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3rd BDS IHD > Renal > Flashcards

Renal Flashcards

1
Q

how much of the cardiac output goes to the kidneys

A

20%

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2
Q

how many nephrons are found in each kidney

A

1,000,000

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3
Q

what are the 4 stages of kidney function

A

Glomerular Filtration (glomerolus)
Tubular re-absorption (descending)
tubular secretion (ascending)
water-reabsorption (collecting tube)

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4
Q

explain glomerular filtration (2)

A

water and solutes move from blood into nephrons.
Important that glomerolus retains plasma proteins and blood cells to avoid these passing to the urine.

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5
Q

explain tubular re-absorption

A

useful substances move from filtrate into blood

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6
Q

explain tubular secretion

A

wastes and excess substances move from blood into filtrate

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7
Q

what are the 4 main importance’s of the kidney

A

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

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8
Q

what are the 3 major hormones regulated by the kidney

A

Vitamin D = bone
Red blood cells (Erythropoietin)
Blood vessels (Renin)

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9
Q

if kidney damage altered salt and water retention, what 3 main changes would we see to a pt

A

Changes in total body water
Changes in blood pressure
Changes in urine volume or concentration

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10
Q

what problems can come if excretion of waste by the kidneys is altered (4)

A

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

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11
Q

if there is barrier failure in the kidney, what might we find in the urine (3)

A

Haematuria - blood
Proteinuria - protein
Lipiduria - lipids

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12
Q

what is GFR

A

glomerular filtration rate

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13
Q

what two values can we get, based on GFR

A

estimated GFR (most common)
measured GFR (if severe case, more accurate)

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14
Q

how do we estimate GFR

A

testing concentration of urea in the blood

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15
Q

what is a normal and a healthy range of GFR

A

normal is 120ml/min and ‘healthy range’ is 60-120 ml/min

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16
Q

what GFR counts as severe life threatening, kidney disease and ‘normal’

A

<15 = life threatening
15-60 = kidney disease
60-120 is normal

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17
Q

what does an estimated GFR < 60 indicate (2)

A

renal disease
take a MEASURED GFR to get more accurate

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18
Q

when do we take a measured GFR and why

A

when the estimated GFR is < 60
need a more accurate finding to classify renal disease
and for better monitoring

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19
Q

what are the main three clinical consequencs of renal disease

A

Hypertension
Anaemia
Renal Bone disease

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20
Q

explain renal hypertension (2)

A

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)

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21
Q

at what point in renal failure do we start seeing anaemia (2)

A

GFR < 30mil/min
at GFR < 5mil/min we see anaemia in every pt

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22
Q

how do we treat renal anaemia

A

weekly injections of EPO

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23
Q

explain renal rickets

A

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

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24
Q

how od we treat mild/moderate renal failure (3)

A

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

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25
Q

what supplements might be given to a mild renal failure pt (4)

A

EPO for anaemia
IV iron
activated Vitamin D
Sodium bicarbonate to prevent acidosis

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26
Q

why is IV iron given to renal failure patients

A

iron has reduced absorption in the gut during kidney disease

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27
Q

what two options are given to patients with GFr < 15

A

severe / life threatening
kidney dialysis or transplantation

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28
Q

Explain dialysis

A

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

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29
Q

what are the 5 main causes of renal failure

A

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

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30
Q

what is ESRF

A

end stage renal failure
GFR < 15ml/min

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31
Q

what is glomerulonephritis

A

nephrotic syndrome
group of diseases that injure the glomerulus
caused by genetics, strep throat, hepatitis, HIV

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32
Q

what is PKS and what is its main symtpoms (4)

A

Polycystic Kidney Disease
autosomal dominant genetic disease PKD
pain due to liver/kidney cysts / bursting cysts
high blood pressure

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33
Q

what are some main symptoms of glomerulonephritis

A

high blood pressure
swollen face in the morning
leg oedema
infrequent urination and often night-time urination
blood in urine

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34
Q

what three cardiac complications come with kidney failure, relevant to dentistry

A

hypertension = pt more likely heart problems
calcific aortic valves = increased risk of infective endocarditis
K-related arrhythmias = hyperkalaemia

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35
Q

with a patient who has had a renal transplant, what complications may come of this (3)

A

on immunosuppressants so more likely to get atypical diseases
some immunosuppressants (cyclosporine) cause gingival enlargement
increased risk of cancer

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36
Q

what dental implications might renal disease have (6)

A

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

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37
Q

what part of dentistry is directly affected by hyperkaliaemic risk of renal failure

A

use of GA
monitor K before and after

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38
Q

what is the main cause of hyperkalaemia

A

renal disease

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39
Q

what are some causes of hyperkalaemia

A

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

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40
Q

what are the 4 main classifications of pathology with the kidney

A

tumour growth
acute renal failure
chronic renal failure
infection

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41
Q

how much fluid is filtered and reabsorbed in the average healthy kidney

A

180L is filtered
178L is reabsorbed
2L is excreted

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42
Q

very briefly explain the function of the kidney filtration (2)

A

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.

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43
Q

give three causes of ‘not enough filtration’ in the glomerulus

A

not enough blood supply
blocked glomerulus
not enough glomeruli

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44
Q

why is low BP bad for renal function

A

less blood is filtered
not enough filtration occurs
build up of waste products in blood
toxic

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45
Q

if a patient has a slightly blocked filter in one of their kidneys, what will this result in

A

very little
can survive off of 1 kidney so a small blockage will make no difference

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46
Q

what 3 types of glomerular filter blockage are there

A

minimal change
Membranous glomerulonephritis
Proliferative glomerulonephritis

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47
Q

what is minimal change glomerulonephritis

A

where there is reduced filtration of blood
but light microscopically, we cannot see structural change in kidney
possible electron microscopy

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48
Q

what is membranous glomerulonephritis

A

Protein attachment to glomerular basement membrane
= straight line on light microscope
reduced filtration

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48
Q

what is membranous glomerulonephritis

A

Protein attachment to glomerular basement membrane
= straight line on light microscope
reduced filtration

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49
Q

what is proliferative glomerulonephritis

A

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

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50
Q

what is the main cause of lack of glomeruli

A

high blood pressure

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51
Q

explain the connection between chronic renal failure and hypertension

A

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

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52
Q

how may glomeruli need to die for problems to occur

A

1/2

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53
Q

what would the kidney of a patient who died of hypertension look like and why

A

granular surface
hypertension leads to artteriole stenosis and ischaemic necrosis within the glomeruli

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54
Q

what are the three types of ‘too much filtration’

A

minimal change
blocked/redcued or inflamed tubules
Leakey tubules –> nephrotic syndrome

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55
Q

what is nephrotic syndrome

A

where we get too much filtration
leaky membranes lead to large potein e.g. albumin being filtered out of the blood into urine

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56
Q

what is the most common sign of nephrotic syndrome and why

A

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

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57
Q

if albumin is found in blood, what is this caused by and what ios this called

A

nephrotic syndrome
caused by leaky membranes in the glomerulous

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58
Q

what is the major sign of too much filtration in kidneys

A

polyuria
proteinuria if leaky membranes = nephrotic syndrome

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59
Q

what is acute tubular necrosis

A

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

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60
Q

what 3 things can cause tubular necrosis

A

embolism from cholesterol or hypertension
myoglobin from muscle breakdown acts as toxin = marathon runners
antifreeze = ethylene glycol = cheap alcohol for alcoholics

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61
Q

what is pyelonephritis (3)

A

severe acute or chronic infection of the kidney
usually from ascending infection from bladder and urinary tract
common cause = UTI

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62
Q

what does pyelonephritis cause and how

A

blocked or inflamed tubules in kidney
infection and inflammation ascends up the urinary tract filling with bacteria, neutrophils and macrophages (mainly chronic)

63
Q

what 3 things can cause blockage of kidney tubules

A

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

64
Q

why is it risky to give elderly patients laxativesbefore e.g. endoscopy

A

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

65
Q

what laxative can cause blocked tubules

A

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

66
Q

what is papillary necrosis of the kidney

A

this is blocking off the drainage system causing necrosis of the tubules

67
Q

what can cause papillary necrosis of the kidney

A

Stone in the collecting system of kidney and infection can grow on the surface of stone easily

68
Q

what is the major cancer of the kidney

A

renal cell carcinoma

69
Q

what are the risk factors for renal cell carcinomas (3)

A

cigarette smoking
obesity
genetics

70
Q

what is the treatment, 5 year survival rate and prognosis of renal cell carcinoma

A

Treatment = resection
40% 5 year survival rate
prognosis dependant on diagnosis staging and tx

71
Q

why might renal cell carcinoma have a low prognosis

A

usually very late diagnosis and very few symptoms

72
Q

what would be the major symptom of renal cell carcinoma

A

blood in urine

73
Q

what is our major defence against UTIs

A

urinary flow and hydration

74
Q

what is the route of UTIs

A

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

75
Q

give two reasons why women are more likely to get UTIs

A

urethra is shorter
urethra is closer to anus = easier for contamination

76
Q

what is cystitis

A

inflammation of the bladder

77
Q

what is dysuria

A

painful urination

78
Q

what is pyelonephritis

A

inflammation of the kidney causing fever and back pain

79
Q

give some risk factors of UTIs

A

gender = women more likely
catheterisation
prostate enlargement or pregnancy
dehydration and reduced urination
any enlargement preventing excretion from bladder

80
Q

what are the diagnostic steps of UTIs

A

midstream urine sample
-cloudy or clear?
-haematuria?
-culture on agar
-nitrite testing (E.coli = nitrites in urine)

81
Q

what do we look for in a urine sample

A

clear or cloudy
pink/red? blood
nitrite levels = e.coli
agar growth + Gram Stain of isolated bacteria or direct staining from urine sample

82
Q

what is the main causative bacteria of UTIs

A

E. Coli

83
Q

what are the three main causative bacterium of UTIs

A

E.coli- Gram Negative rod
Proteus mirabilis- Gram negative pleomorphic rod- swarming motility
Staphylococcus saprophyticus- Gram positive coccus

84
Q

who is more liekly to get Staphylococcus saprophyticus

A

sexually active young women

85
Q

compare community and hospital aquired UTIs

A

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

86
Q

why are hospital acquired UTIs more potentially dangerous than community acquired

A

higher proportion of gram negatives e.g. Klebsiella which is very antibiotic ressitant = part of ESKAPE

87
Q

which 2 main medias do we grow UTI suspects on

A

CLED (can be CLED andrade with pH indicator) and Macconkey agar if E.coli suspected

88
Q

what is CLED agar and how is it significant

A

cycstine-lactose-electrolyte deficient agar
Lack of electrolytes suppresses proteus swarming
Cystine promotes growth of some e.coli strains
Lactose gives lactose fermentation

89
Q

what does Macconkey agar test

A

lactose vs non-lactose fermenters
detects E.Coli

90
Q

compare CLED agar of E.coli, Proteus, Staph Aureus and Staph Saprophyticus

A

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

91
Q

compare E.Coli on CLED and CLED adrade

A

CLED = yellow colonies, opaque with centre being slightly deeper yellow
adrase = pink

92
Q

why is E.coli good at UTIs

A

Possesses potent adhesins for attachment to epithelium
type I pili Binds mannose receptors, common on glycoproteins in uroepithelium

93
Q

what strains of E.Coli specifically cause UTIs

A

UPEC

94
Q

what glycoproteins are commonly found on uroepithelium and why is this relevant to UTIs

A

mannose receptors
type I pili found on UPEC bind to these receptors strongly
causing E.Coli infections

95
Q

what two bacteria would cause nitrite levels to be increased in a urinary dipstick

A

E.coli and Proteus

96
Q

explain Proteus Mirabilis gram stain and motility (4)

A

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

97
Q

what is Proteus Mirablis main virulnece factor

A

produces ureases
urea –> ammonia –> CO2, raises pH of urine»> can cause precipitation of minerals to form kidney and bladder stones

98
Q

what would high urine pH and nitrite in urine indicate

A

Proteus Mirablis UTI

99
Q

what UTI bacteria is diagnostic by a natural resistance to a certain antibiotic, and what is this anti-biotic

A

Staph. Saprophyticus
Novobiocin resistant (diagnostic)

100
Q

when do we give anti-biotics for UTIS

A

not in uncomplicated lower GU infections
if involvement with kidney, pregnant or lower back pain = antibiotics

101
Q

how does antibiotics for UTIs in men and women differ

A

7 days - longer in men as higher risk of kidney infection
3 days in women

102
Q

after how many days is it unlikely to NOT have a UTI after catheterisation

A

14 days
2-3% increased risk every day

103
Q

which two ESKAPE bacteria are likely to cause UTIs in catheterised patients

A

Klebsiella and Enterococcus

104
Q

how do we treat hospital aquired UTIs (2)

A

IV - nitrofurantoin, cefalexin, Penicillins
removal and change of catheter and catheter bag

105
Q

what are the main 3 STIs

A

Neisseria gonnorhoea &raquo_space;> Gonnnorhoea
Chlamydia trachomatis &raquo_space;> chlamydia
Treponema pallidum&raquo_space;> Syphilis

106
Q

can Neisseria gonnorhoea be found as a commensal

A

no, only ever going to cause disease

107
Q

with gonnorhea, what is the likelihood of getting acute urethritis

A

in 95% males
only ~ 50% women show discharge, dysuria

108
Q

why is gonorhea more dangerous for women

A

only ~50% of women show symptoms
more damage can be done:
-ascend the fallopian tubes
-acute salpingitis
-pelvic inflammatory disease
-Sterility

109
Q

what is the shape and gram stain of Neisseria gonnorhoea

A

gram positive diplococci

110
Q

what risks come with pregnancy and gonnorhea

A

Ophthalmia neonatorum
infant blindness through ‘natural birth’ of parent who is positive - do c section

111
Q

what is Ophthalmia neonatorum and what causes it

A

infant blindness through ‘natural birth’ of parent who is positive - do c section

112
Q

why is oral goonorrhea rare

A

the bacteria prefer columnar epithelium, not squamous

113
Q

how does Neiserria Gonnorhoea evade the immune system (3)

A

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

114
Q

what can 1-3% of gonorrhoea cause

A

bloodstream infection can lead to arthritis, fever and infective endocarditis

115
Q

how do we diagnose and test for gonorrhoea (3)

A

urethral swab
Sub-culture on chocolate agar
Sugar fermentation tests–glucose +ve (will not ferment sucrose or maltose)
Oxidase test positive (strict aerobe)

116
Q

how did we used to treat gonorrhoea and how do we now treat it

A

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

117
Q

describe the different phases of Syphilis

A

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

118
Q

a baby is born with a rash. what might this be an indication of

A

congenital syphilis

119
Q

what causes syphylis and what type of bacteria is this

A

Treponema pallidum
spirochaete

120
Q

what is the sore called in syphlyis

A

Chancre

121
Q

what can vertical transmission of syphilis cause (3)

A

still birth
congenital syphilis rash
Birth deformities, silent infection – presents as facial and tooth deformities at 2 years of age

122
Q

what is the most common STD in the UK

A

Chlamydia

123
Q

why is chlamydia probably underestimated in its cases

A

Often asymptomatic in females
50% symptomatic in males
Incubation period 7 – 14 days so quick transmision

124
Q

which STD is conjunctivitis related to

A

chlamydia

125
Q

what is and what causes Trachoma

A

chlamydia related blindness
biggest cause of preventable blindness in the world

126
Q

what are the signs of gonorrhoea

A

pus discharge
dysuria

127
Q

what are the signs and symptoms of chlamydia

A

Asymptomatic infection ~ 50%
Non specific urethritis
Strong associations with

128
Q

how might chalmydia cause infertility

A

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

129
Q

what is and what causes pelvic inflammatory disease

A

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

130
Q

what is Reiter’s syndrome

A

Reactive arthritis (mainly men) – acute onset urethritis, genital swelling. Involves mostly knees, ankles, toes.

131
Q

how does chlamydia avoid immune system

A

very few antigens on surface
avoid and not stimulate immune responses

132
Q

what type of pathogen is chlamydia caused by

A

Very small obligate intracellular parasite
Small genome
Enters through minute abrasions

133
Q

what typs of cells does Chlamydia infect

A

non-ciliated columnar and cubiodal epithelium: genital tract from urethra up to fallopian tubes and rectum
Also respiratory and conjunctival cells

134
Q

how do we test and treat chalmydia

A

Culture in cells
Direct immunofluorescence and ELISA
PCR tests (known as NAAT)

Azithromycin (single dose).
Doxycycline (longer course)

135
Q

what percent of HIV is undiagnosed in the uk

A

15%

136
Q

when should we routinely do HIv testing

A

in a reigon of >2 in 1000

137
Q

what are the CD4+ count for no HIV, intermediate and advanced HIV

A

> 500/microlitre
500>200 intermediate
<200 advanced = aids defining diseases

138
Q

what is PLWH

A

people living with HIV

139
Q

how do we know if someone has oral candidiasis

A

white makrs back of mouth
rub off if brushed, leaving erythema underneith

140
Q

how common is oral candidiasis in health and PLWH

A

very unusal in health
84-100% in PLWH

141
Q

what are 4 causes of oral candidiasis

A

HIV (84-100%)
on antibiotics
oral inhaler without washing mouth
diabetes
steroid use
immunocomprimised

142
Q

how can we tell the difference between shingles rash and a HIV shingles rash

A

normal shingles is dermatomal = 1 belt rash that doesnt cross the midline

HIv shingles may be mutlidermatomal and may cross the midline

143
Q

if a pt presents with HIV symptoms, how would we go about asking for a HIV test1

A

try gain consent
explain that mouth candidiasis like this = routine test
if they refuse, investigate why

144
Q

how do we test for HIV

A

`send clotted blood to lab
4th generation test
test for antibody and antigen
repeat test to make sure coorect test

145
Q

explain the 4th generation HIV test and why this isdifferent to conventional testing

A

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

146
Q

how long after potential infection should we wait to do a 4th generation HIV test

A

1 month

147
Q

after a patient has a HIV test and it is positive, what do we do (4)

A

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

148
Q

describe a Kaposis sarcoma in the mouth

A

very hard, purple lump in mouth
very vascular and would bleed a lot if proded

149
Q

what causes oral hairy leukoplakia

A

Epstein Barr virus

150
Q

what virus causes Kaposis Sarcoma

A

HHV-8

151
Q

compare HIV cold sores to normal cold sores

A

last longer
bigger
more frequent

152
Q

what virus causes cold sores

A

HHV-1 and HHV-2

153
Q

what are the 4 main pathways of HAART

A

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

154
Q

why is triple therapy needed for HAART

A

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

155
Q

what are most antiretroviral metabolised by and what are the implications of this

A

cytochrome CYP450
no metronidazole, amoxicillin, azole antifungals and macrolides

156
Q

do you need written or verbal consetn for HIv test

A

verbal

3rd BDS IHD (14 decks)

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