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CHRONIC WOUNDS PRESSURE ULCERS
DIABETIC FOOT ULCERS AND VENOUS STASIS
ULCERS TEST BANK ELITE REVIEW WITH 100%
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◉Enteric nervous system (ENS). Answer: Neural control of the gastrointestinal tract. ◉Gastrin. Answer: A hormone that stimulates gastric acid secretion. ◉CCK (Cholecystokinin). Answer: A hormone that stimulates digestion of fats and proteins. ◉Secretin. Answer: A hormone that regulates water homeostasis and digestive processes. ◉GIP (Gastric Inhibitory Peptide). Answer: A hormone that inhibits gastric motility and secretion. ◉Gastroesophageal Reflux Disease (GERD). Answer: A condition caused by lower esophageal sphincter dysfunction and increased gastric pressure.
◉Barrett's esophagus. Answer: A complication of GERD that increases the risk of esophageal adenocarcinoma. ◉Peptic Ulcer Disease. Answer: A condition primarily caused by H. pylori infection, NSAIDs, or Zollinger-Ellison syndrome. ◉H. pylori mechanism. Answer: Urease production leading to ammonia and mucosal damage. ◉Crohn's Disease. Answer: An inflammatory bowel disease characterized by transmural inflammation and skip lesions. ◉Ulcerative Colitis. Answer: An inflammatory bowel disease characterized by mucosal/submucosal inflammation and continuous lesions. ◉Irritable Bowel Syndrome (IBS). Answer: A functional gastrointestinal disorder with altered gut-brain axis and visceral hypersensitivity. ◉Rome IV criteria. Answer: Recurrent abdominal pain occurring at least 1 day per week for 3 months.
◉MELD score. Answer: A scoring system that predicts 3-month mortality in patients with liver disease. ◉Cholelithiasis/Cholecystitis. Answer: Risk factors: 4 F's (Female, Fat, Forty, Fertile) ◉Pancreatitis. Answer: Acute causes: Gallstones (40%), alcohol (30%), medications, trauma ◉Developmental considerations. Answer: GI system maturation continues after birth ◉Congenital anomalies. Answer: Structural defects requiring surgical intervention ◉Pediatric-specific disorders. Answer: Different presentations than adult diseases ◉GI tract development. Answer: Foregut, midgut, hindgut derivatives ◉Functional immaturity. Answer: Reduced gastric acid, immature liver enzymes
◉Intestinal microbiome. Answer: Establishment in first years of life ◉Cleft Lip and Palate. Answer: Incidence: 1 in 700 births ◉Esophageal Atresia/Tracheoesophageal Fistula. Answer: Types: EA with distal TEF most common (85%) ◉Pyloric Stenosis. Answer: Demographics: Males 4:1, firstborn, 2- 8 weeks old ◉Hirschsprung Disease. Answer: Pathophysiology: Absence of ganglion cells in bowel wall → functional obstruction ◉Necrotizing Enterocolitis (NEC). Answer: Risk factors: Prematurity, formula feeding, hypoxia, infection ◉Intussusception. Answer: Peak age: 6 months - 2 years ◉Gastroenteritis. Answer: Viral causes: Rotavirus, norovirus, adenovirus ◉Nephron components. Answer: Glomerulus, tubules, collecting duct
◉Prerenal AKI Lab findings. Answer: BUN:Cr ratio >20:1, low FENa (<1%), concentrated urine ◉Prerenal AKI Reversal. Answer: Often reversible with correction of underlying cause ◉Intrinsic AKI Acute Tubular Necrosis (ATN). Answer: Most common intrinsic cause ◉Intrinsic AKI Causes. Answer: Ischemia, nephrotoxins (aminoglycosides, contrast, NSAIDs) ◉Intrinsic AKI Pathophysiology. Answer: Tubular cell death → tubular obstruction, backleak ◉Intrinsic AKI Recovery phases. Answer: Initiation, maintenance, recovery ◉Postrenal AKI Causes. Answer: BPH, stones, tumors, strictures ◉Postrenal AKI Pathophysiology. Answer: Obstruction → increased intratubular pressure → decreased GFR
◉Postrenal AKI Diagnosis. Answer: Hydronephrosis on imaging ◉Chronic Kidney Disease Staging Stage 1. Answer: GFR ≥90 with kidney damage ◉Chronic Kidney Disease Staging Stage 2. Answer: GFR 60-89 with kidney damage ◉Chronic Kidney Disease Staging Stage 3a. Answer: GFR 45- 59 ◉Chronic Kidney Disease Staging Stage 3b. Answer: GFR 30- 44 ◉Chronic Kidney Disease Staging Stage 4. Answer: GFR 15- 29 ◉Chronic Kidney Disease Staging Stage 5. Answer: GFR <15 or on dialysis ◉Chronic Kidney Disease Common Causes. Answer: Diabetes mellitus, Hypertension, Glomerulonephritis, Polycystic kidney disease ◉Chronic Kidney Disease Complications. Answer: Cardiovascular, Bone disease, Anemia, Metabolic acidosis
◉Specific Glomerulonephritides IgA nephropathy. Answer: Most common worldwide, Henoch-Schönlein purpura variant ◉Specific Glomerulonephritides Rapidly progressive GN. Answer: Crescents on biopsy, ANCA-associated ◉Cystitis Pathogens. Answer: E. coli (80%), Staphylococcus saprophyticus, Klebsiella ◉Cystitis Risk factors. Answer: Female gender, sexual activity, pregnancy, DM ◉Cystitis Clinical presentation. Answer: Dysuria, frequency, urgency, suprapubic pain ◉Cystitis Diagnosis. Answer: Urinalysis showing pyuria, bacteriuria; urine culture ◉Pyelonephritis Pathogenesis. Answer: Ascending infection from lower urinary tract ◉Pyelonephritis Clinical presentation. Answer: Fever, flank pain, CVA tenderness, systemic symptoms
◉Pyelonephritis Complications. Answer: Renal scarring, abscess formation, sepsis ◉Pyelonephritis Treatment. Answer: Longer antibiotic course than cystitis ◉Embryology. Answer: Pronephros → mesonephros → metanephros ◉Nephron development. Answer: Continues until 36 weeks gestation ◉Functional maturation. Answer: GFR reaches adult levels by 2 years ◉Concentrating ability. Answer: Limited in infants, mature by 1 year ◉Polycystic Kidney Disease. Answer: Autosomal Recessive (ARPKD): Presents in infancy/childhood ◉Posterior Urethral Valves. Answer: Most common obstructive uropathy in boys ◉Vesicoureteral Reflux (VUR). Answer: Primary: Congenital short intravesical ureter
◉BPH Pathophysiology. Answer: DHT-stimulated growth of stromal and epithelial cells ◉BPH Zones affected. Answer: Transition zone enlargement → urethral compression ◉BPH Clinical presentation. Answer: LUTS (frequency, urgency, weak stream, incomplete emptying) ◉BPH Complications. Answer: Acute urinary retention, UTIs, bladder stones, hydronephrosis ◉Prostate Cancer Epidemiology. Answer: Most common cancer in men, second leading cause of cancer death ◉Prostate Cancer Risk factors. Answer: Age, race (African American), family history, diet ◉Prostate Cancer Pathophysiology. Answer: Androgen-dependent growth, usually adenocarcinoma ◉Prostate Cancer Location. Answer: Peripheral zone (70%), transition zone (20%)
◉Prostate Cancer Screening. Answer: PSA + DRE controversy, individualized approach ◉Prostate Cancer Gleason score. Answer: Histologic grading system (2-10) ◉Erectile Dysfunction (ED) Prevalence. Answer: Increases with age, affects 52% of men 40-70 years ◉ED Pathophysiology. Answer: Vascular, neurogenic, hormonal, psychogenic causes ◉ED Normal mechanism. Answer: NO → cGMP → smooth muscle relaxation → increased blood flow ◉ED Risk factors. Answer: DM, HTN, CVD, smoking, medications ◉ED Treatment. Answer: PDE5 inhibitors, penile injections, vacuum devices, implants ◉Cryptorchidism. Answer: Undescended testis, increased cancer risk ◉Testicular torsion. Answer: Urologic emergency, 'bell clapper' deformity
◉PID Clinical presentation. Answer: Pelvic pain, fever, cervical motion tenderness ◉PID Complications. Answer: Infertility, ectopic pregnancy, chronic pelvic pain ◉Fitz-Hugh-Curtis syndrome. Answer: Perihepatitis with RUQ pain ◉Endometriosis Definition. Answer: Endometrial tissue outside uterine cavity ◉Endometriosis Locations. Answer: Ovaries, uterosacral ligaments, rectovesical pouch ◉Endometriosis Pathophysiology. Answer: Retrograde menstruation, coelomic metaplasia, lymphatic spread theories ◉Endometriosis Clinical presentation. Answer: Cyclic pelvic pain, dysmenorrhea, dyspareunia, infertility ◉Endometriosis Diagnosis. Answer: Laparoscopy with biopsy (gold standard)
◉Leiomyomas (fibroids). Answer: Benign smooth muscle tumors, estrogen-dependent ◉Endometrial hyperplasia. Answer: Unopposed estrogen → atypical hyperplasia → carcinoma risk ◉Endometrial cancer. Answer: Most common gynecologic malignancy, postmenopausal bleeding ◉Functional cysts. Answer: Follicular, corpus luteum, theca-lutein ◉Ovarian torsion. Answer: Surgical emergency, ovarian necrosis risk ◉Ovarian cancer. Answer: 'Silent killer,' often advanced at diagnosis ◉BRCA mutations. Answer: Increased ovarian and breast cancer risk ◉Fibrocystic changes. Answer: Benign, cyclic pain and tenderness ◉Fibroadenoma. Answer: Most common benign breast tumor in young women ◉Breast cancer. Answer: Second most common cancer in women
◉Chlamydia trachomatis - Complications. Answer: PID, infertility, ectopic pregnancy, reactive arthritis. ◉Chlamydia trachomatis - Neonatal. Answer: Conjunctivitis, pneumonia. ◉Chlamydia trachomatis - Treatment. Answer: Azithromycin or doxycycline. ◉Neisseria gonorrhoeae - Clinical presentation. Answer: Urethritis, cervicitis, PID, disseminated infection. ◉Neisseria gonorrhoeae - Complications. Answer: Infertility, Fitz- Hugh-Curtis syndrome, arthritis. ◉Neisseria gonorrhoeae - Neonatal. Answer: Ophthalmia neonatorum (preventable with prophylaxis). ◉Neisseria gonorrhoeae - Antibiotic resistance. Answer: Increasing resistance, dual therapy recommended. ◉Neisseria gonorrhoeae - Treatment. Answer: Ceftriaxone + azithromycin.
◉Treponema pallidum (Syphilis) - Stages. Answer: Primary (chancre), secondary (rash, lymphadenopathy), latent, tertiary. ◉Treponema pallidum (Syphilis) - Primary. Answer: Painless ulcer, highly infectious. ◉Treponema pallidum (Syphilis) - Secondary. Answer: 'Great imitator,' mucous patches, condylomata lata. ◉Treponema pallidum (Syphilis) - Tertiary. Answer: Cardiovascular, neurosyphilis, gummas. ◉Treponema pallidum (Syphilis) - Congenital. Answer: Hutchinson's teeth, saber shins, saddle nose. ◉Treponema pallidum (Syphilis) - Diagnosis. Answer: Darkfield microscopy, serologic tests (RPR, VDRL, FTA-ABS). ◉Herpes Simplex Virus (HSV) - Types. Answer: HSV-1 (traditionally oral), HSV-2 (traditionally genital). ◉Herpes Simplex Virus (HSV) - Pathophysiology. Answer: Latency in dorsal root ganglia, reactivation.
