HY lecture notes:
Recurrent bouts of acute pancreatitis cause chronic pancreatitis –> pancreatic enzymes will usually be normal on the NBME/USMLE because of exocrine pancreas burn out – i.e., recurrent tissue damage leads to defective enzyme secretion. Patients need pancreatic enzyme replacement as the Tx.
Patients with chronic pancreatitis will present with steatorrhea because of decreased lipase secretion –> impaired fat absorption –> can also lead to fat-soluble vitamin deficiencies.
On one of the IM or Surg forms, they have “pancrelipase” as the answer.
44M + fasting glucose of 112 mg/dL + dark skin on forearms + arthritis; Dx? –> hereditary hemochromatosis –> AR, chromosome 6, HFE gene, C282Y or H63D missense mutations account for 90% –> “Bronze diabetes” –> hyperpigmentation (from hemosiderin deposition) + diabetes due to iron deposition in tail of pancreas (normal fasting glucose is 72-99 mg/dL; impaired fasting glucose [pre-diabetic] is 100-125 mg/dL; diabetic is two fasting glucoses 126 or greater, or a single HbA1c >6.5%, or any random glucose >200 mg/dL) + third finding such as arthritis, cardiomyopathy, or infertility.
44M + fasting glucose of 130 mg/dL + hands are sore + x-ray of hands shows DIP involvement; what’s the Dx for the type of arthritis? –> answer = pseudogout, not osteoarthritis. Student says wtf? The two most common etiologies for pseudogout are hemochromatosis and primary hyperparathyroidism (pseudogout is calcium pyrophosphate deposition disease, and will present as either a monoarthritis of a large joint such as the knee, or as an osteoarthritis-like presentation of the hands.
Tx of hereditary hemochromatosis –> serial phlebotomy, not chelation therapy.
44M patient above + USMLE asks what’s the mechanism for his disease –> answer = “increased intestinal absorption of iron.”
44M above + next best step in Dx? –> check serum ferritin (>300 ug/L in men + post-menopausal women; or >200 in premenopausal women; USMLE will always say >300 so don’t worry).
Why do men get hemochromatosis younger + with worse Sx than women? –> menstruation slows progression of disease.
What is secondary hemochromatosis? –> aka transfusional siderosis (amazing to remember if you want to sound sophisticated) –> due to chronic blood transfusions –> each transfusion of RBCs contains iron –> seen classically in beta-thalassemia major or any other patients receiving ongoing transfusions.
Tx for secondary hemochromatosis (transfusional siderosis) –> chelation therapy (e.g., deferoxamine), not serial phlebotomy.
Blind loop syndrome
Normally bacterial growth in small bowel is limited by peristalsis + normal flow of digestive contents. In the case of physical or peristaltic disruption, bacterial overgrowth in the small bowel may ensue, leading to diarrhea and malabsorption. Blind loop syndrome may be seen in the setting of surgery, strictures, fistulae, achlorhydria. Treatment is with doxycycline or rifaximin.
Dumping syndrome
In the setting of roux-en-y procedure (gastric bypass), hyperosmolar chyme from the stomach may enter the duodenum too quickly, leading to a spike in insulin secretion and hypoglycemia. This also can be accompanied by diarrhea. On the USMLE: gastric bypass Hx + hypoglycemia + diarrhea = Dumping syndrome.
Pseudomembranous colitis
For C. difficile, choose “ingestion of spores” as the etiology, not “bacterial overgrowth.” The latter refers to Blind loop syndrome.
Patient takes Abx for several days + has watery diarrhea; Dx? –> difficile (pseudomembranous colitis).
Patient takes Abx for several days + has crampy LLQ pain + bloody diarrhea; Dx? –> difficile à this is on a 2CK NBME –> Yersinia enterocolitica was also listed and was wrong; this is a good distractor because Y. enterocolitica causes pseudoappendicitis due to ileitis / mesenteric adenitis, but is RLQ pain, not LLQ.
Which Abx cause C. diff overgrowth? –> clindamycin, cephalosporins, ampicillin are highest yield.
Dx of C. difficile? –> answer = stool AB toxin test, not stool culture (exceedingly HY).
Tx of C. difficile? –> guidelines as of Feb 2018 say oral vancomycin first-line, not metronidazole –> apparently UW is updated on this too now –> note that vanc is given orally –> apart from C. diff, it’s always given IV because it has terrible oral bioavailability, but in the case of C. diff, where we want the drug confined to the lumen of the colon, that makes sense.
Mechanism of colonic necrosis in C. diff colonic necrosis? –> answer = “cytoskeletal disruption.”
Patient is treated with vanc for C. diff but gets recurrence weeks later; why? –> answer = “regermination of spores.”
C. diff + fever of 104F + tachy + diffuse abdominal pain; next best step in Mx? –> AXR –> look for toxic megacolon –> Tx w/ NPO (nothing by mouth), NG decompression + rectal tube (decompression) + Abx (vancomycin or fidaxomicin) + steroids (if UC) + correct any electrolyte imbalances (sometimes low K) –> if patient doesn’t improve with conservative therapy, must do surgery (subtotal colectomy + ileostomy); do not do a colonoscopy on a patient with toxic megacolon as this will cause perforation.
