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UROLOGY / NEPHROLOGY - Nephritic + Nephrotic Synromes (Nephritic vs.…
UROLOGY / NEPHROLOGY - Nephritic + Nephrotic Synromes
Nephritic vs. Nephrotic Syndrome
*Nephritic Syndrome
blood in the urine
NEPHRITIC BASICS
RBC CASTS need to be there
--> only in nephritic from the kidney
HTN needs to be there
--> since HTN causes the blood to go through the kidneys
*PSGN Nephritis
notes
*PSGN Nephritis
notes
*RAPIDLY PROGRESSIVE Nephritis
notes
NERD CRICKET on RAPIDS is RAPIDLY going to his death in his CRESCENT SHAPED RAFT with his C3B COMPUTER on the side of the boat that ATTRACTS MAC MEN MACROPHAGES to EAT AWAY at his CRESCENT BOAT
NERD CRICKET RAPIDS = rapidly progressive NERD CRICK
NERD CRICKET RAPIDS = CRESCENT SHAPE UTER BOAT
NERD CRICKET RAPIDS = C3B COMPUTER = COMPLIMENT attracts MAC MEN to eat the CRESCENT RAFT
the RAPIDS also grabs onto a GOOD PASTURE man and his GRANULOCYTE CARRIAGE
they all DIE RAPIDLY
Anti-GBM = glomerular basement membrane disease
= Goodpasture's disease
Clinical Cases
Anti-glomerular basement membrane (GBM) disease
= Goodpasture's disease
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Clinical Case
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1 = LINE on the GBM = good pasture
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*DPGN Nephritis = Diffuse Proliferative GN
most common form of death for SLE patients
Wire loops on histology of DPGN
*Alport Collagen 4 Nephritis
X linked
--> look for Alport collagen triad IN FAMILIES
ALPORT COCA COLA NERD CRICKET MUTATION from X GENERAL PILOT splits the GBM BASEMENT in half and the COCA COLA GEM 4 MUTATED NERD CRICKETS multiply by the BASKET LOAD
ALPORT X GENERAL COCA COLA GEM 4 FORK MUTATION = GBM SPLITTING
ALPORT X GENERAL COCA COLA GEM 4 FORK MUTATION = baskefull appearance on IF
ALPORT X GEN COCA COLA GEM 4 MUTATION in NERD CRICKETS = triad of GBM
GBM COCA COLA GEM triad = Can't
SEE
GBM COCA COLA GEM triad = Can't
PEE
GBM COCA COLA GEM triad = Can't
HEAR
the
CRICKETS
or the
BEES
*PSGN Nephritis
notes
Upper *RTI Glom Nephritis
nephritic syndrome SAME TIME as RTI?
or
2 -4 weeks AFTER RTI?
2 -4 weeks AFTER RTI
*PSGN = Post Streptococcal Glomerular Nephritis
most common nephritic in kids
--> COCO COLA
Clinical Cases
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POST STRIPPER on the GRAND MARE CAROSSEL is being watched by NERD CRICKT and his SON who is mesmorized by the POST STRIPPER on the GRAND MARE CARROSEL
POST STRIPPER on GRAND MARE CARROSEL = PSGN
NERD CRICKET and SON = most common in KIDS
NERD CRICKET BOY is drinking his SANTA COCA COLA and peeing it out straight in his URINE while his NERD CRICKET DAD puts an EDEMAME EDEMA over his eyes so he won't see the POST STRIPPER
EDEMA in NERD KIDS
NERD KIDS COCA COLA URINE
also watching POLE STRIPPER on the GRAND MARE CARROSEL is CREEPY LUMPY BUMPY SANTA who also has HTN, FATTY LUMPY BUMPY and EDEMA everyhwere
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nephritic syndrome SAME TIME as RTI
*BERGERS IgA Nephritis
notes
NUMBER 1 NERD CRICKET BERGER JOINT serves NERD CRICKET BERGERS made by a MAZE ANGEL to APPLE GOBLIN and makes everyone sick because in the back there is SICK PHAROH with DIARRHEA on the TOILET coughing APPLE GOBLINS on each NERD CRICKET BERGER
BERGERS NERD CRICKET = #1 causes of NERD CRICKET
BERGERS NERD CRICKET = caused by extra APPLE GOBLIN getting into the MAZE ANGEL cells of the kidney
BERGERS NERD CRICKET = APPLE GOBLIN comes from a current infection with SICK GASTRO PHAROH on the toilet at BERGERS
NERDY NEPHRITIC CRICKET gets into FLAMES MAD with his friend HTN HIKER when they see how bad the RBCs are treating the 3 TREE
NERD CRICKET = nephritic
HTN HIKER
--> necessary forNERD CRICKET to develop
RBCs = blood in NERD CRICKET gets though the GBM
the 3 TREE is treated HALF as BAD as it should be by the RBCs who at teh GBM BASEMENT MEMBRANE of the 3 TREE have set up a BLOODY URINAL that they CHARGE poor OLD GOLFER OLIGURIA the HIGHEST PRICES in NITROGEN just to take a PEE at teh HEMATURIA URINAL at teh GBM of the # TREE TREATED 1/2 BAD
NERD CRICKET = RBS at GBM of 3 TREE
NERD CRICKET = BLOOD in URINAL at GBM of 3 TREE 1/2 BAD
NERD CRICKET = charge OLD GOFERS with no PEE HIGH NITROGEN pricces
--> oliguria
--> high Nitrogen BUN
*Pathoma - nephritic syndrome
Course of PSGN infection
starts with skin infection or throat infection with GAS
--> if the GAS strain has M protein it can possibly cause PSGN
2-3 weeks later you can form PSGN
the IF granulocytes deposits of IgM from the M protein GAS deposit in the GBM of the kidney
--> first have LITTLE DEPOSITS before the GBM
they then get squeezed through the GBM and pile up into BIG HUMPY BUMPY collections behind the GBM
--> the HUMPY BUMPY lumps of GAS PSGN can be seen on lecetron microscope
Tx for PSGN = supportive
--> reason is that
HUMPY BUMPY lump formation
dissapate on their own from the GBM and into the tubules
--> self limiting disease
tx = SUPPORTIVE ONLY
hyperproliferation in the glomerulus = fill most of Bowmans space
2 outcomes of PSGN
based on AGE
KIDS PSGN
--> PSGN is common in kids
--> MOST KIDDS will get through the disease on their WITHOUT AKI or CKD
ADULT PSGN
--> Poor prognosis
OUTCOME 1 = KIDS NORMAL PSGN = goes way on its own
based on AGE
KIDS PSGN
--> PSGN is common in kids
--> MOST KIDDS will get through the disease on their WITHOUT AKI or CKD
ADULT PSGN
--> Poor prognosis
OUTCOME 2 = ADULT PSGN = RAPID PROGRESSIVE GN
very RAPID decline in renal function
--> can DIE within weeks to months
ADULT PSGN
--> Poor prognosis
MAGEMENT of suspect RAPID PROGRESSIVE GN
step 1 = take biopsy to look for CRESSCENT SHAPE
macrophage + fibrin
step 1 = IF stain
INFALMMATION in RAPID PROGGRESSIVE
CRESCENT shape in the glomeruli
macrophages + fibrin
MAC MEN + FIBRE LOGS on the RAPID CRESCENT RIVER
note that CRESCENT is NOT COLLAGEN
Immuno Flourenscence = IF
1 = LINE on the GBM = good pasture
--> Good Pasture = anti-GBM linear ribbon (subtype of rapid progressive nephritic syndrome)
2 = GRANULAR = 2 possibilities
--> GRANULAR LUMPY BUMPY immune complexes piling up on the GBM = PSGN
--> diffuse proliferative = SUB ENDOTHELIAL = SLE complication (this is different than the membranous nephrotic SLE)
3 = IF is NEGATIVE
--> need to do an ANCA test = anti NEUTROPHIL cytoplasm antigen test
4 = IgA deposition in the MESSANGIUM
--> only IF with IgA
--> IgA specific is the number 1 cause nephropathy WORLDWIDE
--> present in KIDS usually
1 = LINE on the GBM = good pasture
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2 = GRANULAR = 2 possibilities
--> GRANULAR LUMPY BUMPY immune complexes piling up on the GBM = PSGN
--> diffuse proliferative = SUB ENDOTHELIAL = SLE complication (this is different than the membranous nephrotic SLE)
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3 = IF is NEGATIVE
need to do an ANCA test = anti NEUTROPHIL cytoplasm antigen test
pANCA = PERI nucleus on the ANCA NEUTROPHIL test
--> CHurg Strauss OR microscopic polyangiitis
cANCA = CYTOPLASM nucleus on the ANCA NEUTROPHIL test
--> C gives you Wegener = weCener syndrome
WeCener syndrome
--> this has both lung + kidney involvement like in Good pasture
--> LUNG inflammation MEDIUM vessel vascultiis = HEMOPTYSIS
--> KIDNEY inflammation MEDIUM vessel vascultiis = HEMATURIA
--> KEY difference is that WEGENER has SINUSITIS (+ kidney + lung) and is from a vasculitis cause
--> Good pasture has NO SINUS involvement and is from Cb3/antibodies to the GBM of alveoli and kidney
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4 = IF is IgA on MESSANGIUM = IgA BERGERS disease
4 = IgA deposition in the MESSANGIUM
--> only IF with IgA
--> IgA specific is the number 1 cause nephropathy WORLDWIDE
--> present in KIDS usually
presents in kids after mucosal infections
--> RIT since it makes IgA
BERGER IgA is usually self limiting and goes away after you fight off the RTI
--> since your IgA levels decrease after
--> can however progress to renal failure though so need support tx
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*Nephrotic Syndrome
protein in the urine
*PSGN Nephritis
notes
*PSGN Nephritis
notes
*PSGN Nephritis
notes
*PSGN Nephritis
notes
*PSGN Nephritis
notes
*PSGN Nephritis
notes
NERD FROG sitting ont he 3 1/2 TREE feeding ADEMAME to the FATTY CAST
*PATHOMA NEPHROTIC syndrome
4 Main changes in the Blood due to protein loss at the glomerulus
HYPO albumin
--> causes decreased oncotic pressure in the blood in the body
--> causes edema
--> especially peri orbidtal
HYPO gammaglobulin
--> leads to increased susceptibility to infection
HYPO antithrombin 3
--> leads to hypercoagulation
--> high risk of DVT ad clots
HYPER cholesterol + HYPER lipid
--> think of the liver trying to compensate for the loss of protein in the blood
Normal 3 layers of the glomerulus for filtering
endothelial cells
GBM = collagen 4
epithelial podocyte foot proccess = charge barrier
3 PAIRS of causes and PATHOPHYS in Nephrotic syndrome
PAIR 1 = cytokines in the blood --> podocyte defacement
--> MCD
--> Focal Segregation G Sclerosis
PAIR 2 = immune complex complement deposition in ONE of the 3 layers
PAIR 3 = systemic disease that cause nephrotic syndrome
--> diabetes
--> systemic sclerosis
PAIR 1 = cytokines in the blood --> podocyte defacement
--> MCD
--> Focal Segregation G Sclerosis
FSGS = focal segmental glomerular SCLEROSIS
FOCAL SEGREGATION of BLACKS and HISPANICS
also high in HIV, IV drugs and SCD = sickle cell disease
think of all the racist things that people can think aboout BLACK people in FOCAL SEGMENT GS
--> HIV
--> IV drug use
--> Sickle cell disease
note that BOTH MCD and FSGS have efacement of the GBM in common
ANYONE with these characteristics who gets NEPHROTIC syndrome
FOCAL SEGMENTAL GS until proven otherwise
FSGS --> each letter tells you the type of nephrotic syndrome
F = focal = means only SOME of the GLOMS are affected
--> example = 1 of 3 glomerulus are affected
S = Segmental SEGREGAION = only 1 LOBULE
--> the rest of the lobules are normal
G = GLom
S = Sclerosis = measn there will be RED SCLEROSIS on the HISTO
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FSGS tx
FSGS does NOT respond well to steroids
--> thus it follows that if you thought a person had MCD and you gave them steroids and they didn't respond
--> they are probably progressing towards FSGS
FSGS has a POOR PROGNOSIS and will progress to RENAL FAILURE
--> is there any treatment?
Dx and histopath of FSGS
note that BOTH MCD and FSGS have efacement of the GBM in common
as the name implies there is SCLEROSIS of the capillaries
NO immune complex --> IF negative
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MCD = minimal change disease
FLATTENNING of the FOOT processing
main cause = cytokines that cause inflammation
same process as in Hodgkin's lymphoma
--> REED STERNBERG = RED STONE BIRD cells
--> secrete high amounts of cytokines in HOG KING lymphoma from their lymph nodes they are in
cytokines in HOG KING LIME FOAM = these cytokines are what cause the constitutional B Symptoms
--> night sweats
--> fatigue / weight loss
--> general fever
MCD can be one way that a HOG KING LIME FOAM can present
--> need to rule this out
MCD Histology
BOTH H and E stain and IF are NEGATIVE in MCD
--> this is becasue the flatenned foot processes are so SMALL
MCD can only be seen in Light MIcroscopy
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MCD treatment
because MCD is only caused by circulating cytokines the main goal is to just lower the cytokines
MCD thus responds extremely well to steroids
--> MCD is the ONLY nephrotic syndrome that is easily treated
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MCD Blood labs
MCD is so MINIMAL since it is ONLY the foot processes that are effected
MCD only has albumin loos
--> there is NO LOSS of gammaglobulins, etc.
PAIR 2 = immune complex complement deposition in ONE of the 3 layers
MEMBRANOUS nephropathy
most common nephropathy among CAUCASIAN ADULTS
MEMBRANOUS also common in
--> HEB B and C
--> SLE
--> common drugs like NSAIDs
SLE patients with kidney problems
note that SLE MOST COMMON CAUSE of death is RENAL FAILURE
SLE nephritic
--> is ALWAYS diffuse proliferative = recall with SLE you have to DIFFUSE the NOOSE in SLE and stop the WIRE LOOP hanging themselves
SLE nephrotic
--> MEMBRANOUS
--> think to have SLE you have to get MEMBRANOUS GN to TRULY be a MEMBER of the club
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MEMBRANOUOS HISTO
MEMBRANOUS = means the GBM membrane gets THINK
always look for the membrane of capillaries they shoul be nice and THIN
MEMBRANOUS = also means that the GBM is thickenned due to IMMUNE COMPLEX deposition on the GBM
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*MEMBRANO PROLIFERATIVE Glomerular Nephritis
think of as 2 separate things happening
MEBRANO
= whenver you see "membrano" = think of GBM THICKENNING that is due to Immune complex deposition
PROLIFERATIVE
= recall that the cells that are the most abundent in the GLOM are the messangial cells that hold all the capillaries of the lobules together
--> thus PROLIFERATIVE = means PROLIFERATION of the messangial cells
--> give the TRAM TRACK appearance on IF
MEBRANO
= whenver you see "membrano" = think of GBM THICKENNING that is due to Immune complex deposition
PROLIFERATIVE = recall that the cells that are the most abundent in the GLOM are the messangial cells that hold all the capillaries of the lobules together
--> thus PROLIFERATIVE = means PROLIFERATION of the messangial cells
PROLIFERATIVE
= recall that the cells that are the most abundent in the GLOM are the messangial cells that hold all the capillaries of the lobules together
--> thus PROLIFERATIVE = means PROLIFERATION of the messangial cells
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TYPE 1 vs TYPE 2 - MEMBRANO PROLIFERATIVE GN
Membrano PRolif GN is further categorized based on which LAYER the Immune complex deposits on
TYPE 1 MPGN = sub ENDOTHELIAL
--> think under the first layer
--> type 1 asscoiated with HEPATITIS = HBV and HBC
--> TYPE 1 = more asscoiated with TRACKS = think IV drug TRACKs = type 1 = HBV and HCV
TYPE 2 MPGN = GBM
--> think in the second layer = GBM
--> type 2 is caused by C3 NEPHRITIC FACTOR
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PAIR 3 = systemic disease that cause nephrotic syndrome
--> diabetes
--> systemic amyloidosis = most common spot is the kidney
*DIabetic Nephropathy
hyperglycemia
NEG = non enzymatic glycosylation of the arterial walls
--> causes hyaline artierosclerosis in the VASCULAR BASEMENT MEMBRANES
--> same as in HTN
EFERENT ARTERIOLE constricted and damaged from NEG
--> EFFERENT causes backflow
--> HIGH GFR
--> microalbuminemia
--> then finally leads to nephrotic syndrome
Kimmelstiel-Wilson Nodules
PAthophys of diabetic nephropathy
note that the whole thing that start DN is that the NEG and arteriosclerosis is MAINLY at the EFFERENT arteriole of the GLOM
--> this makes the back pressure into the GLOM increase
first you get higher pressures in the GLOM
then you get messangial sclrosis just like you did in the EFFERENT arteriole
finally you get nephrotic syndrome and leakage of albumin
KEY to EFFERENT arteriole being the main target of diabetic nephropathy damage
--> EFFERENT is where Angiotensin 2 acts to constrict using A2 receptors
--> thus ACE inhibitors help SLOW the prgression of diabetic nephropathy
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Diabetic - Kimmelstiel-Wilson Nodules
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*systemic amyloidosis
systemic amyloidosis = most common spot is the kidney
*Histology for Glomerular Disease
*Kimmelstiel-Wilson THICK MESSANGIAL Lesion = DIABETES
round pink areas within the glomerulus
found from diabetic nephropathy
*Crescents in Glomerular GOOD PASTURE
seen in GBM (Good Pastures Disease)
*Amyloid Deposits
found in renal amyloidosis
stains on CONGO red stains
*PSGN = Post Streptococcal Glomerular Nephritis
most common nephritic in kids
--> COCO COLA
*LUMPY BUMPS IMMUNE COMPLEX Deposits - PSGN
stains on CONGO red stains
found in
post strep Glom Nephritis
*Granular Deposits - PSGN
found in granular or spotted immunoflourenscent images vs full out green seen in GBM amyloidosis
stains on CONGO red stains
--> think GONGO RED = SANTA COCA COLA
found in
post strep Glom Nephritis
*DIRTY USMLE
NEPHRITIC and NEPPHROTIC syndromes
LUMP 3 BUMP 3 = PSG = C3B = type 3
2 PASTURE
type 2 = IgM x IgG = 2 x 2 = 4 collagen
-->
2 organs
= LUNGS + KIDNEY
TRAM TRACK appearance of the GBM membrane
the arrow pointing here shows the GBM has split in 2
--> looks like a TRAM TRACK
*Antibiotics
PIC
*Bacteril Cell Wall Inhibitors
beta lactams = penicillins
*Bacteril Cell Wall CROSS LINKING
beta lactams = penicillins
stop the "building" and "cross linking" of D-ALA D-ALA building blocks
*Beta Lactams
Penicillins ("RSP respect" penicillins)
--> penicillinase sensitive penicillins
--> penicillinase resistant penicillins
--> Anti-pseudomona penicillins
Cephalosporins
Carrbapenems
*Penicillins ("RSP respect" penicillins)
penicillinase
sensitive
penicillins
--> penicillin V,G
--> ampicillin
--> amoxicillin
penicillinase
resistant
penicillins
Anti-
pseudomona
penicillins
--> piperacillin
--> ticarcillin
*penicillinase sensitive penicillins
penicillin V,G
ampicillin
amoxicillin
*penicillinase resistant penicillins
Oxacillin
--> "the stronger
OX version of amoxacillin
"
*Anti-pseudomona penicillins
piperacillin
ticarcillin
*Cephalosporins
5 generations of Cephs
*Carrbapenems
-
*Bacteril Cell Wall Synthesis
stop the actual synthesis of bacterial cell wall
on reserve = last line for resistant bugs
*Beta Lactams
Vancomycin
Bacitracin
--> bacitracin sensitive = strep. pneumo
--> bacitracin resistant = strep. agalactae
*Vancomycin
note have VRE = vancomycin resistant E. Coli
*Protein Synthesis = Ribosome subunit inhibitors
bacteria ribosomes = 70s
--> 30s + 50s
*50s ribosome inhibitors
"CCEL as 50s"
C = chloramphenicol
Clindamycin
Erythromycin + other ACE MACs
--> azithromycin
--> clarythromycin
--> erythromycin
L = linezolid
*Chloramphenicol = 50s
"Chloraline = Grey Baby Syndrome"
*Macrolides ACE = 50s
A = azythromycin
C = Clarythromycin
E = Erythromycin
*Clindamycin = 50s
Chloramphenicol + Clindamycin both part of
-->
"SAFe Children Take Good Care"
--> both are teratogenic
*Anaerobic tx - ABOVE vs BELOW diaphragm
Clindamycin
= tx Anaerobic infections ABOVE diaphragm
--> "Clean mycins of my SOUL"
= your soul is ABOVE the diaphragm
Metronidazole
= tx Anaerobic infections BELOW diaphragm
"
GET GAP
on the METRO train to HELL"
--> your METRO train to HELL = ABOVE the diaphragm
--> GAP = Giarda + anaerobes (C Diff.) + Pylori both BELOW the diaphragm
*Linezolid = 50s
"Linezolid = strong OX used for resistant VRE and MRSA"
--> Linezolid reserved for last line tx
*30s ribosome inhibitors
"AT 30s"
A = aminoglycosides
T = tetracyclines
*Aminoglycosides = 30s
"forgive MYCINS. AMIN."
--> "Septuagent + Tobra + aMika + Neo"
streptomycin
gentamycin
tobramycin
Amikacin
neomycin
*tetracyclines = 30s
tetracyclines
doxicycline
Tetracyclines are teratogenic --> part of:
-->
"SAFe Children Take Good Care"
*DNA/RNA inhibitors for bacteria
DNA blockers
--> metronidazole
RNA POL blockers
--> "RIFF with RNA" = rifampin
DNA GYRASE blockers
--> flouroquinolones + quinolones
*DNA GYRASE (=Topoisomerase 2) Inhibitors
flouroquinolones
Quinolones = Nalidixic Acid
*Flouroquinolones
"GEMs FLOXAS IN... to LEVO 3 bar... then TOPS nightclub to GYRATE"
--> -
floxacins
block topoisomerase 2 =
DNA GYRASE
1 = "GEMs FLOX IN"
--> -
floxacin
ending
--> gemfloxacin
2 = "to LEVO 3 bar"
--> levofloxacin
2 = CIP a drink of Nalidixic acid from Ken NALLY bartender
--> Nalidixic acid = only quinolone
*Nalidixic Acid = Quinolone
DNA GYRASE blocker
2 = CIP a drink of Nalidixic acid from Ken NALLY bartender
--> Nalidixic acid = only quinolone
*RNA Pol Inhibitors
"RIFF with RNA"
=
rifampin
Rifabutin
= rifampin alternative
Rifabutin
= alternative
--> Rifabutin = Rfiampin "BUT" no CYP "REFUSE Greasy Carbz"
*Rifampin
*Rifampin main part of RIPE tx for TB tuberculosis
RIPE tx for TB
--> R = rifampin
--> I = isoniozid
--> P = pyrazinamide
--> E = ethambutol
*Rifabutin
Rifabutin
= rifampin alternative
--> Rifabutin = Rfiampin "BUT" no CYP "REFUSE Greasy Carbz"
*DNA Inhibitors
"RIFF with RNA"
=
rifampin
Rifabutin
= rifampin alternative
Rifabutin
= alternative
--> Rifabutin = Rfiampin "BUT" no CYP "REFUSE Greasy Carbz"
*Metronidzole
DNA blocker
Metronidazole = tx Anaerobic infections BELOW diaphragm
"GET GAP on the METRO train to HELL"
--> GAP = Giarda + anaerobes (C Diff.) + Pylori both BELOW the diaphragm
*Anaerobic tx - ABOVE vs BELOW diaphragm
Clindamycin
= tx Anaerobic infections ABOVE diaphragm
--> "Clean mycins of my SOUL"
= your soul is ABOVE the diaphragm
Metronidazole
= tx Anaerobic infections BELOW diaphragm
"
GET GAP
on the METRO train to HELL"
--> your METRO train to HELL = ABOVE the diaphragm
--> GAP = Giarda + anaerobes (C Diff.) + Pylori both BELOW the diaphragm
*Folate Synthesis Inhibitors / UTI ABX
DHP synthase blockers
--> SMX = sulfamethoxazole
DHF reductase blockers
--> TMP = Trimethroprim
SMX-TMP are used in combo for most UTI
*SMX = sulfamethoxazole
DHP synthase blocker
--> blocks folate synthesis pathway
SMX-TMP are used in combo for most UTI
*TMP = Trimethroprim
DHF reductase blockers
--> blocks folate synthesis pathway
SMX-TMP are used in combo for most UTI
*Home
*Home