Mehl. Ulcers some info from IM PDF tables Flashcards
Helicobacter pylori = Dx? 2
Urease breath test or stool antigen.
Treat H. pylori with CAP = ? 3
clarithromycin, amoxicillin, PPI (e.g., omeprazole).
H. pylori mechanism?
“secretes proteinaceous substrates that damage mucosal lining” !!!!!
event bacteria incr. gastrin => incr. gastric acid. Still choose the first one.
!!!!! H. Pylori. Antral/pyloric ulcers can lead to …….. What CP mentioned in surg?
Gastric outlet obstruction.
They will mention this in a Surg Q as a “succussion splash.”
H pylori incr. risk for what?
MALT lymphoma, a type of B-cell lymphoma.
H pylori. If suspected perofration => Mx?
DO ABDOMINAL XRAY
Nsaids - gastric ulcers. 2 Tx???
PPIs are first-line for ulcer treatment in general, but that misoprostol is a PGE1 analogue that is used in NSAID-induced ulcers
Vignettes can be tricky with gastrinoma and tell you the patient has 8-10 watery stools daily, where you say, “That sounds like VIPoma.” But they’ll also tell you the patient has history of abdo pain after meals. Q on IM form 8 does this as example.
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gastrinoma = Zollinger-Ellison syndrome causes recurrent duodenal ulcers and sometimes jejunal or ileal ulcers.
Pernicious anemia = Autoimmune antibody-mediated destruction of parietal cells. CP?
Ultra-HY cause of B12 deficiency ( MCV + hypersegmented neutrophils +/- neuropathy) on USMLE.
Chronic gastritis will be an atrophy or autoimmune destruction of the mucosa associated with decr. mucosal thickness, decr. HCl production (achlorhydria), incr. gastrin production, and enterchromaffin-like cell hyperplasia (histamine production to compensate for decr. acid). NBME will give you this constellation of findings and then just simply have “chronic gastritis” as the answer, with acute gastritis not even listed. It’s not hard, but I’ve seen students miss this a lot.
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Acanthosis nigricans can be associated with gastric cancer (even though most of the time, it just means insulin resistance).
Virchow node (Troisier sign) -> palpable supraclavicular lymph node that can reflect visceral malignancy, especially gastric cancer.
Gastric cancer spread to ovaries.
Glucagonoma will present as ?
Incr. serum glucose and a body rash called necrolytic migratory erythema.
Don’t confuse with the facial flushing seen with VIPoma; in addition, VIPoma doesn’t glucose levels.
Essentially, patients with diabetes, or chronic pancreatitis, or pancreatectomy and not just prone to losing the b-islet cells, but they can also lose the a-cells.
Patients who receive insulin for diabetes can sometimes have prolonged or exaggerated hypoglycemic effects. If this occurs, an answer for why this occurs on USMLE is “lack of counter-regulatory glucagon.” Sounds weird, but it shows up more than once on NBMEs
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Somatostatinoma (delta cells) presents as?
Steatorrhea; decr. secretion of most GI hormones, as well as growth hormone.
If patient has high insulin but low C-peptide, answer =?
exogenous injection.
If C-peptide is normal/high, insulin production is = ?
endogenous
Insulinoma.
First step is checking serum hypoglycemic levels (“serum hypoglycemic” = type II diabetes med that ̄ glucose, such as sulfonylureas and meglitinides).
If serum hypoglycemics are negative, then do CT of abdomen to check for insulinoma.
insulinoma CP?
Whipple triad:
1) hypoglycemia;
2) symptoms of hypoglycemia (tachycardia, tremulousness);
3) improves with a meal / gets worse between meals.
Hyperinsulinemia causes anovulation / polycystic ovarian syndrome (see my Repro PDF).
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Ghrelin (produced by GI cells) = makes you hungry. blood levels are highest when?
Blood levels are highest just at the start of the meal.
USMLE will show you a graph of ghrelin levels, and they ask where on the graph corresponds to the start of a meal, and the answer is at the peak. Not complicated. But I’ve seen innumerable students get this wrong.
Leptin = makes you feel fulls (produced by adipocytes). Low in what condition?
Leptin is low. in those with low BMI/anorexia –> GnRH –> low. LH and FSH -> amenorrhea.
Autoimmune hepatitis = what antibodies?
Young adult with LFTs who has (+) anti-smooth muscle antibodies.
Celiac tx = gluten free diet
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Lactose intolerance can be secondary to viral gastroenteritis.!!!!
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Lactase intolerance Tx? 2
lactose-containing products, or with lactase pills.
Milk protein allergy highest risk factor?
Not being exclusively breastfed for the first 6 months of life.
Milk protein allergy CP?
Will present as blood in the stool in a child who they say is, e.g., 4 months old, who was started on formula 3 weeks ago.
Milk protein allergy Tx?
Treatment is switching to hydrolyzed casein formula.
Switching to soy-based formula is wrong fucking answer. There is up to 50% crossover of allergy cases with kids who have milk- and soy-protein allergy.
Milk protein allergy.
Vignette can say kid was started on either a cow-milk or soy formula when symptoms started. It doesn’t matter. Just choose hydrolyzed casein as answer.
For statins = myopathy is more common than toxic hepatitis (on NBME).
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Diabetes GI. diabetes + diarrhea = what nerve?
hypogastric nerves are fucked up.
Sympathetic nerves are “anti-peristalsis,” so if we knock them out, we get too much peristalsis.
Diabetes GI. diabetes + Constipation = what nerve?
pelvic splanchnic nerves are fucked up.
parasympathetic nerves are pro-peristalsis, so if we knock them out we get unopposed hypogastric.
Iron and Aluminum cause what? also calcium
Verapamil causes?
constipation
Magnesium cause what?
diarrhea
Macrolides, orlistat, and a-glucosidase inhibitors (e.g., acarbose) cause what?
diarrhea.
“bronze diabetes” Dx?
Hemochromatosis
Hyperpigmentation due to hemosiderin deposition in skin + fasting sugars (iron deposition in tail of pancreas).
Miscellaneous other findings can be seen like infertility (iron deposition in hypothalamus, anterior pituitary, or gonads), cardiomyopathy, or arthritis (pseudogout).
3 most important causes of pseudogout?
Hereditary hemochromatosis, primary hyperparathyroidism, and hypothyroidism
Tx of hereditary hemochromatosis?
Treat with serial phlebotomy, not chelators.
Tx of SECONDARY hemochromatosis?
Chelators such as deferoxamine or deferasirox
Wilson = Copper levels, CP?
incr. urinary copper + decr. serum ceruloplasmin.
CP = Keiser-Fleischer rings (“slit-lamp exam.”); incr. LFTs with cirrhosis and Parkinsonism.
Wilson. Copper deposits where?
In basal ganglia, especially the putamen.
Parkinsonism in a young patient = Wilson until proven otherwise.
Wilson Tx?
Treat with the copper chelator penicillamine.
Patient with cardiovascular disease (CVD) + blood in the stool. Dx?
Ischemic colitis
Caused by bleeding at ischemic ulcers at watershed areas in the colon (i.e., splenic flexure and rectosigmoid junction).
Ischemic colitis = Can occur randomly or due to inciting event like recent AAA surgery.
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Ischemic colitis = Dx?
Diagnose with colonoscopy to visualize the ischemic ulcers.
“Inflammatory mass and fecalith in the cecum” is phrase used on 2CK NBME form to describe appendicitis.
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USMLE wants you to know appendicitis pain can be RUQ in pregnancy due to displacement of bowel and a shift in appendiceal location. What they will do is tell you pregnant woman in 3rd trimester has RUQ pain, fever, and vomiting + negative abdo ultrasound (meaning not cholecystitis)àanswer = “appendicitis.”
A 2CK NBME Q gives 9 packs of RBCs given during surgery -> days later, total bilirubin is 5.0 and direct bilirubin 2.3. answer =?
“overproduction of bilirubin.
In the setting of hemolysis or incr. RBC turnover (i.e., sickle cell, hereditary spherocytosis, blood given during surgery), where we have incr. RBC breakdown, we get incr. indirect bilirubin
Unconjugated jaundice can occur in neonates because of incr. RBC turnover where HbF is replaced with HbA.
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If ALP is high but direct bilirubin not incr. this can be due to things like bone fractures or Paget disease.
GGT will also go up with bile duct obstruction, since it is also secreted by bile duct epithelium, but USMLE actually rarely mentions this one.
What they want you to know is GGT spikes with acute alcohol consumption / binge drinking.
In other words, “dark urine + pale stools” is buzzy for bile duct obstruction the same way “ incr. ALP and direct bilirubin” is.
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Highest yield cause of incr (2 arrows) direct bilirubin on USMLE is biliary atresia in neonates (discussed later).
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Acute hepatitis can also cause incr. direct bilirubin due to decr. secretion into bile, in addition to incr. indirect. But this makes sense, since it is literally an intra-hepatic pathology.
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Gilbert = Partial deficiency of bilirubin uptake enzyme at the liver (UDP glucuronosyltransferase). CP? Tx?
Presents as isolated indirect bilirubin with yellow eyes in young adult with stress factor, such as studying for exams, or recent surgery/trauma. The patient will otherwise be completely healthy.
Tx not necessary.
Crigler-Najjar = Near-absence of UDP-glucuronosyltransferase causing …. what?
very incr. indirect bilirubin in neonate.
,,nonexistent”. In neonates is important biliary atresia.
Dubin-Johnson = decr. excretion of bilirubin into bile at the liver due to decr. secretory pumps. CP?
Causes incr. direct bilirubin in otherwise healthy adult.
Can cause black liver in theory.
Asked once on new 2CK NBME. Apart from that, nonexistent on USMLE material
Rotor = Same as Dubin-Johnson but no black liver.
nonexistent on usmle.
