143+ quick-fire dental facts • tap a card to flip
Protease inhibitors are commonly associated with metabolic complications including lipodystrophy, insulin resistance, hyperglycemia, hypercholesterolemia, and hypertriglyceridemia. Patients receiving long-term therapy should undergo regular monitoring of blood glucose and lipid profiles to reduce the risk of cardiovascular disease.
Which of the following is a common adverse effect associated with HIV protease inhibitors?
1). Lipodystrophy and metabolic disturbances
2). Acute renal failure
3). Cardiotoxicity
4). Pancreatic necrosis
Isoproterenol is used in the management of bronchospasm during anesthesia;
adjunctive treatment for shock.
Syncope may be treated with any of the following drug except
1) Phenylephrine
2) Oxygen
3) Ephedrine
4) Isoproterenol
Thromboxane $A_2$ ($TXA_2$) is a potent aggregator of platelets produced by COX-1. Inhibition of COX-1 prevents $TXA_2$ synthesis, thus inhibiting platelet aggregation.
How do NSAIDs affect platelet function?
1) They stimulate platelet aggregation by increasing thromboxane production
2) They inhibit platelet aggregation by reducing thromboxane A2 synthesis
3) They enhance fibrinolysis
4) They increase the half-life of platelets
First-generation antihistamines such as diphenhydramine act as competitive antagonists (inverse agonists) at histamine H1 receptors. They block the effects of histamine in peripheral tissues, reducing itching, vasodilation, increased vascular permeability, and edema. Because they readily cross the blood-brain barrier, they also block central H1 receptors, producing sedation and drowsiness.
How do first-generation antihistamines, such as diphenhydramine, exert their therapeutic effects in allergic reactions?
1). By blocking the release of histamine from mast cells
2). By inhibiting prostaglandin synthesis
3). By competitively blocking histamine H1 receptors in both the central and peripheral nervous systems
4). By increasing the degradation of histamine in the liver
Anticholinergic side effect of antidepressant leads to dry mouth in the patients on these drugs.
Dry mouth is due to the Muscarinic acetylcholine receptor antagonism of these drugs.
Dry mouth during antidepressant therapy is caused by blockade of:
1) Muscarinic acetylcholine receptors.
2) Serotonergic receptors.
3) Dopaminergic receptors.
4) GABA receptors.
Chemotherapy primarily damages rapidly dividing hematopoietic progenitor cells within the bone marrow, resulting in pancytopenia. This manifests as anemia, leukopenia, and thrombocytopenia, increasing the risks of infection, fatigue, and bleeding.
What is the primary cause of bone marrow suppression observed in patients, including those with MDS, undergoing chemotherapy?
1). Direct inhibition of platelet production
2). Damage to rapidly dividing hematopoietic stem cells
3). Immune-mediated destruction of marrow cells
4). Reduced erythropoietin production by the kidneys
Anthracyclines such as doxorubicin intercalate between DNA base pairs, inhibiting DNA replication and transcription. They also generate free radicals and inhibit topoisomerase II, leading to DNA damage and apoptosis.
How do anthracyclines function as chemotherapeutic agents in diseases like MDS?
1). By preventing DNA polymerase from adding nucleotides
2). By intercalating into DNA, inhibiting replication and transcription
3). By binding to tubulin, inhibiting mitosis
4). By inhibiting reverse transcriptase activity
GlycosaminoglycAnswer (GAGs) are heteropolysaccharides. These molecules are long unbranched polysaccharides containing a repeating disaccharide unit. The disaccharide units contain either of two modified sugars N-acetylgalactosamine (GalNAc) or N-acetylglucosamine (GlcNAc) and a uronic acid such as glucuronate or iduronate. The specific GAGs of physiological significance are hyaluronic acid, dermatan sulfate, chondroitin sulfate, heparin, heparan sulfate, and keratan sulfate.
Heparin
1) is a glycosaminoglycan
2) potentiates thrombin
3) has a half life of 3-4 hours
4) is normally given IM
Taxanes bind to microtubules and stabilize them, preventing their depolymerization. This blocks normal mitotic spindle function, arrests cells in mitosis, and ultimately induces apoptosis.
How do taxane chemotherapy agents, such as paclitaxel, interfere with cell division in disorders like MDS?
1). By inhibiting DNA topoisomerase II
2). By forming cross-links in the DNA double helix
3). By preventing the formation of the mitotic spindle
4). By stabilizing microtubules, preventing their disassembly during mitosis
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