Question: What are the key differences between adrenergic and cholinergic receptors in terms of their function and associated neurotransmitters?

Answer:

• Adrenergic receptors: Respond to norepinephrine (NE) and epinephrine (E).
  • α1: Vasoconstriction, increased blood pressure, pupil dilation.
  • α2: Inhibits NE release.
  • β1: Increases heart rate and contractility.
  • β2: Bronchodilation, vasodilation.
• Cholinergic receptors: Respond to acetylcholine (ACh).
  • Muscarinic (M1-M5): Controls gland secretion, heart rate, and smooth muscle contraction.
  • Nicotinic: Controls muscle contraction at neuromuscular junctions.

Question: Explain the two-hit hypothesis in the context of tumor suppressor gene mutations.

Answer: The two-hit hypothesis explains that both alleles of a tumor suppressor gene must be inactivated for cancer to develop:

1. First hit: A germline or somatic mutation in one allele of the tumor suppressor gene (e.g., RB1 in retinoblastoma).
2. Second hit: Loss of the remaining normal allele through mutation, deletion, or epigenetic silencing.

Question: What are the phases of the cardiac cycle and their corresponding events?

Answer:

1. Atrial systole: Atria contract, pushing blood into the ventricles (P wave).
2. Isovolumetric contraction: Ventricles contract but no blood is ejected (QRS complex).
3. Ventricular ejection: Blood is ejected from the ventricles.
4. Isovolumetric relaxation: Ventricles relax and no blood enters the ventricles (T wave).
5. Ventricular filling: AV valves open, and blood flows passively into the ventricles.

Question: What are the mechanisms of action for major classes of antibiotics?

Answer:

• Beta-lactams: Inhibit cell wall synthesis.
• Aminoglycosides: Inhibit protein synthesis by binding to the 30S ribosomal subunit.
• Fluoroquinolones: Inhibit DNA gyrase and topoisomerase IV.
• Macrolides: Inhibit protein synthesis by binding to the 50S ribosomal subunit.
• Sulfonamides: Inhibit folic acid synthesis by competing with PABA.

Question: What is the pathophysiology of pre-eclampsia?

Answer: Pre-eclampsia involves:

• Endothelial dysfunction: Leads to vasoconstriction and increased vascular permeability.
• Placental ischemia: Poor placental perfusion due to insufficient remodeling of spiral arteries.
• Imbalance of angiogenic factors: Elevated sFlt-1 and endoglin inhibit VEGF, leading to endothelial damage.

Question: What are the four types of hypersensitivity reactions?

Answer:

• Type I (Immediate): Mediated by IgE and mast cells.
• Type II (Cytotoxic): Involves IgG or IgM targeting cells.
• Type III (Immune complex): Immune complexes deposit in tissues causing inflammation.
• Type IV (Delayed): T-cell mediated tissue damage.

Question: What are the key steps and enzymes of the Krebs cycle?

Answer:

1. Citrate synthase: Acetyl-CoA + oxaloacetate → citrate.
2. Aconitase: Citrate → isocitrate.
3. Isocitrate dehydrogenase: Isocitrate → α-ketoglutarate (NADH release).
4. α-Ketoglutarate dehydrogenase: α-Ketoglutarate → succinyl-CoA (NADH release).
5. Succinyl-CoA synthetase: Succinyl-CoA → succinate (GTP release).
6. Succinate dehydrogenase: Succinate → fumarate (FADH2 release).
7. Fumarase: Fumarate → malate.
8. Malate dehydrogenase: Malate → oxaloacetate (NADH release).

Question: What are the long-term complications of poorly controlled diabetes?

Answer:

• Microvascular complications: Diabetic retinopathy, nephropathy, neuropathy.
• Macrovascular complications: Cardiovascular disease, peripheral arterial disease.