3/17 UWorld - GI, Endocrine, Repro, ID, NS, Renal Flashcards
Toxic shock syndrome (TSS) -Presentation -Causes -Mechanism
Fever, vomiting, diarrhea, muscle pains, and erythroderma (diffuse macular rash resembling sunburn). Can rapidly progress to severe hypotension and multisystem dysfunction Causes: -Toxic shock syndrome toxin (TSST) of Staph Aureus -(Exotoxin A of Strep Pyogenes causes Toxic-Shock-like syndrome) Mechanism: Binds to MHC II and TCR outside of antigen binding site to cause overwhelming release of IL-1, IL-2, IFN-gamma, and TNF-alpha
RNA transcription -Enhancers -Promoters -Start codon
Enhancer sequences - bind activator proteins that facilitate bending of DNA which allows interaction with transcription factors; may be located upstream or downstream from gene being transcribed Promotors (act as binding sites for transcription factors and RNA pol II) -CAAT - highly conserved (consensus sequence); usually located 70-80 bases upstream from transcription start site -TATA box - usually located 25 bases upstream from start site
Blood supply to the GI tract: Name structures provided blood supply via: -Celiac: -Superior mesenteric -Inferior mesenteric -Internal iliac
Celiac trunk: Branches include: -Common hepatic (proper hepatic, R gastric, gastroduodenal) -Splenic -L gastric Provides to foregut structures from lower esophagus, stomach, proximal duodenum, liver, gallbladder, pancreas, spleen Superior mesenteric artery: Supplies the midgut (distal duodenum to proximal 2/3 of transverse colon) Inferior mesenteric artery: Supplies the hindgut (distal 1/3 of transverse colon, descending colon, sigmoid colon, superior rectum) Internal iliac artery: Branches: -Middle rectal -Internal pudendal (inferior rectal) Supplies middle and lower rectum an external genitalia
Somatic symptom disorder
Excessive anxiety and preoccupation with >1 unexplained symptoms
Illness anxiety disorder
Fear of having a serious illness despite few or no symptoms and consistently negative evaluations
Conversion disorder (functional neurologic symptom disorder)
Neurologic symptom incompatible with any known neurologic disease; often acute onset associated with stress
Factitious disorder
Intentional falsification or inducement of symptoms with goal to assume sick role - primary (internal) gain (Munchausen syndrome)
Malingering
Falsification or exaggeration of symptoms to obtain external incentives (secondary gain)
Urease test
Gastric biopsy placed into urea-containing solution containing a pH indicator. If H. Pylori is present, it contains urease which will convert urea to CO2 and ammonia (basic) - causing pH to increase and solution to turn pink
Steps of glucose-mediated insulin release
Glucose enters the cell via GLUT-2 –> glucose is metabolized by GLUCOKINASE to glucose-6-phosphate –> G6P is metabolized by glycolysis and Krebs cycle to produce ATP –> increased ATP causes closure of ATP-sensitive potassium channels –> depolarization of cell lead to opening of voltage-gated Ca2+ channels –> high intracellular calcium leads to insulin release
Visual deficits caused by damage to:
- Part of retina
- Optic nerve
- Optic chiasm
- Optic tract
- Meyer’s loop (near the temporal lobe)
- Dorsal optic radiation
- Entire optic radiation (aka geniculocalcarine tract)
Klinefelter Syndrome
47, XXY Most common cause of hypogonadism Due to progressive destruction and hyalinization of the seminiferous tubules (small firm testes) Sertoli and Leydig dysfunction leads to low Testosterone and low Inhibin Lack of negative feedback leads to elevated LH and FSH High estrogen (due to increased LH) and gynecomastia caused by increased aromatase activity stimulated by gonadotropin excess
