RESPI Flashcards
Muller Maneuver (Reverse Valsalva Maneuver)
A maneuver used to evaluate airway collapse (e.g. in the setting of OSA). After forced expiration, the patient attempts inspiration with a closed mouth and nose, which leads to airway collapse that can be detected via hypopharyngoscopy.
Inhibition of stem cell differentiation into megakaryocytes is the mechanism of action of IFN-α, a treatment option for essential thrombocythemia,
Decreased DLCO is a typical finding of emphysema that reflects the reduction of gas exchange due to a loss of diffusion area.
Cardiogenic pulmonary edema thickens the alveolar-capillary membrane and impairs oxygen diffusion capacity. As a compensatory mechanism, minute ventilation increases, resulting in increased CO2 elimination.
Increased pulmonary capillary permeability is seen in acute respiratory distress syndrome (ARDS).
Transpulmonary pressure is the difference between the alveolar pressure and the pleural pressure. The transpulmonary pressure helps to keep the lungs expanded. This pressure falls to zero in pneumothorax.
The hallmark of Takayasu arteritis (TA) is granulomatous inflammation of the arterial wall affecting the large arteries (typically the aorta and its branches). TA is more common among women with Asian ancestry, and its peak incidence is between 15 and 45 years of age. This condition manifests with systemic features that include fever, malaise, and arthralgia. Other features of TA include decreased brachial and radial pulses (pulseless disease), syncope, carotid bruit, angina pectoris, impaired vision, and Raynaud phenomenon, all of which are due to narrowing of the large arteries. Erythema nodosum and urticaria may also be seen in TA. Microscopic examination of the diseased vessels would show granulomatous inflammation of the vessel walls, with inflammatory cells infiltrating the tunica media and tunica adventitia.
Pulmonary hamartoma (PH) is the most common cause of a benign solitary pulmonary nodule. This diagnosis is further supported by the tumor size (PH are typically 1–3 cm in diameter), the benign appearance on imaging (round, well-circumscribed, calcified mass; 90% of PH are in peripheral lung areas), and the histology findings (typical features of PH include cartilage lobules that calcify or undergo osseous changes and fibromyxoid tissue with clefts of ciliated epithelium). PHs are usually asymptomatic and only occasionally cause symptoms by obstructing a bronchus (e.g., atelectasis, pneumonitis, cough, expectoration, chest pain).
An inactivating mutation in the G-protein coupled calcium-sensing receptors (CaSRs) of the parathyroids and kidneys is characteristic of familial hypocalciuric hypercalcemia (FHH). A defect of the parathyroid CaSRs causes a reduced sensitivity to serum calcium levels, requiring higher calcium levels to suppress parathyroid hormone (PTH) secretion. On serum analysis, the PTH levels can be normal or increased. An increase in PTH levels and the defect in the renal CaSRs increases renal calcium reuptake, which leads to hypocalciuria and mild hypercalcemia. Increased PTH also increases renal phosphate elimination and can cause hypophosphatemia.
Intravenous labetalol, a nonselective antagonist of beta receptors and alpha-1 receptors, is used to treat severe gestational hypertension and hypertensive emergencies. Alpha-1 blockade causes peripheral vasodilation, which decreases blood pressure. Beta-1 receptor blockade decreases cardiac contractility and renin secretion, which further lowers blood pressure. In addition, the beta-1 blockade also decreases the heart rate by causing sinoatrial and AV node depression. Carvedilol and the nondihydropyridine calcium channel blocker diltiazem can cause a similar decrease in both blood pressure and heart rate. Antihypertensives that only have a vasodilatory effect (e.g., hydralazine, nitroprusside, nicardipine, fenoldopam) cause an increase in heart rate (reflex tachycardia).
Hereditary pancreatitis is usually caused by a mutated PRSS1gene that promotes intrapancreatic trypsinogen activation.
Other genetic variants associated with chronic pancreatitis are mutations in SPINK 1 and CFTR genes.
SPINK1 gene (serine protease inhibitor, Kazal type 1 gene, PSTI gene, Pancreatic secretory trypsin inhibitor gene) is a gene that encodes a pancreatic trypsin inhibitor. Mutations of this gene are associated with hereditary pancreatitis.
Calcineurin is a phosphatase that activates the nuclear factor of activated T cell (NFAT) by dephosphorylating its serine and threonine residues. Activation of NFAT induces the transcription of IL-2, which, in turn, activates NK cells and T cells. Immunosuppressants such as pimecrolimus, tacrolimus, and cyclosporine inhibit calcineurin and thereby prevent dephosphorylation of serine on NFAT.
