regulate blood pressure?
through increasing or decreasing secretion of water according to ADH/aldosterone present
through secretion of renin
which hormones do the kidneys produce?
calcitriol
erythropoietin
what is the normal osmolarity of blood, as regulated by the kidneys?
about 275-299 mOsm/L
what are some of the wastes removed from the body by the kidneys?
ammonia urea bilirubin creatinine uric acid toxins/chemicals from the diet drugs
what percentage of cardiac output do the kidneys receive?
about 20-25%
why is anaemia associated with acute renal failure?
lack of production of EPO (can now by supplemented artificially)
how do the kidneys help to regulate blood glucose levels
gluconeogenesis (secondary to the liver) in the renal cortex
describe renal blood flow
Blood enters renal artery → branches out into afferent arterioles (one per nephron) → glomerulus (capillary network)→ efferent arterioles→form peritubular capillaries → VASA RECTA (surrounds Nephron loop (of Henle) → blood exits kidneys via renal vein.
describe the regulation of renal blood flow
- autoregulation - stretch (myogenic effect) from increased flow → constriction of the afferent arterioles → ↓blood flow
- regulation by the SNS
- RAAS
where is angiotensinogen produced?
the liver
what is renin?
an enzyme
effects of angiotensin II?
vasoconstriction
release of aldosterone from the adrenal cortex → ↑ reabsorption of Na+ and H2O follows passively
release of antidiuretic hormone (ADH) from posterior pituitary gland → ↑reabsorption of H2O and ↑vasoconstriction
↑ thirst
what triggers RAAS?
decreased renal flow causes release of renin
which meds will affect kidney function?
NSAIDs e.g. large doses of aspirin, ibuprofen
some antibiotics e.g. gentamycin, vancomycin
alcohol
some blood pressure medications
about how much filtrate is produced each day?
how much (very roughly) per minute?
180L/day
120 ml/min
why do proteinuria and haematuria occur in inflammation/infection?
inflammation causes the pores in the glomerular capillaries to enlarge and this allows protein and blood into the urine
what are the processes/functions of the nephron that allow for urine production?
glomerular filtration
tubular reabsorption
tubular secretion
renal function tests?
creatinine clearance - estimates GFR - 24hr urine collection + bloodtest
Blood Urea Nitrogen (BUN) - rough estimate of GFR
Cystatin C - a protein produced in most cells which gets filtered but reabsorbed - good marker of renal function
what is transport maximum (Tmax)?
the limit to which the amount of a solute (e.g. glucose) can be reabsorbed from the filtrate into the blood. When exceeded the solute appears in the urine
what is renal threshold?
the concentration of a substance dissolved in the blood above which the kidneys begin to remove it into the urine
describe Tmax and renal threshold using glucose as an example
Tmax for glucose is roughly 10mmo/L. If blood glucose is < 10mmol/L all the filtered glucose will be returned to the blood → no glucose in the urine.
if blood glucose is > than 10mmol/L then the renal threshold is exceeded and not all glucose can be returned to the blood → glucose in the urine (glycosuria)
difference between urethritis, cystitis and pyelonephritis?
urethritis – inflammation of the urethra
cystitis – inflammation of the bladder
pyelonephritis – inflammation of the ureters/renal pelvis
why are UTIs so common in hospital?
what percentage of nosocomial infections do they represent?
largely due to use of IDCs
about 40% of nosocomial infections
main organisms involved in UTIs?
E. coli mostly, also staph et al.
about how long does it take for a catheter to become colonised?
about 48 hrs, therefor IDCs should be avoided and removed ASAP
risk factors for UTIs?
urinary stasis
foreign bodies ie. stones, catheters
anatomical factors: congenital defects, fistulas
compromised immune (ageing, DM, HIV)
functional disorders (constipation)
other factors - pregnancy, menopause, poor hygiene, habitual delay of urination, spermicide/diaphragm use
what can cause urinary stasis?
intrinsic obstruction - stone, tumour of urinary tract,
urethral stricture, BPH (benign prostatic hyperplasia)
extrinsic obstruction (tumour, fibrosis compressing urinary tract)
urinary retention
renal impairment
pathophysiology of UTI?
introduction of organisms into a normally sterile bladder
NB: lower urethra colonized by perineal organisms which are flushed out with urine flow.
UTI signs and symptoms?
burning/stinging when passing urine - dysuria
urgency with small volumes passed each time and incontinence (dribbling) of urine after voiding
ascending infections can cause severe pain
why is urinary incontinence associated with UTI?
indicates dysfunction or urinary sphincters, less ability to keep out pathogens
potential consequences of untreated UTI?
bacteraemia (organisms in blood)
sepsis (bacterial toxins in blood)
death from septic shock
which bacteria cause nitrites in the urine?
gram -ve only
management of UTIs?
Ural from chemist alkalinises urine to relieve burning on voiding
antibiotics should match the infective organism
adequate fluid intake
antipyretics & analgesia – care in patients with renal dysfunction
diagnosis of UTIs?
urinalysis - nitrites/proteins/blood
MSU and urine cultures
which AB commonly used to treat UTIs is contraindicated in people with renal failure? why?
co-trimoxazole as it increases serum potassium
nursing management of UTIs?
recognise risk factors
teach preventative measures: emptying the bladder regularly and completely & wiping from front to back
drinking adequate amount of liquid (1.5-2L/day depending on renal and cardiac function)
avoid unnecessary catheterisation and early removal of indwelling catheters
what is acute kidney injury also known as?
acute renal failure (old name for it)
why is acute kidney injury potential fatal?
inability to excrete ions leads to electrolyte imbalances (hyperkalaemia can mean cardiac arrest)
common causes of AKI?
low fluid volume
nephrotoxic drugs e.g. vancomycin, gentamicin, NSAIDs
common causes of low fluid volume?
dehydration, haemorrhage, diuretics, vomiting, diarrhoea, heart failure, sepsis
pathophysiology of AKI?
RAAS → constriction of renal arterioles → ↓GFR
low fluid volume → blood diverted from kidneys to maintain heart and brain circulation
assessment for AKI?
signs of dehydration: dry mucous membranes, hypotension, oliguria
urinalysis is normal or near normal
AKI classifications?
prerenal- develops outside the kidneys
intrarenal –develops in the kidneys
postrenal –develops in ureters, bladder or urethra
causes of prerenal AKI?
sudden or severe drop in BP:
hypovolaemia sepsis burns fluid losses dehydration
or flow obstruction to the kidneys due to:
atherosclerosis
ischemia
causes of intrarenal AKI?
direct damage to kidney
inflammation or infection of the kidney including pyelonephritis or glomerulonephritis
toxins/drugs
autoimmune diseases such as lupus
causes of postrenal AKI?
obstruction of urine flow due to enlarged prostate, stones, tumour, injury, benign prostatic hyperplasia
what is pyelonephritis?
ascending bacterial infection from bladder to kidneys (renal pelvis)
signs and symptoms of pyelonephritis?
fever back pain signs of UTI nausea and vomiting haematuria pyuria WBCs and bacteria in urine
what is glomerulonephritis?
Inflammation of the glomeruli in the nephrons due to diabetes, genetics, following streptococcal infection or viral infections e.g. hepatitis A or C
signs and symptoms of glomerulonephritis?
haematuria proteinuria hypertension fluid retention oedema
difference between chronic kidney disease and acute kidney injury?
CKD is decrease in function that happens over three months; acute happens in less than three months
acute is usually reversible
most common form of acute kidney injury?
intrarenal AKI
four main causes of intrarenal AKI?
acute glomerular nephritis
acute tubular nephritis
acute interstitial nephritis
vascular causes - vasoconstriction, endothelial dysfunction, increased adhesion of inflammatory cells
what percentage of intrarenal AKI is caused by acute tubular nephritis?
what are the most common causes of acute tubular nephritis?
about 50%
cause is usually ischemic (from prolonged hypotension) or nephrotoxic (from an agent that is toxic to the tubular cells)
you need to remember that prerenal, intrarenal and postrenal AKI are heavily interrelated -
especially that prerenal and postrenal AKI will often then cause intrarenal AKI
two main changes that cause decreased GFR?
vascular changes (particularly in the afferent arteriole)
tubular change including damaged cells, necrotic bodies causing obstruction
characteristics of AKI?
functional changes:
decreased GFR
decreased urine output
increased nitrogenous wastes present in blood (urea, creatinine)
and structural changes:
cell death
loss of adhesion to intrinsic renal cells
what is acute interstitial nephritis mostly due to?
allergy or infection
examples of nephrotoxic drugs?
aminoglycosides (gentamicin, tobramicin), vancomycin, NSAIDS
what are the four phases of AKI, and their duration?
onset phase - hours to days
oliguric phase - 8 - 14 days
diuretic phase - 7 - 14 days
recovery phase - several months to a year
describe the first phase of AKI?
onset phase:
renal blood flow 50% of normal
tissue perfusion 50% of normal
urine output <0.5ml/kg/hr
describe the second phase of AKI?
oliguric phase:
urine output <400 ml/day (can be as low as 100ml/day)
increases in blood urea nitrogen (BUN) and creatinine
electrolyte disturbances, acidosis, fluid overload
describe the third phase of AKI?
diuretic phase:
occurs when cause of AKI corrected
renal tubule scarring and oedema
increased GFR
daily urine output > 400ml
possible electrolyte depletion from excretion of more water and osmotic effects of high BUN
describe the fourth phase of AKI?
recovery phase:
decreased oedema
normalisation of fluid and electrolyte balance
return of GFR to 70% - 80% of normal
what happens if there is no recovery phase in AKI?
leads to CKD
what are the electrolyte imbalances associated with the oliguria phase of AKI?
↑ K+, ↓ Na+, H+ and metabolic acidosis due to kidneys unable to excrete ions
clinical manifestations of oliguria phase of AKI?
fluid retention, oedema
kussmaul’s respirations as a result of metabolic acidosis
neurological disorders (fatigue, poor concentration, seizures, coma) due to neurotoxic effects of nitrogenous wastes
if Na+ < 135mmol/L → cerebral oedema
describe urine output in the diuretic phase of AKI?
daily urine output > 400ml as distinct from oliguric phase
1 to 3L urine/day, but may be > 5L
management of AKI?
Prerenal:
• Correction of fluid volume deficit
• Improve cardiac function with inotropic agents
• Correct hypotension
Intrarenal:
• Correct cause e.g. antibiotics for infection Postrenal:
• Correct cause of the obstruction
Postrenal:
• Correct cause of the obstruction
nursing management of AKI?
- Monitor blood electrolyte levels
- Daily weight (fluid load)
- Monitor urine output
- Strict fluid balance record
- Restriction of sodium and potassium intake
- Fluid restriction – based on patients clinical condition
- Health education for the person and family
define CKD?
progressive and irreversible loss of kidney function
either the presence of kidney damage, or a decreased GFR < 60 mL/min/1.73 m2 for longer than 3 months
main causes of CKD?
hypertension (20%),
diabetes and metabolic syndrome (30%)
glomerulonephritis (25%)
main systemic effects of CKD?
increased blood volume (can lead to CCF)
uremia, azotemia - CNS abnormalities, GIT upset
hyperkalaemia - disrhythmias/cardiac arrest
anaemia
hypocalcaemia leading to bone disease
blood clotting disorders
increased infections
what is azotemia?
increased nitrogenous wastes in blood
what is uraemia?
increased urea in blood
