CVS 7 Flashcards
zero order kinetics drugs
WATTP Warfarin Aspirin Theophyline Tolbutamide ( first gen sulfonylurea) Phenytoin
failure of therapy caused by enzyme inducer or inhibitors
INDUCER
list of enzyme inducers
My New GPRS Cell Phone
Modanifil —- increase DA (narcolepsy ADHD)
Nevirapine —– NNRTI
Griseofulvin —– microtubules
Phenytoin —– Na in heart and brain
Rifampin —— Rna polym II
Smoking/ St john wart ——— increase 5HT
Carbamezapine (na-) and CHRONIC alcohol
Phenobarbital —— GABA duration cl- channels
what is the eukaryotic RNA polymerase inhibitor
Amantina phelloides death cap mushroom
most common types of RNA
R rna—— I
M rna—— II
T rna —— III
CYP 450 inhibitors 3A4 most common type
Sodium valproate Na - / gaba transaminase -/ t typ ca Isoniazid Cimetidine Ketoconazole Fluconazole Acute alcohol / avirs / amiodarone ( 5' deiodinase) Chloramphenicol / cipro/ clarythro Erythromycin Sulfa --------- dehypteroate synthase C Omeprazole Metronidazole Grapefruit juice
tiagabine MOA
blocks reabsp of GABA
Gabapentin
acts on GABA receptors +ve
vigabatrin
gaba transaminase inhibitor
GABA doesnt break down —– increase levels of GABA
for infantile spasms
sodium valproate
gaba transaminase inhibitor
Na channels inhib
t type calcium channels
pregabalin
increases releae of GABA
Chemical mediators are divided into CELLULAR AND PLASMA
what are the plasma ones?
made in liver
complement
kinin
clotting
Cellular chemical mediators
PREFORMED
hsitamine
serotonin
lysosomal enzymes
FRESHLY FORMED prostaglandins leukotreines cytokines nitric oxide PAF
TLR CD 14
Gram negative endotoxin
cytokines and mast cells degenerate to make
hsitamines
how do steroids function
induce lipocortin —– breaks PLP to AA
innactivating NF-κB
NF-κB is the transcription factor that induces the production of TNF-α and other inflammatory agents
antibodies against PLP A2
the enzyme that breaks PLP to AA
membranous nephropathy
lipoxigenase inhibiotor drug
zileuton
highly hepatotoxic
blocks leukotreine receptors
zafirleukast moteleukast
Prostacyclin PGI2 function and drug name
inhibits platelet agg
EPOPROSTENOL
ILOPROST
Prostaglandins PGE1
decrease vascular tone
ALPROSTADIL
PGE2
increase uterine tone
pain
pyrexia
DINOPROSTONE
PGF2 alpha
increase uterine tone
CARBOPROST
Thromboxane 2
increase platelet agg
increase vascular tone
ASPIRIN ihibits this
LOX pathway makes LTB4 and LTC D E 4
LTB4 —– neutrophil chemotaxis
LTC D E 4 —— vasodialation and increase bronchial tone
chemotactic agents include
LTB4 IL 8 C5a Kallikrenin formyl methionine
what are the physiological functions of COX 1
gastric mucose protection
increase renal perfusion
platelett aggregation
COX 2 has physiological and pathological functions
PHYSIOLOGICAL
increase renal perf
vasodialation
tissue repair
PATHOLOGICAL
increase pain sensitivity
inflammation
asprin induced asthma mechanism
blocks COX 1 2 …. shifts towards LOX —— LTC D E 4 increase and case bronchospams
drugs that inhibit mast cell degranulation
cromolyn
nedocromil
ketotifen
igE INDEPENDENT mast cell degranulation
morphine opiods
Vancomycin
Radiocontrast
histamine bradykinin released —- localised swelling and urticaria
what activates teh classical pathway
IgG and IgM
C3 derivatives
C3a —— anaphylotoxin
C3b —– opsonin IgG
what are the three pathways of complement cascade
classical —- IgM IgG
lecithin——- mannose binding lecithin C4
alternate—– spontaneous C3
c1 c2 c4 c3 ——-
c5b6-9– MAC
mac is cytotoxic
mac can also bind to self cells like RBC and WBC but normally what blocks this?
PIGA gene is responsible for formation of GPI ( glycosyl phosphatidyl inositol )
this makes DAF ( CD55) and MIRL ( CD59)
these prvent complent mediated desctruction
paroxysmal nocturnal hemoglobinemia
normocytic anemia
at night because of shallow breathing—- retntion of CO2 — acidic ph activates ALTERNATIVE pathway
PNH what can be seen in this condition
dark urine hemoglobinuria
decrease haptoglobin levels
hemosiderinuria
PLT microthrombi —- hepatic vein thrombosis— budd chiari
hemosiderin laden macrophages can be seen in
heart failure
what is the most common cause of budd chiari
polycythemia vera
c1 esterase def
hereditary angioedema
treatment for hereditary angioedema
DANAZOL
ECALLANTIDE
which drugs to avoid in pts with HAE
ACEi
sacubitril
If funny channels
IVABRIDINE
increases BP
visual brightness
bradycardia
what is the function of neprilysin
breaks down ANP BNP and ang II
what is the function of Ag II
increases aldosterone which increases Na and dec K+
constricts efferent arteriole
ADH secretion
sacubitril must be given with ? and why
ARBS
because AgII levels also increase
ANP and AgII will work against each other
what are teh side effects of sacubitril
decrease BP
hypokalemia
angioedema
Captopril side effects
Cough Angioedema Pregnancy CI ----- renal failure/ potter seq Taste disturbance Orthostatic hypoT Prodrugs (activate in liver) RAS Increase K contraindication ( ACE i increases K) Lowers ag II formation
deficiency in C2 C4
risk of pyogenic infections and increase risk of AUTOIMMUNE disease
def in C5-C9
increase risk of infection due to nisseria and txoplasma
neprilysin breaks down
substance p and bradykinin
so when neprilysin is blocked by sacubitril these increase
substance p —- pain
bradykinin —- angioedema
steps of leukocyte extravasation
Margination Rolling Adhesion Transmigration (DIAPEDESIS) Chemotaxis Opsonization Phagocytosis O2 dep killing
Margination cell adhesion molecules include
vasculature and leukocyte
VASCULATURE
P selectin
E selectin
L selectin
LEUKOCYTE
sialyl lewis
E L selectin
IL 1 TNF alpha
P selectin
released from weibel palade bodies
what else is secreted from weibel palade bodies
VWF
can be induced by desmopressin
Adhesion molecules
vasculature and leukocytes
VASCULATURE
ICAM 1 CD54
VCAM 1 CD 106
LEUKOCYTES
CD 11/18 integrin
what induces integrin
C5a
LTB4
Transmigration diapedesis
vasculature and leukocytes
VASCULATURE
PECAM 1 CD31
LEUKOCYTES
PECAM 1
Migration
LTB4 C5a IL8 kallikrein platelet activating factor
CGD and the tests
def in NADPH oxidase XLR nitrobluetetrazolium test ---- blue test positive means no deficiency
DHR test —- O2 —> O2- requires NADPH oxidase
O2- is needed to convert DHR —> rhodamine
so in NADPH oxidase def no O2- is made hence no rhodamine made so INCREASE IN DHR
organisms that can cause infection in CGD
catalse +ve Cats Need PLACESS to Belch their Hairballs Candida Nocardia Pseudomonas Listeria Aspergillus Candida E coli Staph Serratia Burkolderia cepaciae H.pylori
O2 independent mechanism of killing
major basic protein
lactoferrin
lysozyme (tears /saliva)
