Renal Flashcards
how much of the cardiac output goes to the kidneys
20%
how many nephrons are found in each kidney
1,000,000
what are the 4 stages of kidney function
Glomerular Filtration (glomerolus)
Tubular re-absorption (descending)
tubular secretion (ascending)
water-reabsorption (collecting tube)
explain glomerular filtration (2)
water and solutes move from blood into nephrons.
Important that glomerolus retains plasma proteins and blood cells to avoid these passing to the urine.
explain tubular re-absorption
useful substances move from filtrate into blood
explain tubular secretion
wastes and excess substances move from blood into filtrate
what are the 4 main importance’s of the kidney
Salt and water homeostasis
Excretion of waste
Humoral regulation of other organs - producing or modifying several hormones (vit D, renin, Erythropoietin)
Selectivity barrier - prevention of blood into the urine
what are the 3 major hormones regulated by the kidney
Vitamin D = bone
Red blood cells (Erythropoietin)
Blood vessels (Renin)
if kidney damage altered salt and water retention, what 3 main changes would we see to a pt
Changes in total body water
Changes in blood pressure
Changes in urine volume or concentration
what problems can come if excretion of waste by the kidneys is altered (4)
Uraemia - breakdown of proteins = high urea in blood
Acidosis eg lactic acid, ketoacids not being removed = pH of blood change
Others: Potassium, Phosphate, Uric acid = many patients gain hyperkalaemia
Reduced clearance of drug
if there is barrier failure in the kidney, what might we find in the urine (3)
Haematuria - blood
Proteinuria - protein
Lipiduria - lipids
what is GFR
glomerular filtration rate
what two values can we get, based on GFR
estimated GFR (most common)
measured GFR (if severe case, more accurate)
how do we estimate GFR
testing concentration of urea in the blood
what is a normal and a healthy range of GFR
normal is 120ml/min and ‘healthy range’ is 60-120 ml/min
what GFR counts as severe life threatening, kidney disease and ‘normal’
<15 = life threatening
15-60 = kidney disease
60-120 is normal
what does an estimated GFR < 60 indicate (2)
renal disease
take a MEASURED GFR to get more accurate
when do we take a measured GFR and why
when the estimated GFR is < 60
need a more accurate finding to classify renal disease
and for better monitoring
what are the main three clinical consequencs of renal disease
Hypertension
Anaemia
Renal Bone disease
explain renal hypertension (2)
Kidney is important for producing renin in the renin-angiotensin aldosterone system for controlling hypertension
Also for volume of fluid in blood which alters blood pressure (ADH)
at what point in renal failure do we start seeing anaemia (2)
GFR < 30mil/min
at GFR < 5mil/min we see anaemia in every pt
how do we treat renal anaemia
weekly injections of EPO
explain renal rickets
Vitamin D can be made at the skin but has to be activated in a2 step process, with the final step being in the kidney
if not completed, vitamin D cannot aid the absorption of calcium and to keep calcium serum levels correct, the body is forced to take calcium from the bones through resorption
This leads to reduced calcium in bones and weak, brittle, bendy bones
this is rickets caused by the kidney
how od we treat mild/moderate renal failure (3)
moderate/mild = 60 < GFR < 15
diet - so body doesn’t have to remove toxins e.g. less protein
Supplements- Alkali (sodium bicarbonate to prevent acidosis), activated Vitamin D, IV Iron (as liver/kidney disease reduces absorption from the gut)
Drugs for – Hypertension, Anaemia
what supplements might be given to a mild renal failure pt (4)
EPO for anaemia
IV iron
activated Vitamin D
Sodium bicarbonate to prevent acidosis
why is IV iron given to renal failure patients
iron has reduced absorption in the gut during kidney disease
what two options are given to patients with GFr < 15
severe / life threatening
kidney dialysis or transplantation
Explain dialysis
blood is filtered artificially
flows counter-current to a dialysis fluid that is of the correct concentrations of plasma proteins, acid, pH, urea, wateretc
across a partially permeable membrane
any excess urea, water or other toxins are filtered out by diffusion
what are the 5 main causes of renal failure
Glomerulonephritis - affecting glomerulus
Pyelonephritis - affecting tubules
Diabetes (increasing in cause prevalence - can cause both ^)
Polycystic Kidney Disease (autosomal dominant genetic disease PKD)
Hypertension/Renovascular - particularly older patients
what is ESRF
end stage renal failure
GFR < 15ml/min
what is glomerulonephritis
nephrotic syndrome
group of diseases that injure the glomerulus
caused by genetics, strep throat, hepatitis, HIV
what is PKS and what is its main symtpoms (4)
Polycystic Kidney Disease
autosomal dominant genetic disease PKD
pain due to liver/kidney cysts / bursting cysts
high blood pressure
what are some main symptoms of glomerulonephritis
high blood pressure
swollen face in the morning
leg oedema
infrequent urination and often night-time urination
blood in urine
what three cardiac complications come with kidney failure, relevant to dentistry
hypertension = pt more likely heart problems
calcific aortic valves = increased risk of infective endocarditis
K-related arrhythmias = hyperkalaemia
with a patient who has had a renal transplant, what complications may come of this (3)
on immunosuppressants so more likely to get atypical diseases
some immunosuppressants (cyclosporine) cause gingival enlargement
increased risk of cancer
what dental implications might renal disease have (6)
hypertension and increased calcification of heart valves = increased risk of endocarditis
immunosuppressed if transplant = cyclosporine = more likely to get atypical diseaseHigher risk of Anaemia
Has bleeding tendency - reduce loss of blood chance and have blood ready
more likely to have fluid overload so don’t keep reclined for long periods or can flood lungs and cause breathlessness
Risk of hyperkalemia so be very careful with GA and monitor potassium pre and post op
what part of dentistry is directly affected by hyperkaliaemic risk of renal failure
use of GA
monitor K before and after
what is the main cause of hyperkalaemia
renal disease
what are some causes of hyperkalaemia
renal disease (most common)
Addison’s disease (adrenal insufficiency)
Hypertensive drugs e.g.
Angiotensin II receptor blockers
Angiotensin-converting enzyme (ACE) inhibitors
Beta blockers
Dehydration
Destruction of red blood cells due to severe injury or burns
Excessive use of potassium supplements
Type 1 diabetes
what are the 4 main classifications of pathology with the kidney
tumour growth
acute renal failure
chronic renal failure
infection
how much fluid is filtered and reabsorbed in the average healthy kidney
180L is filtered
178L is reabsorbed
2L is excreted
very briefly explain the function of the kidney filtration (2)
Large molecules like blood cells and proteins e/g. Albumin stays in the blood. Small molecules like urea will diffuse out of the glomerular capillaries into the interstitium and into the collecting tubules.
give three causes of ‘not enough filtration’ in the glomerulus
not enough blood supply
blocked glomerulus
not enough glomeruli
why is low BP bad for renal function
less blood is filtered
not enough filtration occurs
build up of waste products in blood
toxic
if a patient has a slightly blocked filter in one of their kidneys, what will this result in
very little
can survive off of 1 kidney so a small blockage will make no difference
what 3 types of glomerular filter blockage are there
minimal change
Membranous glomerulonephritis
Proliferative glomerulonephritis
what is minimal change glomerulonephritis
where there is reduced filtration of blood
but light microscopically, we cannot see structural change in kidney
possible electron microscopy
what is membranous glomerulonephritis
Protein attachment to glomerular basement membrane
= straight line on light microscope
reduced filtration
what is membranous glomerulonephritis
Protein attachment to glomerular basement membrane
= straight line on light microscope
reduced filtration
what is proliferative glomerulonephritis
Inflammatory cells e.g. neutrophils blocking the perforations in membrane of blood vessels
We can see histologically the leukocytes pushing the glomerular cells to the side
what is the main cause of lack of glomeruli
high blood pressure
explain the connection between chronic renal failure and hypertension
chronic hypertension = arteriole stenosis and ischaemic necrosis causes glomeruli to die
When >½ of the glomeruli die (hypertension common cause) there becomes a problem
Leads to reduced filtration in the glomerulus
Leads to a granular appearance to the kidney, rather than smooth
This happens over a long time so falls under the category of chronic renal failure
how may glomeruli need to die for problems to occur
1/2
what would the kidney of a patient who died of hypertension look like and why
granular surface
hypertension leads to artteriole stenosis and ischaemic necrosis within the glomeruli
what are the three types of ‘too much filtration’
minimal change
blocked/redcued or inflamed tubules
Leakey tubules –> nephrotic syndrome
what is nephrotic syndrome
where we get too much filtration
leaky membranes lead to large potein e.g. albumin being filtered out of the blood into urine
what is the most common sign of nephrotic syndrome and why
generalised oedema especially around face
albumin filtered out of blood into urine
albumin usually acts as a fluid modulator
no albumin = fluid doesn’t go back into blood = fluid remains in tissues
= swelling
if albumin is found in blood, what is this caused by and what ios this called
nephrotic syndrome
caused by leaky membranes in the glomerulous
what is the major sign of too much filtration in kidneys
polyuria
proteinuria if leaky membranes = nephrotic syndrome
what is acute tubular necrosis
This occurs if the blood supply to the metabolically very active tubular cells is cut off e.g. embolism
This can also occur if certain toxins are present which are toxic to tubular cells e.g. myoglobin (high muscle breakdown - marathon runners) or antifreeze (ethylene glycol) which has been used by alcoholics as cheap alcohol
what 3 things can cause tubular necrosis
embolism from cholesterol or hypertension
myoglobin from muscle breakdown acts as toxin = marathon runners
antifreeze = ethylene glycol = cheap alcohol for alcoholics
what is pyelonephritis (3)
severe acute or chronic infection of the kidney
usually from ascending infection from bladder and urinary tract
common cause = UTI
what does pyelonephritis cause and how
blocked or inflamed tubules in kidney
infection and inflammation ascends up the urinary tract filling with bacteria, neutrophils and macrophages (mainly chronic)
what 3 things can cause blockage of kidney tubules
blood clots e.g. embolsism
Inflammatory cells when we get urinary tract infections or acute pyelonephritis where infection and inflammation ascendes up the urinary tract filling with bacterial ,enurtropihls and macrophages (mainly chronic)
Crystals e.g. calcium phosphate crystals which are given in bowel prep before e.g. endoscopy as a laxatives but in older people with mild renal failure, this can clog up the tubules
why is it risky to give elderly patients laxativesbefore e.g. endoscopy
Crystals e.g. calcium phosphate crystals which are given in bowel prep before e.g. endoscopy as a laxatives but in older people with mild renal failure, this can clog up the tubules
what laxative can cause blocked tubules
calcium phosphate crystals which are given in bowel prep before e.g. endoscopy as a laxatives but in older people with mild renal failure, this can clog up the tubules
what is papillary necrosis of the kidney
this is blocking off the drainage system causing necrosis of the tubules
what can cause papillary necrosis of the kidney
Stone in the collecting system of kidney and infection can grow on the surface of stone easily
what is the major cancer of the kidney
renal cell carcinoma
what are the risk factors for renal cell carcinomas (3)
cigarette smoking
obesity
genetics
what is the treatment, 5 year survival rate and prognosis of renal cell carcinoma
Treatment = resection
40% 5 year survival rate
prognosis dependant on diagnosis staging and tx
why might renal cell carcinoma have a low prognosis
usually very late diagnosis and very few symptoms
what would be the major symptom of renal cell carcinoma
blood in urine
what is our major defence against UTIs
urinary flow and hydration
what is the route of UTIs
Infection usually ascends from the external site up the UT continuum.
This can in some cases also lead to involvement of the kidneys
Catheterisation a common route of infection
Contamination with GI tract, more common in women
give two reasons why women are more likely to get UTIs
urethra is shorter
urethra is closer to anus = easier for contamination
what is cystitis
inflammation of the bladder
what is dysuria
painful urination
what is pyelonephritis
inflammation of the kidney causing fever and back pain
give some risk factors of UTIs
gender = women more likely
catheterisation
prostate enlargement or pregnancy
dehydration and reduced urination
any enlargement preventing excretion from bladder
what are the diagnostic steps of UTIs
midstream urine sample
-cloudy or clear?
-haematuria?
-culture on agar
-nitrite testing (E.coli = nitrites in urine)
what do we look for in a urine sample
clear or cloudy
pink/red? blood
nitrite levels = e.coli
agar growth + Gram Stain of isolated bacteria or direct staining from urine sample
what is the main causative bacteria of UTIs
E. Coli
what are the three main causative bacterium of UTIs
E.coli- Gram Negative rod
Proteus mirabilis- Gram negative pleomorphic rod- swarming motility
Staphylococcus saprophyticus- Gram positive coccus
who is more liekly to get Staphylococcus saprophyticus
sexually active young women
compare community and hospital aquired UTIs
community = mainly E.Coli and Staph. Saprocyticous
hospital aquired = much more gram positive e.g. staph. epidermidis and staph. Aureus . more gram negatives e.g. klebsiella
why are hospital acquired UTIs more potentially dangerous than community acquired
higher proportion of gram negatives e.g. Klebsiella which is very antibiotic ressitant = part of ESKAPE
which 2 main medias do we grow UTI suspects on
CLED (can be CLED andrade with pH indicator) and Macconkey agar if E.coli suspected
what is CLED agar and how is it significant
cycstine-lactose-electrolyte deficient agar
Lack of electrolytes suppresses proteus swarming
Cystine promotes growth of some e.coli strains
Lactose gives lactose fermentation
what does Macconkey agar test
lactose vs non-lactose fermenters
detects E.Coli
compare CLED agar of E.coli, Proteus, Staph Aureus and Staph Saprophyticus
E.Coli = Large Yellow colonies, opaque, centre slightly deeper yellow
Proteus = Translucent blue colonies
Staph Aureus = yellow colonies, uniform in colour (coagulase positive, only staph)
Staph. Saprophyticus = (coagulase-negative) Pale yellow colonies
compare E.Coli on CLED and CLED adrade
CLED = yellow colonies, opaque with centre being slightly deeper yellow
adrase = pink
why is E.coli good at UTIs
Possesses potent adhesins for attachment to epithelium
type I pili Binds mannose receptors, common on glycoproteins in uroepithelium
what strains of E.Coli specifically cause UTIs
UPEC
what glycoproteins are commonly found on uroepithelium and why is this relevant to UTIs
mannose receptors
type I pili found on UPEC bind to these receptors strongly
causing E.Coli infections
what two bacteria would cause nitrite levels to be increased in a urinary dipstick
E.coli and Proteus
explain Proteus Mirabilis gram stain and motility (4)
Gram negative pleomorphic rod - Changes from normal looking rod to a much larger bacteria with hundreds of flagella
swarming motility - swarms out from the centre and can swarm over catheters in 4 hour waves
what is Proteus Mirablis main virulnece factor
produces ureases
urea –> ammonia –> CO2, raises pH of urine»> can cause precipitation of minerals to form kidney and bladder stones
what would high urine pH and nitrite in urine indicate
Proteus Mirablis UTI
what UTI bacteria is diagnostic by a natural resistance to a certain antibiotic, and what is this anti-biotic
Staph. Saprophyticus
Novobiocin resistant (diagnostic)
when do we give anti-biotics for UTIS
not in uncomplicated lower GU infections
if involvement with kidney, pregnant or lower back pain = antibiotics
how does antibiotics for UTIs in men and women differ
7 days - longer in men as higher risk of kidney infection
3 days in women
after how many days is it unlikely to NOT have a UTI after catheterisation
14 days
2-3% increased risk every day
which two ESKAPE bacteria are likely to cause UTIs in catheterised patients
Klebsiella and Enterococcus
how do we treat hospital aquired UTIs (2)
IV - nitrofurantoin, cefalexin, Penicillins
removal and change of catheter and catheter bag
what are the main 3 STIs
Neisseria gonnorhoea »_space;> Gonnnorhoea
Chlamydia trachomatis »_space;> chlamydia
Treponema pallidum»_space;> Syphilis
can Neisseria gonnorhoea be found as a commensal
no, only ever going to cause disease
with gonnorhea, what is the likelihood of getting acute urethritis
in 95% males
only ~ 50% women show discharge, dysuria
why is gonorhea more dangerous for women
only ~50% of women show symptoms
more damage can be done:
-ascend the fallopian tubes
-acute salpingitis
-pelvic inflammatory disease
-Sterility
what is the shape and gram stain of Neisseria gonnorhoea
gram positive diplococci
what risks come with pregnancy and gonnorhea
Ophthalmia neonatorum
infant blindness through ‘natural birth’ of parent who is positive - do c section
what is Ophthalmia neonatorum and what causes it
infant blindness through ‘natural birth’ of parent who is positive - do c section
why is oral goonorrhea rare
the bacteria prefer columnar epithelium, not squamous
how does Neiserria Gonnorhoea evade the immune system (3)
special type of Lipo-oligosaccharide: sialylated acid on end
this is a self-antigen so not recognised as a foreign body
can also switch OPA proteins on outside, changing its antigenicity
IgA proteases
what can 1-3% of gonorrhoea cause
bloodstream infection can lead to arthritis, fever and infective endocarditis
how do we diagnose and test for gonorrhoea (3)
urethral swab
Sub-culture on chocolate agar
Sugar fermentation tests–glucose +ve (will not ferment sucrose or maltose)
Oxidase test positive (strict aerobe)
how did we used to treat gonorrhoea and how do we now treat it
Historically penicillin and tetracyclines were drugs of choice
Ceftriaxone (IM) and azithromycin (1g orally) recommended first line choice (also kills chlamydia). - cases of super-gohnerrea resistant to all of these drugs
describe the different phases of Syphilis
Primary lesion: chancre at site of infection
- Resolves spontaneously
-Painless ulcer which goes after a few weeks
Secondary syphilis:
- 6-8 weeks post-infection, Bacteria disseminate around body
- Flu-like illness: myalgia, headache, fever, rashes.
Latent syphilis: 3-30 years- no symptoms
Tertiary Syphilis:
- Neurosyphilis- invasion of CNS
- CV sequelae- aortic lesions, heart failure
- skin and bone deformity - in childrens teeth
a baby is born with a rash. what might this be an indication of
congenital syphilis
what causes syphylis and what type of bacteria is this
Treponema pallidum
spirochaete
what is the sore called in syphlyis
Chancre
what can vertical transmission of syphilis cause (3)
still birth
congenital syphilis rash
Birth deformities, silent infection – presents as facial and tooth deformities at 2 years of age
what is the most common STD in the UK
Chlamydia
why is chlamydia probably underestimated in its cases
Often asymptomatic in females
50% symptomatic in males
Incubation period 7 – 14 days so quick transmision
which STD is conjunctivitis related to
chlamydia
what is and what causes Trachoma
chlamydia related blindness
biggest cause of preventable blindness in the world
what are the signs of gonorrhoea
pus discharge
dysuria
what are the signs and symptoms of chlamydia
Asymptomatic infection ~ 50%
Non specific urethritis
Strong associations with
how might chalmydia cause infertility
Pelvic inflammatory disease in up to 40% of cases - ascending infection involving uterus, fallopian tubes, and other pelvic structures
Complications include chronic pelvic pain, ectopic pregnancy and infertility
scarring can narrow the fallopian tubes and block egg descent to the uterus
what is and what causes pelvic inflammatory disease
up to 40% of cases of chlamydia- ascending infection involving uterus, fallopian tubes, and other pelvic structures which can lead to chronic pelvic pain, ectopic pregnancy and infertility
what is Reiter’s syndrome
Reactive arthritis (mainly men) – acute onset urethritis, genital swelling. Involves mostly knees, ankles, toes.
how does chlamydia avoid immune system
very few antigens on surface
avoid and not stimulate immune responses
what type of pathogen is chlamydia caused by
Very small obligate intracellular parasite
Small genome
Enters through minute abrasions
what typs of cells does Chlamydia infect
non-ciliated columnar and cubiodal epithelium: genital tract from urethra up to fallopian tubes and rectum
Also respiratory and conjunctival cells
how do we test and treat chalmydia
Culture in cells
Direct immunofluorescence and ELISA
PCR tests (known as NAAT)
Azithromycin (single dose).
Doxycycline (longer course)
what percent of HIV is undiagnosed in the uk
15%
when should we routinely do HIv testing
in a reigon of >2 in 1000
what are the CD4+ count for no HIV, intermediate and advanced HIV
> 500/microlitre
500>200 intermediate
<200 advanced = aids defining diseases
what is PLWH
people living with HIV
how do we know if someone has oral candidiasis
white makrs back of mouth
rub off if brushed, leaving erythema underneith
how common is oral candidiasis in health and PLWH
very unusal in health
84-100% in PLWH
what are 4 causes of oral candidiasis
HIV (84-100%)
on antibiotics
oral inhaler without washing mouth
diabetes
steroid use
immunocomprimised
how can we tell the difference between shingles rash and a HIV shingles rash
normal shingles is dermatomal = 1 belt rash that doesnt cross the midline
HIv shingles may be mutlidermatomal and may cross the midline
if a pt presents with HIV symptoms, how would we go about asking for a HIV test1
try gain consent
explain that mouth candidiasis like this = routine test
if they refuse, investigate why
how do we test for HIV
`send clotted blood to lab
4th generation test
test for antibody and antigen
repeat test to make sure coorect test
explain the 4th generation HIV test and why this isdifferent to conventional testing
old tests used to only test for antibodies which can take 2-3 months before they show, highly likely to get false negatives
4th generation tests test for antibodies and antigens
antigens are produced within 1 month of infection, so less likely to give false negatives
how long after potential infection should we wait to do a 4th generation HIV test
1 month
after a patient has a HIV test and it is positive, what do we do (4)
do another test to ensure correct diagnosis
send to specialist to go over treatment
contact tracing of any sexual partners
PCR test to chekc current HIV viral load
describe a Kaposis sarcoma in the mouth
very hard, purple lump in mouth
very vascular and would bleed a lot if proded
what causes oral hairy leukoplakia
Epstein Barr virus
what virus causes Kaposis Sarcoma
HHV-8
compare HIV cold sores to normal cold sores
last longer
bigger
more frequent
what virus causes cold sores
HHV-1 and HHV-2
what are the 4 main pathways of HAART
HAART = higly active anti-retroviral treatment
this includes 3 of the 4 main pathway drugs
CCR5 c-receptor inhibitor - entry (not used anymore)
MAIN: NRTIs- nucleoside reverse transcriptase inhibitors
integrase inhibitors
protease inhibitors - exit, budding and breaking protein into CCR5 and CD4
why is triple therapy needed for HAART
HIV has very high mutation rate
1 in every 2 new viruses
resistance builds quickly
if 3 different pathways are inhibited, there is a 1 in 1 trillion chance of a mutation against all 3
what are most antiretroviral metabolised by and what are the implications of this
cytochrome CYP450
no metronidazole, amoxicillin, azole antifungals and macrolides
do you need written or verbal consetn for HIv test
verbal
