Block 10 Flashcards
Describe the process of events that occur in pre renal acute kidney injury.
Low blood supply to kidneys —> reduced GFR —> accumulation of H2O and solutes in the blood. If severe hypo perfusion, glomerular necrosis may occur.
= oligurea or anurea
Blood supply to the kidneys has to fall quite low before AKI due to necrosis becomes apparent (~20% of normal). This is because the majority of energy of renal cells is used for powering Na+ pump. As perfusion and GFR decreases, there is less need for the Na+ pumps and so the cells require less energy and O2 etc.
THIS IS THE MOST COMMON CAUSE OF AKI
What is intra renal acute renal failure?
Failure of the flirtation function of the kidneys due to an abnormality within the kidney itself. The most common cause is glomerulonephritis (especially post streptococcal).
Other causes: acute tubular necrosis & acute interstitial nephritis
Describe the pathophysiology of glomerulonephritis
Commonly a hypersensitivity reaction usually caused post infection with a streptococcal sore throat.
It is a type 3 reaction where antigen/antibody complexes precipitate into the micro vessels of organs, especially the kidney. They become trapped in the glomerular basement membrane and cause an inflammatory reaction.
LOTS of different causes and usually results in one or both or nephritic and nephrotic syndrome.
What is the difficulty with acute post renal failure?
Depending on where the blockage is, it can present very late on where irreversible kidney damage has already occurred.
This is because a blockage of one kidney can be compensated for (in most part) by the other kidney, leaving very few, if any, symptoms. This is only the case in partial or one sided blockages however.
What are the physiological effects of acute renal failure and how these occur.
Oedema and hypertension
Reduced GFR –> retention of Na+ and H2O
Arrhythmia
retention of K+ –> hyperkalaemia
Metabolic acidosis
retention of H+ –> acidosis –> respiratory compensation
(A patient will die within 7-14 days if no treatment is given!)
What is the definition of of chronic renal failure?
A progressive and irreversible loss of functioning nephrons.
Unfortunately, there are no/few symptoms until the number of nephrons drops by ~70% as the remainder can hypertrophy and compensate
What are some causes of chronic renal failure?
Metabolic disorders (diabetes)
Hypertension
Renal vascular disorders (stenosis and atherosclerosis)
Immunological (glomerulonephritis)
Infections
Urinary tract dysfunction (prostatic hyperplasia)
Congenital disorders (PKD)
Describe the ‘vicious cycle’ in CKD.
Decrease in nephron number –> Increased arterial pressure –> increased glomerular pressure –> glomerular stenosis
Hypertrophy and vasodilation of the remaining nephrons can somewhat compensate the increased GFR and delay diseases progression.
What is the method of decreasing the progression of CKD?
Only way is to lower arterial pressure and reduce the resultant pressure on the glomeruli. This is done though antihypertensive medication (A/B/C/D)
What are the other functions of the kidney (other than filtration) that are impaired in CKD.
EPO production –> anaemia
Vit D synthesis –> osteomalacia
Renin secretion –> hypotension (probably not common as major cause of CKD is hypertension!)
What are some common symptoms of kidney disease?
Hypertension
Loin pain
Kidney mass
Ureteral bleeding
Loss of excretory function (oligurea, frequency, hesitancy)
Loss of solute homeostasis (malaise, sweats, heavy breathing)
Name some lower urinary tract symptoms.
Hesitancy Delay Straining Incomplete emptying Terminal dribbling Frequency Nocturea Urgency Incontinence Dysurea
What are the visible features of urine to note?
Volume Colour Odour Cloudiness Consistency Frothiness Debris
What are the common causes of polyurea?
Early CKD (loss of ability to concentrate) Osmotic diuresis (glucose in diabetes mellitus) Post-renal obstruction (very common) UTI
What are the common causes of oligurea?
Acute Kidney Injury
What are the common causes of anurea?
Complete post-renal obstruction
Severe renal failure
What are some changes of colour in urine to note and their meanings?
Pale = dilute = excess water Dark = concentrated or bile pigments Pink = blood or beeturea Red = blood Brown/red = muscle breakdown
What are the tests of a urine dipstick and their common meanings?
Leucocyte esterase = presence of white cells Nitrites = created from nitrates by bacteria Urobilinogen = haemolysis Protein = glomerular injury pH = high in bacterial infection/RTA Blood = damage to urinary system Specific gravity = dilute of excess ADH Ketones = ketoacidosis Bilirubin = Obstructive jaundice Glucose = Diabetes mellitus
Advantages and disadvantages of screening an asymptomatic family member for PKD or any other inherited condition.
Advantages:
Aware of possible problems
Able to monitor and treat early
If female, can monitor effect in pregnancy
Disadvantages;
Employment difficulty
Insurance
Ethical issues about passing disease onto children.
What are the advantages and disadvantages of dialysis?
Immediately life saving! Close intact with hospital MDT Bridge to transplantation Relief from isolation and loneliness? Opportunity for further social interaction
Impact of dialysis on a patients life.
Not 100% effective so still have some level of kidney failure and accompanying symptoms
Takes up A LOT of time (travel, clinics, dialysis)
Limitation of travel
May make it hard to get out of the hose
Depression and other psychological illnesses are common
What is GFR auto regulation?
A mechanism within the kidney to maintain a constant GFR.
low BP –> reduced GFR –> reduced solute in kidney –> detected by juxtaglomerular cells –> renin release –> RAAS –> angiotensin 2 causes efferent arteriole vasoconstriction
This increases the BP in the glomeruli (among many other things) which causes a resultant GFR
What are the hormonal and neural influences which determine if Na+ is retained or lost?
Retaining: RAAS Renal nerve stimulation Noradrenaline ADH
Loosing: ANP Prostaglandins Bradykinin Dopamine
What is the main change which causes vasopressin release?
An increase in blood osmolarity (measured by osmoreceptors in hypothalamus)
What are the consequences of basement membrane damage of the glomeruli (glomerulonephritis)?
Protein loss: (usually >3.5g/day)
Nephrotic syndrome = peripheral oedema, proteinurea, hypoalbuminaemia, hypercholesterolaemia
Blood loss:
Nephritic syndrome = haematurea, hypertension, AKI, oligurea, proteinurea, oedema (2˚ to oligurea)
What are the main causes of nephrotic syndrome in both adults and children?
Adults: Membranous glomerulonephritis IgA nephropathy Diabetic nephropathy SLE Amyloidosis
Children:
Minimal change glomerulonephritis
Focal-segmental glomerulonephritis
What is sensitivity?
The number of people WITH the disease who will have a positive result.
No. of true positives / ALL those with disease
What is specificity?
The number of people WITHOUT the disease who will have a negative result.
No. of true negatives / ALL those without disease
What is positive predictive value?
No. of true positives / ALL those testing positive
What is negative predictive value?
No. of true negatives / ALL those testing negative
What happens to sensitivity, specificity, PPV and NPV as prevalence of the disease rises?
sensitivity and specificity remain constant
PPV value will RISE
NPV value will FALL
What can a test with a high sensitivity but a low specificity be used for?
Ruling out a disease.
A positive result may be a false positive , however, a negative result is very unlikely to be a false negative.
What can a test with a low sensitivity but a high specificity be used for?
Ruling IN a disease.
A negative result may be a false negative, but having a high specificity means that a positive result is very unlikely to be a false positive.
What are the signs and symptoms of nephritic syndrome?
Blood in the urine:
Haematurea
Proteinurea
Oligurea
Oedema (2˚ to oligurea)
What are the signs and symptoms of nephrotic syndrome?
Protein in the urine:
Proteinurea
Hypoalbuminaemia
Hypercholesterolaemia (reduction in lipoprotein lipase leads to reduced breakdown of LDL)
Oedema
What are the main classes of post-renal failure? Give some examples of each
Kidney:
prolapse, calculus, neoplasm, narcotising papillitis
Ureters:
stricture, stenosis, kinks, infection, valve, retrocaval, neoplasm, calculus, compression, peri-ureteral inflammation (appendicitis)
Bladder:
uterocele, neoplasm, calculus, foreign body
Urethra:
Neoplasm, stricture, stenosis, diverticulum
Prostate:
BPH, prostatitis, neoplasm, cyst
What are the symptoms of post-renal failure?
Abdo pain Unrelenting full bladder Frequency Retention Dysurea Hesitancy Slow flow Recurrent UTIs Intermittency Nocturea
What are the 3 TYPES of obstruction that post-renal failure can be classified as?
MURAL (to do with the wall)
LUMINAL
EXTRA-MURAL
What are the two muscles of the bladder and their function?
Detrusor = major muscle of the bladder, rugaeted on inside, contracts to high pressure (~50mmHg)
MAIN MUSLCE OF MICTURITION
Trigone = forms triangle between ureters and urethra. A smooth muscle. Detects stretch of the bladder
What is the sympathetic innervation to the bladder?
L2 –> hypogastric plexus –> detrusor and trigone
Innervates blood vessels and mediates their contraction. Not to do with the muscles directly.
What are the two sphincters within the bladder?
Internal sphincter = functional sphincter within the elastic tissue of the bladder neck. Natural tone which prevents emptying until a certain pressure is reached.
External sphincter = muscle within the perineum under somatic control. Function to prevent micturition in the presence of autonomic impulses.
What and where are the sensory and motor fibres innervating the bladder?
S2-S4 –> pelvic nerves –> sacral plexus –> bladder
Sensory mainly comes from the trigone and strong impulses from the INTERNAL SPHINCTER
Skeletal motor fibres to the external sphincter to via the pudendal nerve.
