Free NPLEX Part I Exam Flashcards

The left anterior descending artery supplies the anterior two-thirds of the interventricular septum through septal branches. Occlusion can therefore impair conduction pathways running in that region.

Stroke volume and cardiac output initially fall because the ventricle must eject against greater pressure. Compensation may increase end-systolic volume and, over time, promote hypertrophy.

Impaired left ventricular ejection raises left atrial and pulmonary venous hydrostatic pressure. Fluid then moves from pulmonary capillaries into the interstitium and alveoli.

Plaque disruption exposes thrombogenic material, activating platelets and coagulation. A superimposed coronary thrombus can abruptly reduce blood flow enough to cause ischemic myocyte necrosis.

A dissection is blood tracking through a tear into the aortic media and separating wall layers. An aneurysm is a localized abnormal dilation involving the vessel wall, although either condition may coexist with the other.

Friable vegetations composed of organisms, platelets, and fibrin can detach from left-sided valves and travel through systemic arteries, causing infarction or seeded infection in distant organs.

Hypothalamic TRH stimulates pituitary TSH, which stimulates thyroid hormone production. Circulating T3 and T4 suppress both TRH and TSH release, stabilizing hormone output.

Metabolic alkalosis is promoted because aldosterone increases distal sodium reabsorption while enhancing potassium and hydrogen ion secretion. Hypertension and hypokalemia commonly accompany it.

Absolute insulin deficiency and excess counter-regulatory hormones accelerate lipolysis. The liver converts released fatty acids to acidic ketone bodies, while hyperglycemia drives osmotic diuresis and dehydration.

Cortisol is low and ACTH is high because the adrenal cortex cannot respond to pituitary stimulation. Loss of aldosterone may also cause hyponatremia, hyperkalemia, and volume depletion.

The primitive gut tube divides into foregut, midgut, and hindgut domains. Their major arterial supplies are the celiac trunk, superior mesenteric artery, and inferior mesenteric artery, respectively.

Duodenal S cells release secretin in response to acid. Secretin stimulates pancreatic duct cells to secrete bicarbonate-rich fluid that helps neutralize the duodenal contents.

The terminal ileum absorbs the intrinsic factor–B12 complex and reclaims bile salts. Damage can therefore cause B12 deficiency and reduce the bile salt pool, contributing to fat malabsorption.

Elevated portal pressure diverts blood through portosystemic collateral veins. Dilation of submucosal veins at the lower esophagus creates fragile varices that can rupture and bleed.

In genetically susceptible people, gluten-derived peptides trigger a T-cell-mediated immune response in small-intestinal mucosa. The resulting inflammation damages villi and reduces absorptive surface area.

Hepatocyte injury disrupts bilirubin uptake, conjugation, and excretion. Conjugated and unconjugated bilirubin can accumulate in blood, producing yellow discoloration of skin and sclerae.

Reduced renal tissue oxygenation stabilizes hypoxia-inducible factors in renal interstitial cells, increasing erythropoietin production and stimulating erythroid progenitors in bone marrow.

B12 deficiency impairs DNA synthesis through the folate cycle. Nuclear maturation lags behind cytoplasmic growth, producing enlarged erythroid precursors and macrocytic red cells.

Factor VIII deficiency impairs the intrinsic coagulation pathway, so activated partial thromboplastin time is prolonged. Prothrombin time and platelet count are typically normal.

B lymphocytes differentiate into plasma cells. With T-cell help, activated B cells may also undergo class switching, affinity maturation, and memory-cell formation.

MHC I on nearly all nucleated cells presents endogenous peptides to CD8 T cells. MHC II on professional antigen-presenting cells presents exogenous peptides to CD4 T cells.

C3b covalently coats microbial surfaces and acts as an opsonin, making pathogens easier for complement-receptor-bearing phagocytes to ingest. It also helps amplify complement activation.

Type I hypersensitivity. Allergen cross-linking of IgE bound to mast cells triggers rapid mediator release, leading to vasodilation, vascular leak, bronchoconstriction, and other systemic effects.

The stratum basale. Its keratinocytes divide and move outward through the epidermal layers as they differentiate and eventually form the protective stratum corneum.

Loss of the skin barrier and inflammatory increases in vascular permeability allow plasma-rich fluid to leave the circulation. Evaporative water loss also rises, promoting hypovolemia.

Pemphigus targets desmosomal proteins between keratinocytes, producing intraepidermal separation. Bullous pemphigoid targets hemidesmosomal proteins at the basement membrane, producing subepidermal blisters.

Opposing articular surfaces are separated by a fluid-filled joint cavity, covered by hyaline cartilage, and enclosed by a capsule lined with synovium. This arrangement minimizes friction while permitting motion.

Calcium binds troponin C, shifting the troponin-tropomyosin complex away from actin's myosin-binding sites. Cross-bridge cycling can then proceed while calcium and ATP are available.

Reduced vitamin D activity lowers intestinal calcium and phosphate absorption. Inadequate mineral availability prevents normal deposition of hydroxyapatite in osteoid, causing rickets in children or osteomalacia in adults.

Rheumatoid arthritis is a systemic autoimmune synovitis that can erode cartilage and bone. Osteoarthritis is dominated by degeneration and remodeling of articular cartilage and subchondral bone.

Infection and inflammation can compromise local blood supply, creating a necrotic sequestrum. Reactive periosteal bone may form around it as an involucrum.

Selective membrane permeability, especially potassium leak conductance, combines with ion gradients maintained by the sodium-potassium ATPase. The inside remains electrically negative relative to the outside.

Myelin normally raises membrane resistance and lowers capacitance, enabling saltatory conduction between nodes of Ranvier. Its loss increases current leakage and can slow or block propagation.

The dorsal column–medial lemniscus pathway. Primary fibers ascend ipsilaterally in the spinal cord, synapse in the medulla, cross, and then ascend to the thalamus.

Loss of oxygen and glucose depletes ATP, causing ion-pump failure, depolarization, excitotoxic calcium entry, cellular swelling, and ultimately irreversible neuronal injury.

Reduced dopamine alters basal ganglia direct and indirect pathway activity, decreasing thalamic drive to motor cortex. The result includes bradykinesia and rigidity.

Pulmonary surfactant from type II pneumocytes lowers surface tension, especially as alveoli shrink. This increases compliance and reduces the tendency toward atelectasis.

Alveolar carbon dioxide removal falls, so arterial carbon dioxide rises. Carbonic acid formation increases and pH falls, producing respiratory acidosis unless renal compensation develops.

Variable, usually reversible airflow obstruction results from bronchial smooth-muscle constriction, airway inflammation, and mucus production. Increased resistance is most evident during expiration.

The embolus blocks perfusion to ventilated alveoli, creating high ventilation-perfusion regions and increasing physiologic dead space. Redistribution and associated low-V/Q areas can lower arterial oxygenation.

The paired paramesonephric, or Müllerian, ducts form the uterine tubes, uterus, cervix, and upper portion of the vagina. Their fusion creates the uterine primordium.

A midcycle luteinizing hormone surge triggers follicular rupture and oocyte release. Sustained high estradiol from the dominant follicle switches to positive feedback that produces the surge.

Testosterone supports Wolffian duct differentiation, while its metabolite dihydrotestosterone drives development of external genitalia and prostate. Defects at different steps therefore produce different patterns.

Viral oncoproteins disrupt tumor suppressor pathways: E6 promotes loss of p53 function and E7 inactivates retinoblastoma protein. Persistent dysregulated cell cycling can progress to neoplasia.

Pathogens ascend from the lower genital tract into the endometrium and fallopian tubes, provoking inflammation. Healing can scar the tubes, increasing infertility and ectopic-pregnancy risk.

The proximal tubule reabsorbs most filtered sodium and water, along with nearly all filtered glucose and amino acids under normal conditions. Water follows solute, keeping tubular fluid roughly iso-osmotic.

ADH binds V2 receptors on collecting-duct principal cells, increasing apical aquaporin-2 channels. Water then moves into the hypertonic medullary interstitium, lowering urine volume and raising its osmolality.

Renal tubules increase hydrogen ion secretion and generate or reclaim more bicarbonate. This raises plasma bicarbonate and partially restores pH while elevated carbon dioxide persists.

Inflammatory damage disrupts the glomerular capillary barrier, allowing red cells into urine. Swelling and capillary injury reduce glomerular filtration, which may cause oliguria and azotemia.

Organisms colonize the lower urinary tract and ascend through the ureter to the renal pelvis and parenchyma. Vesicoureteral reflux or urinary obstruction increases the risk of pyelonephritis.