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- Impaired in Alcoholism.
*Amanita Toxin - Binds to DNA dependent RNA Polymerase II, halts mRNA synthesis.
*anti-dsDNA - SLE.
*Glycine - M/C (every third) amino acid in collagen fibers. D/t its smallest size, it
gets fit into the restricted space of triple helix.
*Proline - essential for alpha helix in collagen fibers, as it's ring structure produces a
bend into polypeptide chains.
*Ketone Body Utilizing parts- Skeletal Muscles, Cardiac muscles, Renal Cortex, Brain.
*Poly A tail - at 3' end. Gene has consensus sequence (AAUAAA) at 3' end, after
which poly A tail is added.
*Only Vit. B12 & folate are reserved in Liver in sufficient amount to last for YEARS.
Other Vit. (Viz. A,E,K) last only for few months.
- unconjugated jaundice.
*Tumor lysis syndrome - large quantity of Uric acid is produced which can cause
Acute Renal Failure.
*Late division of Monozygotic twins results in 1 amniotic sac and 1 chorionic sac.
*Sertoli cells will inhibit the involution of Mullerian (paramesonephric) ducts. Thus
inhibiting the development of internal female genitalia.
*Leydig cells produce testosterone, thus developing wullfian duct and male external
genetalia.
*hCG - Glycoprotein Hormone Produced by the placenta, which resembles LH, FSH &
TSH.
*Triple Test - afp, hcg & estriol levels. B/w 16-18 weeks.
- If triple test is abnorml, then usg. If usg is consistent with pregnancy dates
n there r no anatomic abnormalities, then Amniocentesis.
*Freckles - Ephelides
*The secondary Oocytes remain frozen until fertilization occurs in Fallopian tube.
*Dorsal Pancreatic Bud - Forms Tail, body and most of head of pancreas along with
dorsal (accessory) Pancreatic duct of Santorini.
- Both, Ventral and dorsal buds are derived from the duodenal portion of the
foregut.
*Vit. A overdose in pregnancy - Craniofacial Deformity, Posterior fossa CNS Defects,
Auditory defects and abnormalities of great vessels. (similar to DiGeorge
Syndrome).
*Apple Peel Atresia - Atresia of small intestine in neonate d/t SMA obstruction.
*Polyhydramnios causes -
- in CNS, It's also thought to regulate mood, anxiety, and stress behavior.
MOA - 1.) D1 receptor activation -> activayes adenylyl cyclase ->raises cyclic
AMP -> Arterial dilatation (espacially Renal, Coronary and mesenteric) -> decreases
SVR
*During continuous infusion of a drug metabolized by first order kinetics, the steady
state concentration is reached in 4-5 lives.
*Dopamine -
*Nor-epinephrine - I/v may cause Indurations and pallor of the surrounding tissue,
D/t extravasation of NE-> intense alpha1 mediated vasoconstriction which can lead
to local tissue necrosis.
*Statins are metabolized in the liver (except Pravastatin) by Cyt3A4. So, enzyme
inhibitors will increase their Concentration and enzyme inducers will decrease their
concentration.
*Hydrocholothiazide - I line T/t for HTN with osteoporosis (since it increases the
Serum calcium) and Isolated Systolic HTN.
*Niacin MOA - 1.) decreases the synthesis of hepatic triglycerides and VLDL ->
SUPPRESSED RELEASE of free fatty acids from peripheral tissues.
*Fibrates and niacin - decrease hepatic VLDL production. Thus mainstay of T/t for
Primary hypertriglyceridemia (increased VLDL).
*ApoB 100 - Apoprotein on VLDL &LDL. Decreased serum concentration of these will
cause decreased ApoB 100.
- For rate control in AF with rapid ventricular response d/t ability to slow
conduction through the AV node.
ADR- Constipation and gingival hyperplasia.
*Nor-epinephrine-
*Cardio selective beta blocker - pts. With coronary artery Ds. with CHF and HTN
*ACE-I - increase in Serum creatinine by 30% within 2-5 days is common, which
stabilizes in 2-3 weeks.
*Ticlopidine & Clopidogrel - block platelet ADP receptor-> disllow GP IIb/IIIa receptor-
> inhibit platelet aggregation.
*Abciximab - monoclonal antibody that inhibits platelet aggregation by targeting the
platelet IIb/IIIa receptor.
*Bile acid binding resin (Cholestyramine) increases the bile acid production, thus
increasing hepatic triglyceride & VLDL production.
eg.- 1.) alpha adrenergic agents used as nasal decongestant. use >3 days
causes negative feedback, resulting in decreased norepinephrine synthesis and
release from nerve endings, resulting in relative vasodilation. It is rebound
rhinorrhoea/ rhinitis medicamentosa.
*Glucocorticoids- High doses are used for ophthalmopathy A/w Graves Disease.
They are helpful in decreasing the severity of inflammation and decreasing
extraocular volume. Conventional antithyroid drugs do not improve
ophthalmopathy.
* SERMs- Tamoxifen, Raloxifen. Agonist in Uterus and antagonist in Breast.
- Also improve the lipid levels and partial agonist to bone, thus increase BMD.
-Adiponectin (Adipocytokinin) levels are low in type 2 DM. T/t with TZDs
increases its levels.
W Increases Adiponectin
W increases fatty acid transport protein
W increases insulin receptor substrate
W increases glucose transporter-4 (Glut-4)
- increases circulating levels of von Wille brand factor (factor VII:R) and
promote the coagulant activity of factor VII:C.
- acts through G-protein coupled cell surface receptor, which act by adenylate
cyclase activation.
- starts working in 2 hours, peaks in 4-12 hrs and lasts about 18 hours.
* Detemir- Long acting insulin analogue with a fatty acid bound to 1 of the lysine
amino acid on the insulin molecule. This fatty acid side chain allows the detemir to
bind to albumin and slowly dissociate afterwards, resulting in prolonged action.
- it usually starts working in with-in 2 Hours, peaks in 3-9 hours and lasts
about 24 hours.
*Beta-blocker- initially increases the PVR as it blocks beta2
*ANti arrhythimic drugs do not affect phase 4 (the resting membrane potential) of
myocyte, but these do affect the phase 4 of pacemaker cell action potential, which
is mediated by Na influx.
*Digitalis ADR- fatigue, blurry vision, changes in color perception, nausea &
vomiting, diarrhoea, abdominal pain, headache, confusion, dizziness and delirium.
*Drugs causing acne - Androgens, epidermal growth factor receptor inhibitors and
Lithium.
Causes- PCOs, Cushing syndrome, ovarian and adrenal tumour and idiopathic.
eg.-Propylthiouracil, Methimazol.
*PTU- decreases peripheral conversion of T4->T3, has a shorter half-life and is the
drug of choice in pregnancy.
*Flutamide- non-steroid antiandrogen that comppetes with testosterone and DHT for
testosterone receptors.
*Lepirudin and Argatroban- Direct thrombin inhibitor, used for Mx of heparin induced
thrombocytopenia
*Gardos channel ( calcium dependent K ion channel) blockers hinder the efflux of
potasium and water from the cell, preventing dehydration of erythrocytes and
reducing the polymerization of HbS.
*Hyroxyurea icreases fetal hemoglobin (HbF) synthesis by an unknown mechanism.
*At low doses, aspirin inhibits COX1 alone, whereas at high doses, it inhibits both
isoenzymes irreversibly.
Uses- Following PCI and T/t of unstable angina and non-Q wave myocardial
infarction.
*Enfuvirtide- HIV Fusion Inhibitor. Binds to the envelope GP41 of HIV-1 and blocks
conformational changes necessary for the fusion of viral and cellular membrane.
*Imatinib- inhibits BCR/ABL protein Tyrosin kinase. thus inhibits the cellular
proliferation of BCR/ABL cells without inducing apoptosis.
- ORAL medication.
1.Infections
2.Drugs- Dapsone,Antimalarials,Sulfonamides
3.DKA
4.Favism
*Raltegravir- Integrase inhibitor. Disrupts the ability of HIV to integrate it's genome
into the host cell's chromosomes, thus preventing host cellular machinery from
being used to synthesize HIv mRNA.
*Fusion inhibitor - Attaches to gp41 and ihibits virus entry into CD4+ cells.
*HIV attachment to target cells is mediated by the binding of viral envelope protein
gp120 to the CD4 membrane protein of T-helper cells.
*RT inhibitor- HIV DNA Synthesis from RNA Template.
*Aminocaroic acid and tranexamic acid- inhibit fibrinolysis. they inhibit plasminogen
activation.
*AZT- can bind to and inhibit some mammalian cellularand mitochondrial DNA
polymerases, particularly beta and gamma polymerases.
*Biotin (B7) & Pantothenic acid (B5) - via sodium dependent multivitamin
transporter.
*Penicillin - inhibits transpeptidase, the enzyme that catalyzes the final crosslinking
step in peptidoglycan cellwall formation.
*Sulfonamides - compete with Para Aminobenzoic Acid (PABA) for incorporation into
folic acid.
*Drugs with high intrinsic hepatic clearance tend to have high lipophilicity and a
high volume of distribution, with penetrance into the CNS and other tissues.
*MU Opiod Analgesic-> contraction of smooth muscle cells-> -> constriction and
spasm of of the Sphincter of Oddi-> Increased CBD pressure-> increased Gall
bladder pressure-> Billiary colic.
*the risk of CVA due to OCPs is very much increased in smokers and >35 Yrs.
4. Hypertriglyceridemia
5. Pregnancy
*Lead Poisoning-
T/t- Dimercaprol, which displaces arsenic ions from the sulfhydryl group of
enzymes.
Ribivirin MOA- Lethal Hypermutation, inhibiting RNA polymerase and IMP (depleting
GTP), causing defective 5'-cap formation on viral mRNA transcript and modulating a
more effective immune response.
*Bioavailability = Area under the oral curve* IV dose/ area under the IV curve*oral
dose
*Lyme disease vaccine- contains aa recombinant outer surface protein from Borrelia
burgdorferi bacteria
*Etambutol ADR- optic neuritis causing visual acuity, central scotoma or color
blindness.
*Aminoglycosides & Vancomycin ADR- direct damage to the 8th cranial nerve.
Therefore can cause deafness, vertigo and tinnitus.
*aerosolised Ribavirin- for RSV infection, espacially in infants and children who are
at risk for disease progression.
*Amphotericin B- MOA- binds to ergosterol with higher affinity than with cholesterol.
5. Thrombophlebitis.
Prophylaxis- weekly Azithro and pharamcological HIV T/t to bring CD4 cells
>200.
*Mycolic acid- long branched chain saturated fatty acid that contain aproximately
ninety carbon molecules.
*pyrimidines (Flucytosine):- convorted to 5FU and interferes with fungal RNA and
protein synthesis.
T/t- Dantrolin.
*Physostigmine- Tertiary amine, which can cross BBB and reverse the anti-
muscarinic effect of Atropin.
*Phenytoin -> MOA- inhibits neuronal high frequency firing by reducing the ability if
sodium channels to recover from inactivation, increasing the refractory period.
*Carbamazepine- Uses- GTCS, Partial Seizures, pain relief in trigeminal and diabetic
neuropathy and bipolar disorder.
ADR- Agranulocytosis.
*Aged Pt.s with H/o falls etc., should not be given first generation antihistamines.
*GABA- BZDs bind to allosterically to gaba chloride ion channel and increase the
frequency of Cl ion channel opening. Thus facilitates GABA actions.
- blocks T-type calcium ion channels that trigger and sustain rhythmic pulsed
discharges in thalamic neurons.
- Hepatotoxic.
- Dependence doesn't occur, even with chronic use.thus can be used in Pts.
with h/o of abuse of anti-anxiety drugs.
* Cisplatin- MOA- forms a reactive oxygen species that can form Crosslinks.