Renal Disorders Flashcards
functions of the kidney
homeostasis of the internal environment
maintain fluid and electrolyte balance
secretion of : erythropoietin, renin, dihydroxy vitamin D
Filtration pressure
net pressure forcing fluid out of the glomerulus
GLomerular filtration rate (GFR)
the filtration of plasma per unit of time
renal clearance
volume of blood plasma cleared of a waste produce in 1min
filtration pressure
net pressure forcing fluid out of the glomerulus
factors that affect filtration
changes in hydrostatic pressure
changes in the diameter of the afferent or efferent arterioles
large molecules like plasma proteins cannot move through small pores in glomerular membranes
negative charge along the filtration membrane impedes filtration of negatively charged particles as they repel
GFR is dependent on
permeability of capillary walls
vascular pressure
filtration rate
eGFR
based on blood and calculation of a formula using age, ethnicity and gender
results give the range of variation
Obstructive Uropathy
any condition causing a change in the normal urine flow anywhere within the urinary tract
Consequences of obstructive uropathy
pain caused by distension caused by blockage
urine output varies
renal calculi
masses of crystals, proteins, other substances
usually bilateral
if flow blocked, urine backs up in pelvis
Hydroureter
obstruction of the ureter with accumulation of urine
Hydronephrosis
retrograde increases in hydrostatic pressure in the renal pelvis and calyces can increase accumulation of urine in the renal collecting system
Clinical manifestations of hydroureter or hydronephrosis
pain - colicky with stones
bladder symptoms
unilateral obstruction, complete or partial is often asymptomatic
bilateral partial obstruction - cant concentrate urine
bilaterial complete obstruction - oliguria/anuria
Types of kidney stones
calcium
struvite
uric acid
cysteine
PAtho of kidney stones
high urinary concentration of stone forming substances changes in pH and temp drugs and diet decreased urinary flow grow in the renal papilla or pelvis
Risk factors for kidney stones
calcium stones - smallest, hypercalciuria, hyperuricosuria
struvite stones - women infected by microbes
urice acid stones - ulcerative colitis or regionial enteritis with fluid and bicarbonate loss
cyteinuria
rare hereditary disorder
disorder of amino acid metabolism
decreased tubular reabsorption of cysteine
Patho of cyteinuria
high levels of stone forming substances in plasma and urine, some medications, loss of inhibitors of precipitation
clinical manifestations of cyteinuria
colicky pain, flank pain, nausea and vomiting, haematuria
Bladder-prostate enlargement
stone blocks exit from bladder when muscle contract
treatment and management of bladder-prostate enlargement
adequate analgesia and high fluid intake
treat infection
dissolve stones and prevent reformation
How to dissolve stones
increase fluid intake and urine output
decrease dietary intake of stone forming substances
durgical removal of stones greater than 0.5cm width
percutaneous puncture of kidney with forceps removal
shock wave lithotripsy for large calcium stones
predisposing factors for kidney stones
family history diabetes chronic disease renal calculi urinary tract obstruction immunosuppression pregnancy prostate disease in older men
Autoregulation
the renin-angiotensin aldosterone system (RAA) and antidiuretic hormone (ADH) are the feedback loop systems maintaining homeostasis in the body
keeps pressure in the glomerulus within a wide range of systemic blood pressures
Kidney Dysfunction
inadequate urine output
Impaired homeostasis, conversion of vitamin D to the active form and secretion of erythropoietin
Injury to glomerulus
increased permeability of the capillary membrane
larger molecules can cross: RBC, epithelial casts, proteins
decreased oncotic pressure = decreased GFR = urine output
glomerulonephritis
characterised by inflammation of the glomerulus
primary: rapidly progressive glomerulonephritis
secondary: to other disease such as diabetes
Patho of glomerulonephritis
glomerulus is the high pressure filtration component of the normal kidney tubules
with damage there is swelling, increase permeability and decreased effectiveness of cell junction
Classifications of glomerulonepthritis
Asymptomatic ACute nephritic syndrome rapidly progressing GMN Nephrotic Syndrome Chronic glomerulonephritis (CKD)
Asymptomatic glomerulonephritis causes
IgA nephropathy with haematuria
abnormal IgA binds to cells, complement stimulates inflammation and injury
abnormal IgA produced by bone marrow binds to glomerular mesangial cells, stimulating them to proliferate and release inflammatory mediators
Acute nephritis syndrome
a group of symptoms that occur with some disorders that cause swelling and inflammation of the glomeruli in the kidney
acute onset of gross haematuria and mild-moderate proteinuria
manifestations of acute nephritis syndrome
acute onset of fever, malaise, nausea, oliguria, haematuria
red cell cause in the urine and mild proteinuria
periorbital oedema and mild hypertension
Rapidly progressing GMN
acute nephritis with glomerular damage resulting in proteinuria and rapid progression to AKI with severe oliguria or anuria and irreversible kidney disease
causes of rapidly progressing GMN
immune-mediated
posinfectious GMN
systemic disease
idiopathic
Types of rapidly progressinv GMN
GOodpasture syndrome - characterised by pulmonary haemorrhage
immune complex deposition
Pauci immune glomerulonephritis
Patho of Rapidly Progressing GMN
antiglomerular basement membrane antibodies and antineutrophil cytoplasmic antibodies are associated with glomerular injury
extensive proliferation of cells into the bowman space with cresent formation
Nephrotic Syndrome
heavy protein loss
generalised oedema with characteristic pitting
Pathogenesis of Nephritic Syndrome
damage of alteration of glomerular basement membrane
becmes excessively permeable to plasma proteins
depletion of plasma proteins resulting in hypoalbuminaemia
Causes of nephritic syndrome
systemic disease such as diabetes and SLE
Chronic glomerulonephritis (CKD)
glomerular disease with a progressive course leading to chronic kidney diseases
Diabetic nephropathy pathology
insulin deficiency and altered metabolism, thickening of glomerular basement membrane, in connective tissue matrix and hardening
Acute kidney injury and chronic kidney disease
severe reduction in renal function
Acute kidney injury
rapid and sudden deterioration of renal function
resulting in retention of metabolic wastes , impaired fluid and electrolyte balance
Cases of AKI
prerenal - impaired blood flow: hypotension, ischaemia, low CO, haemorrhage, surgery
Intrarenal - acute glomerulonepthritis or acute tubular necrosis - aminoglycoside antibiotics
Post renal - urinary tract obstruction
Clinical progression of AKI
- initiation phase - reduced perfucion, renal injury evolving
- maintenance phase - period of established renal injury and dysfunction
- recoevery phase - interval when renal injury is repaired
Chronic Kidney disease
gradual loss of nephrons until the remainder cannot carry out normal renal function
results in end stage renal disease requiring dialysis
Risk factors for CKD
intact nephrons can enlarge and increase function
one kidney can take overall function
may not see impaired function until 75-80% loss of nephrons
Stages of CKD
- normal or high GFR - no symptoms
- mild CKD - asymptomatic
- moderate CKD - possible signs of organ dysfunction
- severe CKD - normal blood volume and concentrations not maintained
- end stage CKD - uraemia, oligurua, anuria, vomiting, anorexia,
