Title: MD / Course 1

Q: what is the suffix for a(n):
immature cell: [...]
mature cell: [...] or [...]
A: -blast; -cyte; -phil

Q: when is EPO secreted?
[...]
A: in hypoxic conditions
Extra: EPO = erythropoietin

Q: what does high reticulocyte count indicate?
[...]
A: bleeding or hemolysis
Extra: normal circulating count = 1%
high retic counts = bleeding, hemolysis
low retic counts = marrow disorder

Q: what does low reticulocyte count indicate?
[...]
A: marrow disorder
Extra: normal circulating count = 1%
high retic counts = bleeding, hemolysis
low retic counts = marrow disorder

Q: what does elevated hematocrit % indicate?
[...]
A: polycythemia

Q: what does depressed hematocrit % indicate?
[...]
A: anemia

Q: what are the 2 major nutrient requirements of erythropoiesis?
[...]
A: vitamin B12 and folate
Extra: B12 from dietary intake and transported by IF to store in liver; enough storage for years
folate needed to make nucleotides for DNA and RNA synthesis; quickly depleted from body
other reqs: vit B6, C, E, riboflavin, niacin, pantothenic acid

Q: what %ge of total body iron is bound to hemoglobin?
[...]
A: 70% (i.e., a shitton)

Q: in what cmpd is iron stored in macrophages (mainly in liver)?
[...]
A: ferritin (ferritin = apoferritin + iron)

Q: where are RBCs recycled?
[...]
A: in spleen and liver
Extra: macrophage uptake and breakdown to heme, iron, and globin
iron oxidized to Fe^3+ (ferric), globin metabolized to aas, heme broken into bilirubin

Q: what do lymphoid progenitor cells differentiate into?
[...]
A: B, T, NK

Q: what do myeloid progenitor cells differentiate into?
[...]
A: all cells other than B, T, NK (e.g., neutrophils, basophils, monocytes, eosinophils)

Q: what is the normal count of leukocytes in the blood?
[...]
A: 5-10 billion / L
Extra: <1% of total blood volume
cells stain purple

Q: what is the purpose of granulocytes?
[...]
A: they help destroy pathogens w/ enzymes and vacuoles

Q: what is this cell?
[...]
A: neutrophil

Q: what is the fn of neutrophils?
[...]
A: engulf and destroy bacteria and debris (causes acute inflammation) thru phagocytosis

Q: what type of cell is this?
[...]
A: lymphocyte (B, T, plasma celll)

Q: what type of cell is this?
[...]
A: monocyte

Q: when do monocytes become macrophages?
[...]
A: when they move from blood into tissue

Q: what type of cell is this?
[...]
A: eosinophil

Q: what is the fn of eosinophils?
[...]
A: destruction of parasites and viruses

Q: when might you find a shitton of eosinophils?
[...]
A: during parasitic infections, allergic rxns, and asthma

Q: what type of cell is this?
[...]
A: basophil

Q: why should you be concerned when tons of basophils appear under microscope?
[...]
A: b/c increased presence is almost always pathologic

Q: which cell differentiates into megakaroblasts which turn into megakaryocytes (which forms platelets)?
[...]
A: myeloid stem cell

Q: what are the 2 most common leukocytes in a CBC?
[...]
A: neutrophil and lymphocyte (B, T, NK)

Q: ignoring Hb and hematocrit, what are the 2 major findings in this CBC?
[...]
A: macrocytic cells and pancytopenia

Q: what do the platelet and WBC counts indicate?
platelet: [...]
WBC: [...]
A: thrombocytosis (thrombocythemia); leukocytosis
Extra: RDW = red cell distn width
polycythemia = too many RBCs
thrombocytosis = too many platelets
leukocytosis = too many WBCs

Q: what is hematochezia?
[...]
A: red / maroon blood in stool

Q: what is hemoptysis?
[...]
A: expectoration of blood (i.e., vomiting)

Q: what are the 3 main signs that confirm melena?
[...]
A: blood (50-100 cc), bacteria, and time (8-14 hrs)

Q: when melena is observed, which organs do we suspect of bleeding?
[...]
A: esophagus, duodenum, stomach (all upper GI)

Q: where is the most common site of bleeding that causes melena?
[...]
A: location proximal to ligament of Treitz (band of mesentery tissue that seps duodenum from jejenum)

Q: why should we be concerned about hematochezia?
[...]
A: b/c red / maroon stools can be manifestation of massive UGIB
Extra: hematochezia is usually due to LGIB but better safe than sorry

Q: what are the 2 most common causes of acute hematemesis?
[...]
A: peptic ulcer disease (~55%) and portal hypertension (~15%)

Q: which 2 factors account for 99% of peptic ulcer disease?
[...]
A: H. pylori and NSAIDs

Q: what do the green arrows point to?
[...]
A: a Mallory-Weiss tear (UGIB)

Q: why does hr increase when you stand up after donating blood?
[...]
A: to maintain cardiac o/p with decreased blood volume
Extra: CO = HR x SV

Q: how to assess blood volume status thru vital signs?
[...]
A: heart rate and bp (lying & standing); >30 bpm increase helpful; decrease in >20 mmHg systolic or >10 mmHg diastolic helpful

Q: what is the clinical def of shock?
[...]
A: inadequate end-organ tissue perfusion

Q: what deficits in blood volume counts as mild / moderate / severe hypovolemia?
mild: [...]
moderate: [...]
severe: [...]
A: <15%; 20-40%; >40%

Q: what are the 4 main steps of pt mngmt w/ UGIB?
1. [...]
2. [...]
3. [...]
4. rescue therapy (as needed)
A: resuscitation (saline via 2 large bore IVs); pharmacotherapy (e.g., PPIs); endoscopy

Q: what is the goal in terms of pH of IV PPIs for UGIB?
[...]
A: increase pH > 6 (improves clotting)
Extra: after endoscopic therapy, re-bleeding chances decreases from ~25% TO ~6%

Q: what are the risks of gastroscopy?
[...]
A: sedation, aspiration, bleeding, perforation

Q: what is this?
[...]
A: ulcer (w/ blood vessel)
Extra: tx is to clip the blood vessel to prevent bleeding

Q: in which organ would you find these cells?
[...]
A: stomach
Extra: mucus cells for protection at top
glandular cells to produce stomach acid at bottom

Q: what is the fn diff btw parietal cells and chief cells?
[...]
A: parietal cells produce HCl and IF whereas chief cells secrete pepsin
Extra: IF = intrinsic factor
CC blue b/c they have a lot of ribosomes

Q: what do the most prevalent cells in this picture produce?
[...]
A: mucin
Extra: found in the large intestine

Q: what is being shown in this img?
[...]
A: esophagitis

Q: what can chronic GERD cause?
[...]
A: metaplasia where distal esophagus becomes covered by stratified squamous epithelium
Extra: GERD = gastroesophageal reflux disease

Q: what is metaplasia?
[...]
A: reversible change where one differentiated cell type is replaced by another

Q: what happens in Barrett esophagus?
[...]
A: squamous epithelium of distal esophagus replaced w/ intestinal-type colunar epithelium w/ goblet cells
Extra: goblet cells produce mucin

Q: why is AB plasma so valuable?
[...]
A: b/c they don't have any anti-A or anti-B abs (universal plasma donor)

Q: why do ppl sometimes not test Asians for Rh antigens?
[...]
A: b/c >99% of them are d (no D antigen)
Extra: caucasians ~15% d (no D antigen)

Q: why is pt plasma x donor RBC considered a major crossmatch?
[...]
A: b/c if incompatible, ALL donor cells will be destroyed (serious hemolytic rxn)

Q: why is donor plasma x pt RBC considered a minor crossmatch?
[...]
A: b/c if incompatible, donor plasma becomes diluted (less chance of hemolytic rxn)

Q: what does Coombs test do?
[...]
A: tests for presence of antibody (either bound to RBCs or free)

Q: what do we do if ab is unspecified for RBC transfusion?
[...]
A: donor units tested by serological cross match to find least incompatible blood
Extra: i.e., weakest rxn

Q: what is the most impt test for transfusion of RBC indicated?
[...]
A: type & screen
Extra: step 1. pt's blood group tested (typed) for ABO & Rh; serum tested for presence of anti-A or anti-B
step 2. pt's serum tested for allo & autoimmune abs against common minor blood group abs
type & screen then x-match

Q: what blood type to transfuse in stat transfusions?
[...]
A: O-

Q: how long can you store platelets for?
[...]
A: 5 days, no refrigeration
Extra: increased risk of sepsis as compared to other tx due to non-refrigerated storage (~1 in 10,000)

Q: when should you transfuse w/ platelets?
[...]
A: in cases w/ massive bleeding

Q: how long can you store frozen plasma?
[...]
A: up to 1 yr

Q: when should you not give frozen plasma?
[...]
A: when specific therapy is available OR hypovolemia w/o coagulation defect

Q: other than whole blood transfusions, what are the 3 most common blood products?
1. [...]
2. [...]
3. [...]
A: frozen plasma; platelets; cryoprecipitate

Q: what are some benefits of blood transfusions?
[...]
A: maintains O_2 carrying capacity; helps stop bleeding; alleviates sx of low blood cell counts

Q: what are risks of transfusions?
[...]
A: fever, dyspnea, cytopenia, infection
Extra: dyspnea = intense tightening in the chest, air hunger, difficulty breathing, breathlessness or a feeling of suffocation
'

Q: at what Hg lvl should we provide RBC transfusions to "typical" pts?
[...]
A: <70 g/L

Q: at what platelet count should we provide platelet transfusions to "typical" pts?
[...]
A: <10 billion/L

Q: what are the clinical presentations of transfusion rxns?
[...]
A: fever & chills, tachycardia, hypotension, dyspnea, nausea, vomiting, disseminated intravascular coagulation

Q: what to do immediately if there are problems w/ transfusion?
[...]
A: STOP it then monitor & evaluate

Q: what is the tx for FNHTR?
[...]
A: acetaminophen (Tylenol) 325-650 mg orally; meperidine (Demerol) for severe rigors
Extra: FNHTR = febrile non-hemolytic transfusion rxns
rigors are when temps rise extremely quickly

Q: what are the sx of TRALI?
[...]
A: hypoxia, bilateral pulmonary edema, no evidence of congestive heart failure, hypotension, fever
Extra: FNHTR = febrile non-hemolytic transfusion rxns
rigors are when temps rise extremely quickly

Q: how fast does TRALI present after start of transfusion?
[...]
A: ~2 hours; usually resolves in 24-72 hours
Extra: FNHTR = febrile non-hemolytic transfusion rxns
rigors are when temps rise extremely quickly

Q: what do TACO and TRALI stand for?
TACO: [...]
TRALI: [...]
A: transfusion-assoc circulatory overload; transfusion-related acute lung injury

what does SAMPLE stand for in hx?
1. S: signs and sx
2. A: allergies
3. M: medication (rx, herbal, complementary)
4. P: past hx (family, medical, social, surgical, sexual* - when indicated)
5. L: last oral intake / bowel / bladder
6. E: events proceeding
Extra: SAMPLE + demographic data, review of systems

Q: 70F lost 25 lbs after a month. Presents w/ coffee ground emesis and takes 3 ASA per day w/o relief. Hx of tobacco use and feels weak and tired when climbing stairs. What is likely ddx?
[...]
A: gastric cancer
Extra: other possibilities (less likely): gastric ulcer, duodenal ulcer

Q: 30M born in India has CC of black stool, lightheadnedness, and burning pain. He is single w/ no hx of smoking or drinking. He is hemodynamically unstable and has stomach pain. Father had ruptured ulcer. What is likely ddx?
[...]
A: DU or GU
Extra: DU = duodenal ulcer
GU = gastric ulcer
varices are also a possibility

Q: 50M presents w/ hematemesis, nausea, vomiting, and lightheadedness. He recently separated from his partner and drank 24 beers/day for the past 3 days. What is likely ddx?
[...]
A: Mallory-Weiss tear
Extra: varices and PUD are also possibilities

Q: what constitutes orthostatic hypotension?
[...]
A: fall of SBP of at least 20 mmHg or DBP of at least 10 mmHg w/in 3 min of standing

Q: what is orthostatic tachycardia?
[...]
A: >30 bpm increase w/in 3 min of standing
Extra: resting tachycardia = HR > 100 at rest

Q: how do H2 blockers reduce acid secretion?
[...]
A: by blocking histamine receptors (His activates adenylate cyclase which converts ATP to cAMP to protein kinase which activates the H+/K+ ATPase)

Q: how do PPIs reduce acid secretion?
[...]
A: by directly inhibiting proton pumps

Q: what is the fn of D cells when inhibited by ACh?
[...]
A: to secrete somatostatin which inhibits G cells that produce acid

Q: what are the 3 phases of gastric acid secretion?
1. [...]
2. [...]
3. [...]
A: cephalic phase (~30% of response to meal); gastric phase (50-60% of response to meal); intestinal phase (~5% of response to meal)

Q: what happens in the cephalic phase?
[...]
A: vagus nerve releases ACh on G cell to stimulate gastrin release (stim by smell, taste, chewing, swallowing, hypoglycemia)

Q: what is normal response to stomach pH < 3?
[...]
A: inhibition of acid secretion via D cells releasing somatostatin

Q: when can we dx gastrinoma using secretin stimulation test?
1. [...]
2. [...]
A: gastrin > 1000 pg/mL and increased HCl (pH < 2); gastrin >200 pg/mL following secretin incusion in setting of increased HCl

Q: when should secretin stimulation test NOT be ordered?
[...]
A: when gastrin already >1000 pg/mL OR no abnormal gastric acid secretion

Q: what is Zollinger-Ellison syndrome?
[...]
A: PUD with non-beta islet cell tumour of pancreas (gastrinoma)

Q: when to suspect ZE syndrome?
[...]
A: ages 20-50, diarrhea, ab pain, heatburn, weight loss

Q: how is H. pylori acquired?
[...]
A: water, oral-oral, fecal-oral

Q: what is normal MCV?
[...]
A: 80-100 fL
Extra: MCV = mean corpuscular volume

Q: what are the 3 common non-endoscopic tests for H. pylori?
[...]
A: serologic test, urea breath test, fecal antigen test

Q: what are PUD sx?
[...]
A: ab pain, nausea, bloating, pain aggravated by eating, melena, *asymptomatic*
Extra: ~70% of peptic ulcers are asymptomatic

Q: what are some complications of untx ulcer?
[...]
A: bleeding, obstruction, perforation
Extra: notice free air indicative of perforation

what are 4 major endoscopic therapies to tx PUD?
1. injection therapy (epi and/or saline)
2. thermal (cautery, argon plasma coagulation)
3. mechanical (hemoclips)
4. foam (hemospray)
Extra: endoscopic therapy reduces risk of re-bleeing and reduces mortality

Q: what are some common classes of anti-ulcer drugs?
[...]
A: antacids, H2RA, PPIs, ABx for H. pylori
Extra: H2RA = H2 receptor antagonists

Q: what are the most common cheap options for PPIs?
[...]
A: pantoprazole Mg (Tecta, 40 mg, $30 / 90 days) and omeprazole (Losec, 20 mg, $35 / 90 days)
Extra: all listed PPIs pretty much equivalent; choose based on pt tolerance and cost

Q: when are PPIs most effective?
[...]
A: when given 15-30 min before meals

Q: what are likely causative adverse effects of PPIs?
[...]
A: hypomagnesemia, vit B12 deficiency, small-intestine bacterial overgrowth

Q: what constitutes LT use of PPI?
[...]
A: >8 weeks

Q: what are NSAID side effects due to COX inhibition?
[...]
A: peptic ulcers, GI bleeding, hypertension, stroke, myocardial infarction

Q: what are the 3 ways NSAIDs induce bleeding thru COX-1?
1. [...]
2. [...]
3. [...]
A: reduced mucosal blood flow (impaired defense); reduced mucus & bicarbonate secretion (impaired defense); impaired platelet aggregation
Extra: COX-1 is cytoprotective; COX-2 mediates inflammation

Q: what are the 2 ways NSAIDs induce bleeding thru COX-2?
1. [...]
2. [...]
A: reduced angiogenesis (impaired healing); increased leukocyte adherence (leukocyte activation)
Extra: COX-1 = cytoprotective
COX-2 = inflammatory

Q: what are alternatives to NSAIDs for arthritis tx?
[...]
A: coxibs (COX-2 inhibitors)

Q: what is TAILS short for if MCV < 80?
[...]
A: thalassemia, anemia of chronic disease, iron deficiency, lead poisoning, sideroblastic anemia

Q: what conditions does MCV > 100 indicate?
[...]
A: vit B12 or folate deficiency, drugs, liver disease (w/ EtOH), hypothyroid
Extra: macrocytic
suspect folate if heavily drinking w/o much nutrition
vit B12 deficiency accompanied by neuropathy and elevated levels of methylmalonic acid (MMA)

Q: Supine vitals: bp 90/60 mmHg and hr 110 bpm. Upon standing for 1-2 min, bp 70/40 mmHg and hr 125 bpm and nearly faints. What is immediate tx?
[...]
A: double bore 16 or 18 gage IV (Ringer's lactate or saline)
Extra: orthostatic hypertension: -20/-10 mmHg satisfies conditions
this person is hemodynamically unstable and hypovolemic; showing signs of shock

Q: what are the 3 main investigations for esophageal disease?
1. [...]
2. [...]
3. [...]
A: endoscopy ± biopsy; barium esophagogram; esophageal manometry

Q: what do barium x-rays screen for in esophageal disease?
[...]
A: motor disorders (gross test for ulcer or blockage)

Q: what does esophageal manometry look for in esophageal disease?
[...]
A: checks peristaltic fn and UES and LES responses to swallowing

Q: what acid reflux test results constitutes as a reflux episode?
[...]
A: if pH < 4

what is VITAMIN D short for w/ tissue disease?
V = vascular
I = infectious/inflammatory
T = trauma/toxic
A = autoimmune
M = metabolic
I = inherited/idiopathic
N = neoplastic
D = drug

Q: what are some esophageal defense mechanisms?
[...]
A: salivation, motility, acid reflux, "healthy" bacteria

Q: what is this bacteria in the esophagus?
[...]
A: Candida albicans

Q: what is the clinical presentation for esophageal infections?
[...]
A: dysphagia, odynophagia, heartburn, nausea
Extra: may be accompanied by fever, sepsis, ab pain in immunosuppressed pts
odynophagia = painful swallowing

Q: what is dx?
[...]
A: eosinophilic esophagitis (EOE)

Q: what is tx for EoE?
[...]
A: PPI first line then swallowed topical steroids, dietary elim, or dilation
Extra: EoE = eosinophilic esophagitis

Q: what are typical sx of GERD?
[...]
A: heartburn and regurgitation
Extra: GERD = gastroesophageal reflux disease

Q: what are alarm sx of GERD?
[...]
A: vomiting, bleeding, weight loss, ab mass, dysphagia
Extra: MUST investigate all alarm sx!!!
GERD = gastroesophageal reflux disease

Q: what tests to investigate if pt has GERD?
[...]
A: pH monitor for 24-48 hr

Q: how to tx GERD?
diet: [...]
pharmcological: [...]
A: avoid caffeine, peppermint, citrus, alcohol; PPIs or antacids

Q: what causes achalasia?
[...]
A: selective loss of inhibitory innervation of esophageal myenteric plexus

Q: what are the 2 major tx for achalasia?
1. [...]
2. [...]
A: pneumatic dilation; surgical myotomy (preferred)
Extra: can also try botox for frail/elderly pts

Q: what are the 2 most common malignant esophageal neoplasms?
[...]
A: adenocarcinoma and squamous cell carcinoma

Q: what are risk factors for esophageal or gastric cancer?
[...]
A: chronic gastritis and gastric atrophy

Q: what are the 3 steps to investigate esophageal cancer?
1. [...]
2. [...]
3. [...]
A: endoscopy; CT or PET; endoscopic ultrasound (dets T and N stage)

Q: what does T and N mean for cancers?
T: [...]
N: [...]
A: primary tumour grading; regional node metastasis
Extra: M0 = no distant metastasis, M1 = mets
G: G1 = well differentiated, G4 = undifferentiated

Q: what is vomiting?
[...]
A: forceful expulsion of gastric content

Q: how to manage nausea and vomiting?
1. [...]
2. [...]
3. suppress sx
A: correct any complications (e.g., volume depletion, electrolytes); identify cause

Q: what is diff btw oropharyngeal and esophageal dysphagia?
oropharyngeal: [...]
esophageal: [...]
A: immediate difficulty (swallowing, choking, regurgitation); delayed difficulty (food sticks seconds later)

Q: 27F, nonsmoker, previously well presents to ER w/ food stuck in esophagus. He has occasional reflux sx and has sx of food blocking since his teens. What type of dysphagia is this and what is next step?
[...]
A: esophageal dysphagia - mechanical and endoscopy

Q: 74F w/ stroke complains of difficulty swallowing for ~6 months. She reports choking/coughing when eating. Is this oropharyngeal or esophageal dysphagia?
[...]
A: oropharyngeal

Q: what is tx for this bird's beak deformity?
[...]
A: laparoscopic Heller's myotomy OR pneumatic dilation
Extra: myotomy favoured
bird's beak indicates achalasia (progressive motor dysphagia of the esophagus)

Q: what is diff by trisomy and triploidy?
[...]
A: trisomy is triple copy of a single chromosome whereas polyploidy is triple copy of every chromosome

Q: what are the 3 major themes of precision health?
1. [...]
2. [...]
3. [...]
A: wellness and disease prevention; early dx and prognosis; targeted interventions

Q: what is the improvement to Sanger sequencing?
[...]
A: NGS (massively parallel)
Extra: NGS = next generation sequencing

Q: approx how many base changes does the human exome have?
[...]
A: ~30,000

Q: what is Peto's paradox?
[...]
A: how larger animals have lower lifetime risk of cancer than smaller animals

Q: which cells are primarily involved in innate immunity?
[...]
A: dendritic cells, neutrophils, macrophages, eosinophils
Extra: complement system also involved
NK cells considered innate but also involved in adaptive system

Q: what is fn of NK cells?
[...]
A: surveillance and killing

Q: what is the fn of the complement system?
[...]
A: punching holes into pathogens, opsonization, promiting inflammation

what are the 4 major sx of the inflammatory response?
1. redness (rubror)
2. swelling (tumour)
3. heat (calor)
4. pain (dolor)

Q: what happens in the white pulp of the spleen?
[...]
A: B and T cells hang out and encounter antigens, phagocytosis of bad stuff

Q: what happens in the red pulp of the spleen?
[...]
A: macrophages remove old and damaged RBCs, removal of foreign material

Q: why does the germinal centre of the lymph node enlarge during infection?
[...]
A: b/c B cells proliferate and differentiate

Q: what are the 2 main types of B cells?
[...]
A: plasma cells (make abs) and memory cells

Q: thru which ligand do B and T cells interact?
[...]
A: CD40

Q: what is the diff btw CD4+ and CD8+ T cells?
[...]
A: CD4+ are helper cells whereas CD8+ are cytotoxic cells

Q: which MHC do T cells present / detect?
CD4+: [...]
CD8+: [...]
A: MHC II; MHC I

Q: why are PAMPs so impt?
[...]
A: b/c they're only found on pathogens, NOT on self

after recognizing PAMPs thru PRRs, what does the innate immune response look like?
1. opsonization (complement sys)
2. phagocytosing pathogen
3. activating cytokines (inflamm)
4. inducing apoptosis of infected cell
Extra: OPCA = opsonization, phagocytosis, cytokines, apoptosis

Q: what mobilizes the neutrophil?
1. [...]
2. [...]
3. [...]
A: bacterial cell wall products; complement proteins; cytokines

Q: what are the killing mechanisms employed by neutrophils?
1. intracellular: [...]
2. extracellular: [...]
A: phagosome; ROS and NETs
Extra: NET = neutrophil extracellular traps

Q: what are indications of neutrophil adhesion deficiency?
1. [...]
2. [...]
A: lack of pus at sites of infection; very elevated neutrophil cnt w/ infection
Extra: normal neutrophil count: 3-5.8 billion /L (50-67% of leukocytes)

Q: what is the mechanism of neutrophil oxidative killing post-phagocytosis of microbes?
1. [...]
2. [...]
3. [...]
A: NADPH oxidase generates O^- (transfers e^- from NADPH to O_2); O^- metabolized to H_2O_2 by SOD; H_2O_2 reacts w/ O^- to form HOCl
Extra: SOD = superoxide dismutase
respiratory burst = rapid consumption of O_2 and production of superoxide (O^-) and its metabolites

Q: what is chronic granulomatous disease?
[...]
A: defect in neutrophil oxidative killing resulting in infection w/ catalase +ve organisms

Q: what is ddx if catalase +ve organisms aren't killed but catalase -ve organisms are?
[...]
A: CGD
Extra: CGD = chronic granulomatous disease

Q: how to test for CGD?
[...]
A: dihydrorhodamine test; if oxidative burst dysfnl, fluorescence is DIM
Extra: CGD = chronic granulomatous disease

Q: what is leukemia?
[...]
A: group of conditions characterized by an increase in premature leukocytes released into the bloodstream

Q: what are paraneoplastic syndromes?
[...]
A: disease or sx due to presence of cancer in body, but NOT due to local presence of cancer cells
Extra: mediated by hormones or cytokes excreted by tumour cells OR an immune response against the tumour

Q: what is an ECOG of 2?
[...]
A: capable of ALL self care; confined to bed/chair <50% of waking hours

Q: what is an ECOG of 3?
[...]
A: capable of limited self-care; confined to bed/chair >50% of waking hours

Q: what is adjuvant/neo-adjuvant tx?
[...]
A: tx after primary cancer tx to increase chance of cure

Q: what is stage II of cancer?
[...]
A: cancer larger than stage I; cancer cells may have moved into lymph nodes close to tumour

Q: what is stage III of cancer?
[...]
A: large cancer and possible local metastasis

Q: what is stage IV of cancer?
[...]
A: large cancer and distal metastasis

Q: what are common NSAIDs?
1. [...]
2. [...]
3. non-selective NSAIDs
A: ASA (acetylsalicylic acid; aspirin); coxibs (COX-2 inhibitors)

Q: what are the major sx of COX-1 inhibition?
[...]
A: ulcers and bleeding

Q: what are the major sx of COX-2 inhibition?
[...]
A: reduced inflammation, pain, fever

Q: when does acid secretion resume after PPIs bind to H+/K+ ATPase?
[...]
A: only AFTER synthesis of new enzymes (PPIs bind irreversibly to proton pumps); usually about 24 hr

Q: what are common adverse clinical presentations of PPI use?
[...]
A: headache, nausea, dizziness, diarrhea, rash
Extra: mostly nonspecific

Q: what is the 2003 recommendation for PPIs and bleeding PUs?
1. initially: [...]
2. followed by: [...]
3. after 72 h: [...]
A: 80 mg bolus (e.g., IV pentoprazole); infusion of 8 mg/hr for 72 hr; equiv to omeprazole 40 mg bid orally
Extra: bid = bis in die, twice a day

Q: by definition, a gastric peptic ulcer has breached into which stomach layer?
[...]
A: submucosa or deeper

Q: A 59 year old male presents to the emergency with a 1 day history of small volume coffee ground emesis. The patient also reports daily, severe heartburn for the past 25 years, managed with liberal use of antacids. There has been no significant associated nausea/vomiting, dysphagia, anorexia, or early satiety. The patient also denies any unexplained weight loss, fevers, or drenching night sweats. What is most likely etiology of pt's presentation?
[...]
A: esophagitis

Q: when are IV Octreotide and antibiotics recommended?
[...]
A: ONLY when esophageal varices or cirrhosis are suspected
Extra: Patients should be made NPO during UGIBs, whereas clear fluid diets and NG tubes are not indicated. IR embolization and surgical intervention are warranted if hemostasis cannot first be achieved through endoscopy.

Q: A 38 year old female patient is in your clinic with dysphagia. The patient has intermittent trouble swallowing both solids and liquids. Seems to happen especially when drinking tea. The patient denies heartburn and wait loss. What is the most likely ddx?
[...]
A: esophageal dysphagia - motor disorder - intermittent - esophageal spasm

Q: A 61 year old female presents to the emergency with a 1 day history of bright red emesis and confusion. The patient also complains of generalized abdominal pain. There has been no significant associated nausea/vomiting, heartburn/regurgitation, dysphagia, anorexia, or early satiety. The patient reports increased abdominal distension and weight with associated leg bilateral legs swelling over the past week. The spleen was palpable and Castell's sign was positive. Asterixis, palmar erythema, spider nevi, and Dupuytren's contracture were all noted. DRE revealed bright-red blood. What is the most likely dx for UGIB?
[...]
A: portal hypertension - gastroesophageal varices

Q: what is the diff btw motor disorders and mechanical obstructions in esophageal dysphagia?
[...]
A: motor disorder has trouble w/ solids AND liquids whereas mechanical is only solids

Q: is achalasia an intermittent or progressive motor disorder of esophageal dysphagia?
[...]
A: progressive

Q: what are 5 main dx in microcytic anemia?
[...]
A: TAILS: thalassemia, anemia of chronic inflammation, iron deficiency, lead poisoning, sideroblastic anemia
Extra: sideroblastic anemia: ineffective heme synthesis

Q: what common ddx to expect for normal MCV anemia?
1. [...]
2. [...]
3. [...]
A: bleeding + hemolysis (high retic count); bone marrow failure (low retic count); anemia of chronic inflammation

Q: what test can we use to assess iron storage in bone marrow?
[...]
A: Prussian Blue stain

Q: how does the body naturally lose iron?
1. [...]
2. [...]
A: sloughing of cells from GI tract (~1mg/day); menstruation (~1 mg/day during periods)

Q: what normally happens if hepcidin lvls increase?
[...]
A: hepcidin blocks ferroporitin 1, preventing Fe absorption (e.g., Fe overload, inflammatin)
Extra: The enzyme hepcidin regulates intestinal absorption of iron.
- Hepcidin is synthesized in the liver
- Its production is regulated by the human hemochromatosis protein (HFE protein)
- Increased body stores of iron → ↑ HFE protein → ↑ hepcidin → prevention of iron absorption Iron deficiency → ↓ hepcidin → ↑ iron absorption
Ferric iron (non-heme iron, Fe3+) is mainly reduced to ferrous iron (Fe2+) and then absorbed.
- Vitamin C increases absorption (converts Fe3+→ Fe2+).
- Calcium decreases absorption (due to chelation of iron). Heme iron can be directly absorbed into intestinal cells.

Q: how does Fe enter the enterocyte from the gut?
1. [...]
2. [...]
A: Fe^3+ → Fe^2+ by gastric acid and Dcytb reductase; DMT1 transports Fe^2+ to enterocyte
Extra: Ferric iron (non-heme iron, Fe3+) is mainly reduced to ferrous iron (Fe2+) and then absorbed.
- Vitamin C increases absorption (converts Fe3+→ Fe2+).
- Calcium decreases absorption (due to chelation of iron). Heme iron can be directly absorbed into intestinal cells.

Q: how does Fe^3+ enter the bloodstream and then tissues from an enterocyte?
1. enterocyte to bloodstream: [...]
2. bloodstream to tissue: [...]
A: ferritin transported to bloodstream via ferroportin 1; transferrin binds iron in bloodstream and transports to issues

Q: how can gastric acid and ascorbic acid enhance the bioavailability of inorganic iron?
[...]
A: b/c acids can reduce Fe^3+ to Fe^2+, which can be absorbed by the DMT1 receptor

what are common causes of iron deficiency?
1. decreased Fe intake
2. decreased Fe absorption
3. increased iron loss (chronic bleeding)
4. increased iron requirements

the pink slide shows Fe deficiency: what abnormalities can you see?
1. microcytic RBC (smaller than lymphocyte)
2. hypochromia (enlarged central pallor)
3. anisocytosis (variable shapes and sizes)
4. pencil cells

Q: what ferritin lvls would you expect in Fe deficiency?
[...]
A: <15-30 mcg/L (caution: may be falsely elevated due to inflammation or infection)

Q: what to expect on TIBC in Fe deficiency?
[...]
A: high transferrin lvls
Extra: low transferrin lvls in anemia of chronic inflammation
TIBC = total iron binding capacity

Q: what is tx for iron deficiency?
1. preferred tx: [...]
2. [...]
A: oral Fe replacement (anemia corrects w/in 6 weeks; Fe stores replenish w/in 6 months); IV Fe replacement

Q: what are the main lab test findings of Fe deficiency?
1. ferritin: [increased/decreased]
2. TIBC: [increased/decreased]
3. transferrin saturation: [increased/decreased]
A: decreased; increased; decreased

Q: 24F has long-standing heavy menstrual bleeding presents to family doctor w/ fatigue limiting her ability to work and exercise. CBC shows Hb 72 g/L (normal >120 g/L) and serum ferritin is 3 mgc/L (normal > 30 mcg/L). How would you tx?
[...]
A: IV iron replacement
Extra: oral iron replacement likely takes too long
consider blood transfusion if vital signs show hemodynamic instability

Q: how to differ btw TRALI and TACO?
[...]
A: TRALI has fever (immune mediated by neutrophils) and hypotension whereas TACO has no fever and hypertension

Q: what is Octreotide?
[...]
A: a somatostain analog (decreases portal hypertension)

Q: which chemical should we look for in UGIB?
[...]
A: increased urea lvls (creatinine also increases but not as much as urea)

Q: what pathological process occurs in megaloblastic anemia?
1. [...]
2. [...]
3. ineffective erythropoiesis
A: DNA synthesis impaired (cytoplasm matures faster than nucleus); neutrophil hypersegmentation and presence of maco-ovalocytes

Q: how fast does folate deficiency present?
[...]
A: just a few weeks (i.e., FAST)

what are common causes of folate deficiency?
1. nutritional deficiency (EtOH use, substance abuse)
2. malabsorption (IBD, bowel disease)
3. drugs (e.g., methotrexate, phytoin, EtOH, trimethoprim)
4. increased requirements (pregnancy, chronic hemolysis)

Q: what tests to dx folate deficiency?
[...]
A: serum folate, RBC folate
Extra: homocysteine high, MMA normal
folate deficiency does not cause neurological sx (except for neural tube defects during gestation)

Q: how long before vit B12 deficiency presents?
[...]
A: several years of complete lack of B12

Q: what is pernicious anemia?
[...]
A: autoimmune disorder causing antibodies against gastric parietal cell or IF

Q: what type of diet cause B12 deficiency?
[...]
A: non-supplemented vegan diet (normally diet isn't a huge problem)

what dx tests and results are indicative of B12 deficiency?
1. MCV > 110-115 (macrocytic)
2. serum B12 < 150 pmol/L
3. homocysteine and MMA both increased
4. antibodies to IF or parietal cells

Q: what are 2 common tx of B12 deficiency?
1. [...]
2. [...]
A: parenteral B12 injections (for severe anemia or neurologic changes); oral B12 supplements

Q: 45F presents with fatigue and decreased exercise tolerance. She is on hypothyroid tx for 6 years; her mother has osteoporosis and autimmune thyroiditis; her father died of colon cancer at age 56. She has no weight loss, no GI blood loss, and normal periods. She looks well and has no masses but has skin rashes on her arms and buttocks. The lab has Hgb 91 and normal TSH. What is the most likely micronutrient deficiency in this patient?
[...]
A: iron

Q: 25M presents with fatigue and anemia. He has had 1 year of diarrhea and weight loss, no overt blood loss, and 10-12 loose stools/day. Diagnostic tests reveal terminal ileal Crohn's disease. His Hb is 100 and MCV is 105. What is the most likely micronutrient deficiency in this patient?
[...]
A: vitamin B12
Extra: hint: macrocytic
hint: terminal ileal Crohn's disease

Q: 50M drinks 12 beers/day for the past 10 years. He has had a 10 lb weight loss over the past year. He has poor oral intake. He is unemployed and in a poor financial situation. His Hb is 100 and MCV is 105. What is the most likely micronutrient deficiency in this patient?
[...]
A: folate

Q: what are the 2 recommended first line rx for H. pylori?
1. [...]
2. [...]
A: CLAMET x14 days: PPI, clarithromycin, amoxicillin, metronidazole; BMT x14 days (for pts w/ penicillin allergy or 2nd line if CLAMET fails): PPI, bismuth, metronidazole, tetracycline

Q: what are the MOST common complications of blood transfusions?
1. [...]
2. [...]
3. [...]
A: allergy (hives); fever; fluid overload

Q: what is a qualitative Hb disorder?
[...]
A: mutations in globin chains altering structure and fn

Q: what is a quantitative Hb disorder?
[...]
A: decreased/imbalanced production of globin chains

Q: what mutation causes sickle cell anemia?
[...]
A: glu6val

Q: how to screen newborns for SCD?
[...]
A: heel prick for HPLC
Extra: HPLC = high-performance liquid chromatography

what is the clinical pathology of sickle cell disease?
1. vaso-occlusion
2. chronic inflammatory state
3. hemolysis
4. chronic organ damage

Q: what are the 2 most common manifestations of sickle cell disease?
1. [...]
2. [...]
A: vaso-occlusive crisis (painful!); acute chest syndrome
Extra: VASH = vaso-occlusive crisis, acute syndrome, sequestration crisis, hemolytic crisis

Q: what is the mgmt for acute chest syndrome from SCD?
[...]
A: hydration, pain ctrl, O_2 for hypoxemia, tx infection, transfusion
Extra: SCD = sickle cell disease

Q: what are the 2 main features of chronic organ damage due to SCD?
1. [...]
2. [...]
A: splenic dysfn (higher risk of infection); progressive organ dysfn due to vaso-occlusion and chronic hemolysis

Q: how to prevent a veno-occlusive crisis (SCD)?
1. [...]
2. [...]
3. [...]
A: avoid hypoxia/cold; infection ctrl and prevention; folic acid supplementation

Q: what is the only disease-modifying therapy for SCD in Canada?
[...]
A: hydroxyurea (increases HgbF lvls)
Extra: national guidelines (Canada + USA): consideration of HU for all SCD pts > 10 months/o

Q: when giving frequent transfusions for SCD, what other tx should you also give?
[...]
A: iron chelation therapy
Extra: to prevent transfusional iron overload

Q: what is the main curative therapy for SCD?
[...]
A: bone marrow transplant

Q: what are the cell characteristics observed in anemia of chronic disease ("anemia of inflammation")?
[...]
A: normocytic, normochromic anemia

what investigations to order for normocytic anemia?
1. reticulocyte count
2. PBS
3. iron studies (Fe, TIBC, Fe sat, ferritin)
4. creatinine, TSH, SPEP, liver enzymes
5. CRP
Extra: PBS = peripheral blood smear

Q: overproduction of which chemical results in iron trapped in macrophages in anemia of chronic disease?
[...]
A: hepcidin

Q: what is the pathological result of release of IL-1, IL-6, IFN-beta, and IFN-gamma in anemia of chronic disease?
[...]
A: hepcidin overproduction

Q: what is tx for anemia of chronic disease?
[...]
A: correction of underlying disorder; Fe is NOT useful in absence of Fe deficiency

after tx for anemia of chronic disease, how would you expect Fe indices to change?
1. Fe: higher
2. TIBC: same or higher
3. % saturation: normal
4. ferritin: decreased to normal

what are common etiologies of anemia of chronic disease?
1. infection
2. inflammation
3. cancer
4. kidney/liver disease
5. endocrinopathies
Extra: IICKE

Q: what is an Hb molecule made of?
[...]
A: 4 heme molecules and 4 globin chains

Q: what are the 3 most common Hb molecules in adults?
[...]
A: Hb A (96-98%), Hb A2 (2-3.5%), Hb F (<1%)

Q: which 2 chromosomes contain genes encoding for globins?
[...]
A: 16 (alpha, zeta) and 11 (gamma, delta, beta)

Q: what is the diff btw alpha and beta thalassemia?
[...]
A: alpha is decreased synthesis of alpha globin chain whereas beta is decreased for beta globins

Q: what is genotype for alpha thalassemia?
[...]
A: aa/-- OR a-/a-

Q: what are sx of alpha thalassemia?
[...]
A: mild anemia, microcytosis, hypochromia

Q: which alpha thalasemmias require no tx but genetic counselling?
[...]
A: silent carrier (aa/a-) and alpha thalassemia (aa/-- or a-/a-)

Q: what are sx of HbH disease?
[...]
A: moderate hemolytic anemia, microcytosis, hypochromia; mild splenomegaly

Q: what is tx for HbH disease?
[...]
A: transfusion and iron chelation

Q: which alpha thalassemias are incompatible w/ life?
[...]
A: hydrops fetalis and Hb Barts

Q: which phenotypes of beta thalassemia require no tx?
[...]
A: B/B^0 and B/B^+ (minor; trait)

Q: what are sx of beta thalassemia minor?
[...]
A: mild anemia, microcytosis, hypochromia, basophilic stippling

Q: what is genotype of beta thalassemia intermedia?
[...]
A: B^0/B^+ (moderately severe anemic)

Q: what is tx for beta thalassemia minor?
[...]
A: transfusion, iron chelation, induction of HbF w/ hydroxyurea

Q: what is sx of beta thalassemia major (B^0/B^0)?
[...]
A: severe anemia presenting at 6-12 mo; possible severe organ dysfn; decreased HbA, increased HbA2 and HbF

Q: what is tx for beta thalassemia major (B^0/B^0)?
[...]
A: lifelong transfusion and iron chelation; organ transplant; gene therapy/editing

Q: which liver acinus zone is closest to an artery and venule?
artery: [...]
venule: [...]
A: zone 1; zone 3

Q: what is the oxygen gradient in the liver acinus zones?
[...]
A: zone 1 to 3 via sinusoids (closer to HA, increased O_2)

Q: what is the area btw the portal tract and hepatocytes?
[...]
A: interface

Q: what liver cmpt is illustrated by the blue arrows?
[...]
A: sinusoids

Q: which liver cmpt is the conduit for bile secretion?
[...]
A: bile canaliculi (merges to form canals of hering, which drains into bile duct)

Q: what are Kupffer cells?
[...]
A: specialized macrophages that are part of the liver immune system

Q: what is the likely dx given this is liver tissue?
[...]
A: acute severe hepatitis

Q: what pathological changes occur in hepatitis?
[...]
A: necrosis of hepatocytes, inflammation, Mallory bodies, fatty change

Q: what is the diff etiology btw macrovesicular and microvesicular steatosis?
macrovesicular: [...]
microvesicular: [...]
A: caused by dysregulation of lipid metabolism; caused by mitochondrial toxins
Extra: steatosis = fatty liver disease

Q: what is the progression of non-alcoholic liver disease to cirrhosis?
[...]
A: steatosis to steatohepatitis to fibrosis to cirrhosis

what are the 4 main changes in NAFLD?
1. insulin resistance produces hepatic steatosis
2. oxidative injury to fat-laden hepatocytes
3. liver cell necrosis and inflamm (oxidative injury)
4. activation of stellate cells leads to fibrosis/cirrhosis
Extra: NAFLD = non-alcoholic fatty liver disease

Q: how does XS alcohol cause liver disease?
[...]
A: EtOH metabolism thru CYP2E1 (non ADH) produces ROS, causing hepatocyte damage

Q: what is hemochromatosis?
[...]
A: XS iron absorption and deposition in liver; assoc w/ free radical rxns and formation of collagen

Q: what occurs in Wilson disease?
[...]
A: impaired copper secretion (think Kaiser-Fleischer ring and House MD lol)

Q: which hepatitis viruses never cause chronic hepatitis?
[...]
A: A and E (except in immunocompromised hosts and pregnant females)

Q: how is hep B transmitted?
[...]
A: 3 Bs: blood, birthing, "bonking"

Q: which hep virus most oten leads to chronic hep?
[...]
A: hep C (>80% dev chronic hepatitis, 20% will develop cirrhosis)
Extra: C for chronic; 20% of pts w/ hep C also dev cirrhosis

Q: what is cholangiocarcinoma?
[...]
A: group of cancers that begin in bile ducts

Q: what is dx?
[...]
A: cholelithiasis (gallstones)
Extra: 2 main types: pigment (black/brown) and cholesterol (white/yellow)

Q: what are histologic features of cholecystitis?
1. [...]
2. [...]
A: inflammation (neutrophils if acute; lymphocytes if chronic); Rokitansky-Aschoff sinuses (outpouchings of mucosa)
Extra: cholecystitis = inflammation of gallbladder; typically caused by an obstruction of the cystic duct by a gallstone

Q: what is diff btw exocrine and endocrine pancreas?
exocrine: [...]
endocrine: [...]
A: secretion of digestive enzymes, ions, water into duodenum; produce insulin + glucagon (think islets of Langerhans)

Q: what are the 3 main initiating events of acute pancreatitis?
1. [...]
2. [...]
3. [...]
A: pancreatic duct obstruction; acinar cell injury; defective intracellular transport of proenzymes

Q: what is prognosis of pancreatic adenocarcinoma?
[...]
A: 5-year survival of <5%

Q: what should you immediately think of when you see neurological sx accompanying macrocytic anemia?
[...]
A: vitamin B12 deficiency
Extra: folate is often dietary w/ EtOH abuse

Q: what is structure B called?
[...]
A: left lobe

Q: what is structure A called?
[...]
A: right lobe

Q: what is structure C called?
[...]
A: caudate lobe

Q: what is structure D called?
[...]
A: quadrate lobe

Q: where is inflammation of the liver or gallbladder most commonly felt?
[...]
A: RUQ or epigastrium

Q: what are the 2 inflows of blood to the liver?
[...]
A: hepatic artery (20%) and portal vein (80%)

Q: where does blood leave from the liver?
[...]
A: via hepatic veins (RHV, MHV, LHV) from the caudate lobe

Q: which veins form the liver's main portal vein?
[...]
A: splenic vein, IMV, SMV

Q: thru which zones of a liver lobule does bile and blood flow?
bile: [...]
blood: [...]
A: zone 3 to 1; zone 1 to 3

Q: what is a cholangiocyte?
[...]
A: epithelial cell which lines the bile ducts

Q: what are Kupffer cells?
[...]
A: macrophages of the liver

Q: where do Kupffer and hepatic stellate cells reside in the liver?
[...]
A: in the space of Disse (perisinusoidal space)

Q: what are the 3 main classes of oropharyngeal dysphagia?
[...]
A: structural, neuromuscular/toxic/metabolic, functional

Q: what happens to lvls of serum iron, ferritin, and TIBC in anemia of chronic disesase?
serum Fe: [...]
ferritin: [...]
TIBC: [...]
A: decrease; normal/high; normal/low

what are the main 3 Fe lvls to look out for?

Q: why is stool usually brown and urine usually yellow?
[...]
A: bacteria in colon break down bilirubin to from stercobilin (brown stool) and urobilinogen (kidneys to urine)

Q: what should you suspect when you have jaundice, dark tea-coloured urine, pruritis, and increased ALP?
[...]
A: blockage of bile flow (e.g., common bile duct stone or cancer in head of pancreas)

what are the main fns of bile?
1. transport stuff in liver
2. prevents gallstone formation
3. cholesterol homeostasis
4. detergent molecules
5. body defenses
6. intestinal mobility

Q: where in bowel would you expect bile acids to be absorbed?
[...]
A: terminal ileum

Q: Pt presents w/ jaundice and RUQ pain. Pt has hx of alcohol abuse. What is likely ddx?
[...]
A: hepatitis, cirrhosis

Q: why might pruritis arise in chronic liver disease?
[...]
A: b/c of cholestasis (lack of bile flow)

Q: Pt presents w/ hematemesis, melena (occasional hematochezia), ascites, weight gain, edema, and hepatic encephalopathy. What is likely ddx?
[...]
A: cirrhosis or HCC
Extra: HCC = hepatocellular carcinoma

Q: what does I4M4 mean for injury to organs on hx?
I4: [...]
M4: [...]
A: infectious, immune, inflamm, ischemia; medications (toxins), metabolic, mechanical, malignancy

Q: what are the 3 main qs for the AUDIT-C framework for at risk drinking?
1. [...]
2. [...]
3. [...]
A: how often did you have a drink containing alcohol in the past year?; how many drinks containing alcohol did you have on a typical day when you were drinking in the past year?; how often did you have 6+ drinks on one occasion in the past year?

Q: how does hep A and E spread?
[...]
A: via fecal-oral transmission

Q: how does hep B, C, and D spread?
[...]
A: parenteral transmission

Q: in which small bowel segment is Fe, B12, and folate absorbed?
[...]
A: Fe: duodenum, folate: jejunum, B12: ileum

Q: why might you see neurological sx in B12 deficiency?
[...]
A: b/c B12 needed for myelin in spinal cord tracts (also needed for DNA/RNA synthesis)

Q: how to distinguish btw B12 and folate deficiency using MMA?
[...]
A: B12 MMA increased whereas folate is normal

Q: what are the major categories for stigmata of chronic liver disease?
1. [...]
2. [...]
3. [...]
A: hepatic insufficiency (jaundice, scleral icterus, asterixis); hyperestrogenism (gynecomastia, palmar erythema); portal hypertension (spider angioma, ascites, encephalopathy)

Q: what is the Hook technique?
[...]
A: wrapping fingers around costal margin to feel liver

Q: what does Murphy's sign indicate?
[...]
A: acute cholecystitis (pt suddenly stops inspiration when inflamed gallbladder touches your palpating hand)

Q: how to find top and bottom of liver?
top: [...]
bottom: [...]
A: percussion note changes from resonant over lung to dull over liver; dull over liver to tympanic over gas in bowel

Q: how do the liver and spleen tend to enlarge?
[...]
A: spleen enlarges down to RLQ whereas spleen enlarges diagonally across abs (towards RLQ)

Q: how to feel for spleen?
[...]
A: palpate using LH to pull up ribs while palpating w/ right hand

Q: what is a physical exam sign of splenomegaly?
[...]
A: dull percussion note at Castell's point

Q: what is a sign for ascites in the physical?
[...]
A: shifting dullness or fluid wave

Q: what is normal ALT range for men and women?
[...]
A: men is 29-33 U/L (~30) whereas women is 19-25 (~20)

Q: what is the AST/ALT ratio in most liver diseases (other than cirrhosis)?
[...]
A: ALT > AST

Q: what is the AST/ALT ratio in alcohol related liver disease?
[...]
A: AST/ALT > 2 (AST > ALT)

Q: why does ALP rise in pathological cholestatic liver tests?
[...]
A: due to bile duct obstruction

Q: how can GGT help in dx?
[...]
A: very sensitive to drinking alcohol, being overweight, or w/ certain meds (use in isolation is usually not very significant)

Q: what can decreased albumin lvls indicate?
[...]
A: chronic liver disease, malnutrition, acute inflammation

Header: is US required? if so, where should we look?

Header: is US required? if so, what should we expect?

Q: what does pre-hepatic jaundice result in?
[...]
A: overprod of unconjugated bilirubin and decreased uptake of bilirubin

Q: what test to order if you suspect cholestatic cause of jaundice?
[...]
A: ab US to examine bile ducts

Q: what test to order if you suspect hepatocellular cause of jaundice?
[...]
A: liver panel (ALT usually elevated)

Q: which tests to order for autoimmune liver diseases?
[...]
A: ANA and ASMA

Q: which tests to order for immunoglobulin related liver diseases?
[...]
A: IgA (EtOH), IgG (AIH), IgM (PBC)

Q: what are the major categories to investigate w/ liver disease?
step 1: [...]
step 2: [...]
step 3: other (thyroid, celiac)
A: viral and metabolic; genetic and autoimmune

Q: when should a liver biopsy be performed?
[...]
A: dx uncertainty or to prov prognosis of severity

Q: what are the 3 methods of liver biopsy?
1. [...]
2. [...]
3. [...]
A: blind (thru ribs on RHS); US guidance (underneath ribs anteriorly); transjugular

Q: when is the transjugular route for liver biopsy preferred?
[...]
A: w/ pts w/ low platelets or high INR (high risk of bleeding)

Q: what is grade 1 of the Ludwig Batts scoring system for inflamm?
[...]
A: inflammation around portal space

Q: what is grade 2 of the Ludwig Batts scoring system for inflamm?
[...]
A: inflammation crosses limiting plate (interface hepatitis/piecemeal necrosis)

Q: what is grade 4 of the Ludwig Batts scoring system for inflamm?
[...]
A: inflamm cells spread from portal space to central vein (bridging necrosis)

Q: what is stage 1 of the Metavir scoring sys for fibrosis?
[...]
A: portal space fibrosis

Q: what is stage 2 of the Metavir scoring sys for fibrosis?
[...]
A: fibrosis spreading into lobule towards other portal spaces

Q: what is stage 3 of the Metavir scoring sys for fibrosis?
[...]
A: bridging fibrosis

Q: what is steatosis?
[...]
A: (micro/macro)vesicular fat
Extra: cirrhosis findings (below)

Q: what are common potential pathogens?
[...]
A: prions, virus, bacteria, fungi, parasites
Extra: these are in increasing order of complexity

Q: what are some likely causative factors for CRC?
[...]
A: high-fat and low-fiber diet, red meat

Q: what are the adverse effects of false positive screens?
[...]
A: anxiety, unnecessary biopsy, repeat screening

Q: what are potential adverse effects of false negative screens?
[...]
A: false reassurance, progression of cancer b4 tx

Q: what does FIT do?
[...]
A: tests for blood in stool (can be caused by CRC or polyps)

Q: how often should FIT be tested?
[...]
A: every 1-2 years for ppl aged 50-75

Q: what to do after +ve FIT?
[...]
A: refer to colonoscopy performed w/in 8 weeks

Q: when should FIT not be performed?
[...]
A: in symptomatic pts (e.g., GIB)

Q: what is diff btw sigmoidoscopy and colonoscopy?
[...]
A: sigmoidoscopy only goes to descending whereas colonoscopy goes all the way to ascending

Q: why would we use sigmoidoscopy over colonoscopy?
[...]
A: b/c pts don't necessarily need to be sedated (can work after test)

Q: what are risk factors for GERD?
[...]
A: obesity, increased age, smoking, EtOH

Q: how to investigate GERD w/ sx of heartburn but not dysphagia?
[...]
A: hx of retrosternal burning and see whether pt responds to PPI

Q: what are common GI diseases arising from GERD?
[...]
A: esophagitis, stricture, Barrett's esophagus, esophageal cancer

Q: why are adenomatous polyps more more relieving than carcinomas?
[...]
A: b/c they are ALL benign by definition (but are premalignant)

Q: what are the most concerning types of adenomas?
[...]
A: polyps w/ lots of villous cmpt (more tubular is "better")

Q: what are the big 4 cancers in Canada?
[...]
A: lung + bronchus, CRC, pancreas, breast

Q: what are major risk factors for CRC?
1. [...]
2. [...]
3. world geography + diet/lifestyle
4. occupational risk
A: FMHx and personal hx; IBD

Q: what is diff btw adjuvant and neoadjuvant therapy?
[...]
A: neoadjuvant is for chemo/radiation b4 surgery whereas adjuvant is post-surgery

Q: what are the major clinical presentations of CRC?
[...]
A: asymptomatic, weight loss, fever, night sweats, fatigue

Q: what investigations to investigate CRC?
1. [...]
2. [...]
3. [...]
A: digital rectal exam or flexible sigmoidoscopy; colonoscopy (gold standard); CBC, liver enzymes, CEA
Extra: apple core sign on fluorscopy indicative of CRC

Q: what happens in stage II of CRC?
[...]
A: invasion past muscularis of colon into pericoic tissues or adjacent organs; NOT into lymph nodes

Q: how to tx stage II colon cancer?
[...]
A: surgical resection w/ adjuvant chemo

Q: what is standard of care adjuvant tx for stage III CRC?
[...]
A: FOLFOX (improves 5 yr survival by 10-20% vs placebo)
Extra: surgical resection first

Q: how do platinum chemotherapies (e.g., oxaliplatin and cisplatin) work?
[...]
A: by forming crosslinks btw DNA, preventing syn and transcription

Q: how do chemotherapies targeting the VEGF pathway work?
[...]
A: by inhibiting angiogenesis

Q: 51F with +ve FIT test and mass consistent w/ cancer in colonoscopy. A biopsy is done and comes back as adenocarcinoma of the colon. What is your next step?
[...]
A: order a CT chest/ab to stage the cancer and check for mets

Q: Pt shows up to ER w/ bowel obstruction. The CT shows a mass suggestive of cancer in obstructed colon and another mass in liver suggestive of mets. What is your next step?
[...]
A: refer to surgery b/c the pt is obstructed

Q: what is the diff btw G+ and G- cell wall?
[...]
A: G+ has thick peptidoglycan wall whereas G- has thin wall + LPS + plasma membrane

Q: what does LPS from bacteria do to an infected person?
[...]
A: invokes a strong inflammatory response (LPS is an endotoxin)

Q: how do G+ and G- cells stain in the gram stain?
[...]
A: G+ is purple whereas G- is pink

Q: what are endospores?
[...]
A: resting cells that are highly resistant to dessication, heat, chemical agents

Q: how is C. difficile transmitted?
[...]
A: via inegestion of spores

Q: what type of baccili are E. coli, salmonella, shigella, and yersinia?
[...]
A: G- enterobacteriales

Q: what type of bacteria are campylobacter, H. pylori, and Vibrio cholerae?
[...]
A: curved G- bacilli

Q: what type of bacterium are most bacilli?
[...]
A: G-

Q: what type of bacterium are most cocci?
[...]
A: G+ (except neisseria, moraxella, veillonella)

Q: what are the 3 overall phases of hemostasis?
1. [...]
2. [...]
3. [...]
A: make a clot (platelet plug, clotting cascade); stop clotting (antithrombin, protein C/S); dissolve the clot (plasmin)

Q: how does primary hemostasis work?
[...]
A: injury to endothelium exposes subendothelial matrix; platelets adhere to matrix via VWF

Q: how do platelets change when they are activated?
[...]
A: they secrete substances that activate nearby platelets and change their cytoskeleton to cover more SA

Q: what are the major pathways of secondary hemostasis?
[...]
A: extrinsic initiates the cascade and the intrinsic amplifies it; both culminate in the common pathway

Q: how does the extrinsic pathway initiate the coagulation cascade?
[...]
A: TF exposed when endothelium damaged → F7 binds to TF → TF-7a complex activates F10

Q: how does the intrinsic pathway amplify the coagulation cascade?
[...]
A: F12 → F11 → F9 → F8 → F10

Q: how does the common pathway generate fibrin?
[...]
A: F10 + F5 → prothrombin (F2) to thrombin (F2a) → fibrinogen (F1) to fibrin
Extra: fibrin polymerizes to form clot

Q: what does antithrombin (AT) inactivate to stop clotting?
[...]
A: thrombin (2a) and F10

Q: what does protein C and S inactivate to stop clotting?
[...]
A: F5

Q: what is responsible for clot dissolving?
[...]
A: plasmin which cuts fibrin

what lab tests used to measure coagulation?
1. CBC for platelet cnt
2. INR (extrinsic) and PTT (intrinsic)
3. fibrinogen
4. D-dimer (checks for clots)

Q: all coagulation factors w/ the exception of what is synthesized in the liver?
[...]
A: vWF (endothelial cells) and F8 (endothelial cells + liver)
Extra: F 10, 9, 7, 2 (1972) + proteins C/S req vit K for synthesis
vit K deficiency and liver disease typically only increases INR and not PTT (F7 has shortest half-life of the factors)

Q: what is the diff in bleeding hx btw primary and secondary hemostasis?
[...]
A: primary has mucosal bleeding and petechiae whereas secondary has deeper soft tissue + joint bleeding

Q: what is ddx for Fe deficiency in pts over 40?
[...]
A: CRC until proven otherwise

Q: when does hemolytic disorders turn into hemolytic anemia?
[...]
A: when rate of hemolysis is faster than body's ability to produce new RBCs

Q: what are the 2 main ways hemolysis destroys RBCs?
1. [...]
2. [...]
A: increased clearance/removal by macrophages in RES; increased physical destruction

Q: what are the 3 main ways RBCs lyse intravascularly?
[...]
A: mechanical shearing, complement-mediated lysis, infection
Extra: mech shearing results in RBC fragments (schistocytes)

Q: how does MAHA (TMA) cause mechanical shearing of RBCs?
[...]
A: fibrin strands in microvascular tear RBC as it passes thru (schitocytes and thrombocytopenia)

Q: how does TTP result in clots?
[...]
A: failure to produce ADAMTS13 results in increased vWF in vessels, which attracts platelets and destroys RBCs
Extra: TTP = thrombotic thrombocytopenic purpura

what is the classic pentad in TTP?
1. microangiopathic hemolytic anemia (100%)
2. thrombocytopenia (100%)
3. fever (not from infection; 25%)
4. renal dysfn (45%)
5. fluctuating bizzare neuro manifestations (45%)
Extra: TTP = thrombotic thrombocytopenic purpura

Q: how to tx TTP?
[...]
A: plasmapheresis to replace ADAMTS13 and remove high vWF multimers; plasma infusion for congenital TTP
Extra: TTP = thrombotic thrombocytopenic purpura

Q: what is the pathophys of hemolytic uremic syndrome?
[...]
A: shiga toxin / ab deregs expression of complement regulatory genes, so increased MACs cause intravsacular hemolysis

Q: what is pathophys of cold AIHA/agglutinins disease?
[...]
A: IgM binding to RBCs only at cold temps then hemolysis occurs in liver or intravascularly via MACs

Q: how to manage cold AIHA/cold agglutinins disease?
[...]
A: avoid cold exposure, transfuse blood thru warmer, and tx underlying cause

Q: what are general risk factors for cholangiocarcinoma?
[...]
A: obesity, diabetes, cigarette smoking, FDR
Extra: FDR = first degree relationship

Q: what are sx of pancreatic CA?
[...]
A: asymptomatic, painless jaundice, ab pain, nonspecific (nausea, vomiting, weight loss, anorexia, malaise)

Q: what do you expect on bloodwork for pancreatic CA?
[...]
A: elevated liver enzymes, elevated conjugated bilirubin, new onset diabetes, lipase/amylase usually normal

Q: how to detect intrahepatic CCA?
[...]
A: on physical or dx imaging
Extra: sx: usually not jaundiced
constitutional sx: fatigue, malaise, anorexia, weight loss
ab pain often vague
increased ALP and GGT

Q: what is major sx diff btw intrahepatic and extrahepatic CCA?
[...]
A: extrahepatic usually has painless jaundice whereas intrahepatic doesn't

Q: what imaging technique is best for checking pancreaticobiliary lesions?
[...]
A: CT for masses (u/s for quick checks)

Q: how to perform an ERCP?
[...]
A: insert side-viewing endoscope into duodenum and inject contrast via ampulla of Vater into bile ducts
Extra: bile duct appears dilated; intrahepatic biliary tree also appears dilated

Q: what are the 3 major anastomoses in Whipple surgery?
1. [...]
2. [...]
3. [...]
A: choledochojejunostomy (gallbladder + jejunum); pancreaticojejunostomy (pancreas + jejunum); gastrojejunostomy (stomach + jejunum)

Q: what margins are necessary for surgical resection of intrahepatic CCA?
[...]
A: R0 resection; 1 cm clear margin for ANY survival beneft

Q: how to tx hilar CCA?
[...]
A: excision of the entire extrahepatic biliary tree

Q: how to manage primary AIHA?
[...]
A: suppress immune production of autoantibody (prednisone 1 mg/kg) and decrease RBC rm by spleen (splenectomy if refractory)
Extra: AIHA = autoimmune hemolytic anemia
assess for hemodynamic stability!!!!

Q: what is pathophys of hereditary spherocytosis?
[...]
A: membrane of RBC gets rm each time it passes thru splenic sinusoids

how to manage hereditary spherocytosis?
1. folic acid supplementation
2. supportive blood transfusions
3. splenectomy (for moderate/severe disease)
4. cholecystectomy (if sx for gallstones)

Q: what is pathophys of hemolytic enzymopathy?
[...]
A: unstable Hb denatures under oxidative stress; Hb precipitates outta RBC; spleen removes the RBCs

Q: how does G6PD deficiency cause hemolysis?
[...]
A: w/o G6PD can't create NADPH needed to reduce glutathione, which protects RBC from oxidative stress

Q: how does G6PD deficiency lead to RBCs w/ "bites" taken out of them?
[...]
A: spleen attempts to rm Heinz bodies (leads to extravascular hemolysis)

Q: what would you expect on lab if you see jaundice, scleral icterus, and pigmented gallstones?
[...]
A: increased unconjugated bilirubin

Q: what is normal relative and absolute retic cnt?
[...]
A: 1-2%, 20-100 billion

Q: what happens to retic count in anemia of chronic disease?
[...]
A: normal/low counts

Q: what is the fn of haptoglobin?
[...]
A: prevents Hb from oxidizing and creating free radicals AND consumes NO from vascular smooth muscle cells

Q: how to investigate immune-mediated hemolysis?
[...]
A: test for IgG or C3 complement (look for agglutination)

Q: what is ddx if apple core lesion presents on barium swallow?
[...]
A: annular constriction by colorectal carcinoma

Q: what is dx?
[...]
A: achalasia

Q: what signs on this CT tells you this might be gastric cancer?
[...]
A: eccentric thickening along stomach wall (non-diffuse, inhomogenous growth)

Q: why do we need to image the ENTIRE appendix for RLQ pain?
[...]
A: to check for tip appendicitis

Q: name the anatomical location pointed to by the yellow arrow
[...]
A: ileocaecal junction

Q: what is the arrow pointing towards?
[...]
A: a ventral wall hernia

Q: what is dx in both of these cases?
[...]
A: acute appendicitis

Q: what does the arrow point towards?
[...]
A: diverticulosis

Q: we are looking at RUQ; what is dx?
[...]
A: cholelithiasis

Q: what is the use case of acetominophen (paracetamol, tylenol)?
[...]
A: analgesic and antipyretic
Extra: analgesic for mild to moderate pain (temporary)

Q: what are the 3 phases of hepatic drug metabolism?
phase I: [...]
phase II: [...]
phase III: [...]
A: parent molecule altered (ox/red/hydrolysis); conjugates molecule w/ water-soluble moiety; excretes molecule into bile

Q: how does acetaminophen overdose cause hepatotoxicity?
[...]
A: glucuronidation and sulfation pathways saturated, resulting in more acetaminophen metabolized to toxic NAPQI; oxidatie injury and necrosis of acinar zone 3

Q: what are the 4 stages of acetaminophen toxicity?
Stage 1 (0.5-24 hr): [...]
Stage 2 (24-72 hr): [...]
Stage 3 (72-96 hr): [...]
Stage 4 (4-14 d): recovery (typically complete)
A: asymptomatic, lethargy, normal lab studies; initial sx improvement; AST/ALT, INR, bilirubin elevation begins; nephrotoxicity; jaundice, RUQ pain, encephalopathy, bleeding diathesis, ..., death

Q: how many acetaminophen pills per day can cause OD?
1. [...]
2. w/ NeoCitran b4 bed: [...]
3. chronic XS alcohol: [...]
A: 30 regular strength pills; 8 XS pills; 8 XS pills

Q: what is antidote of acetaminophen toxicity?
[...]
A: N-acetylcysteine (NAC) and activated charcoal

Q: when to tx acetaminophen toxicity w/ NAC?
1. [...]
2. [...]
3. delayed presentation, evidence of liver injury, and hx of XS ingestion
A: >4 hrs following acute ingestion above tx line of nomogram; >66 umol/L and unknown ingestion time

Q: which ribosome subunits can we target in fungi?
[...]
A: 40S and 60S subunits

Q: what are impt targets of antifungal agents?
[...]
A: beta-1,3 glucan synthase AND ergosterol

Q: what are impt target molecules for dx tests for fungal infections?
[...]
A: mannoproteins and beta-1,6 glucans

Q: how do molds reproduce?
[...]
A: asexually via spores

Q: how do yeasts reproduce?
[...]
A: asexually by budding

Q: what are the 2 phases of dimorphic fungi?
[...]
A: yeast at 37 ℃ and mould at 25 ℃

Q: what type of pathogen are fungi?
[...]
A: opportunistic pathogens (immunocompromised hosts or defect in anatomical barrier)

Q: what is diff btw definitive and intermediate parasite host?
[...]
A: definitive is where parasites sexually reproduce; intermediate is where parasites mature or asexually reproduce

Q: what are the 2 forms of parasites?
[...]
A: infective (dormant) and invasive (active)

Q: what are the 4 major types of protozoa?
[...]
A: amoeba, flagellates, ciliates, sporozoa

Q: what bacteria causes malaria?
[...]
A: plasmodium

Q: what are the 3 major groups of helminths?
[...]
A: nematodes (round worms), cestodes (segmented flat worms), trematodes

Q: what are the definitive and intermediate hosts of the Taenia species (tapeworms)?
[...]
A: definitive is humans (in small intestine) and intermediate is cow or pig

Q: why are prions so difficult to get rid of?
[...]
A: b/c they are extremely stable and accumulate in tissue

Q: what are the 2 essential cmpts of a virus?
[...]
A: nucleic acid and protein capsid

Q: how do dsDNA viruses replicate?
[...]
A: by using host polymerase for transcription and replication

Q: how do -ssRNA viruses replicate?
[...]
A: by using viral RNA poly for rep and transcription

Q: how do +ssRNA replicate?
[...]
A: using viral RNA poly for replication (genome itself can act as mRNA)

Q: what is the survival benefit of naked viruses?
[...]
A: lack of envelope allows naked viruses to be more stable to temp, proteases, detergents, and drying

Q: why are enveloped viruses usually spread thru droplets, secretions, and blood/bodily fluids?
[...]
A: b/c their envelope needs to stay "wet" to retain infectivity

Q: what does varicella and zoster mean?
[...]
A: varicella = chicken pox (initial disease) and zoster = shingles (many yrs later)

what are the 4 things a pathogen needs to do to be successful?
1. attach, enter, and establish in host
2. invade, repilicate, and disseminate
3. cause host damage
4. transmit to the next host

Q: what is pathogenicity?
[...]
A: ability for pathogen to cause disease

Q: what is virulence?
[...]
A: degree of pathogenicity of an organism (super virulent organisms usually severely damage the host)

Q: what are primary pathogens?
[...]
A: ones that regularly cause disease even in intact immune system

Q: when do endogenous pathogens become bad?
[...]
A: usually due to breach of site where normal flora is found

Q: which type of bacteria have endotoxins (LPS)?
[...]
A: G- bacteria

Q: how do bacterial capsules increase virulence?
[...]
A: by disabling phagocytosis

Q: why do we have to inoculate against the common flu every year?
[...]
A: b/c of antigen drift (minor) or shift (major)

Q: how to differentiate btw hepatocellular and cholestatic liver disease based on ALT, AST, and ALP?
hepatocellular: [...]
cholestatic: [...]
A: ALT or AST > ALP; ALP > ALT or AST

Q: what ALT lvls are considered mild / moderate / severe lvls of hepatocellular liver disease?
[...]
A: mild is ALT < 5xULN, moderate is 5-15xULN, severe is >15x ULN

Q: what tests to order if you suspect viral or metabolic causes of chronic liver disease?
[...]
A: HBsAg, anti-HCV; glucose, lipids, IgA

Q: what tests to order if you suspect viral or genetic causes of chronic liver disease?
[...]
A: Fe/TIBC (HH), A1AT, ceruloplasmin (Wilson's)

Q: what tests to order if you suspect viral or immune causes of chronic liver disease?
[...]
A: AIH: ANA, ASMA, IgG; PBC: AMA, IgM

Q: what are the best 2 tests for sickle cell anemia?
[...]
A: CBC + PBC (best initial test) and Hb electrophoresis

Q: how to manage chronic SCD that doesn't respond well to hydroxyurea?
[...]
A: chronic transfusion therapy (w/ chelation) and folic acid supplementation to prev macrocytic anemia

Q: is this a benign or malignant ulcer?
[...]
A: benign (flat edges)

Q: is this a benign or malignant ulcer?
[...]
A: malignant (heaped up edges)

Q: what cell types do you expect to see w/ malignant ulcers?
[...]
A: signet ring cells (diffuse) and intestinal cells (glands)

how do these 4 features of H. pylori linked to virulence?
1. urease: elevates local gastric pH to enhance survival
2. adhesins: increased adherence to gastric epithelium
3. toxins: involved in ulcer or cancer dev
4. flagella provides motility in viscous mucus

Q: what are the gross diffs btw Crohn's disease and ulcerative colitis?
[...]
A: Crohn's has transmural inflamm + fissures whereas ulcers usually eat away at least to the submucosa (also more continuous colonic involvement beginning at rectum)

Q: what is the main ddx?
[...]
A: Crohn's disease
Extra: mucosa w/ skip alternative lesion of normal and inflamed mucosa; sharp areas of transition btw inflamed and uninflamed mucosa (aka fistula formation)

Q: what is the issue in terms of colonoscopy w/ colitis-associated neoplasia?
[...]
A: many areas of dysplasia are flat, making them difficult to identify (soln: high resolution imaging)

Q: which of the bottom two adenomatous polyps should you be more worried about?
[...]
A: right side b/c it's more villous
Extra: LHS = tubular (neoplastic growth), RHS = villous (more advanced lesions)

Q: what is this?
[...]
A: tubular adenoma
Extra: usually pedunculated; usually low grade dsyplasia; bigger = more dysplastic = more likely to precede carcinoma

Q: where in bowel does celiac disease damage?
[...]
A: mucosa of duodenum and jejunum

Q: how does gluten sensitivity in celiac disease cause mucosal damage?
1. [...]
2. [...]
A: increases lymphocyte infiltration (inflamm); loss or blunting of villi (decreased ability to absorb nutrients)

Q: which two genes predispose ppl to celiac disease?
[...]
A: HLA DQ2 and DQ8
Extra: tTG is an intracellular enzyme released from epithelial cells as a result of inflammation or mechanical irritation. It also functions as an antigen. The detection of tTG is central to the diagnosis of celiac disease.

Q: what histological feature is a hallmark of celiac disease?
[...]
A: hyperplastic crypts

Q: what are 2 major presentations of celiac disease?
1. [...]
2. [...]
A: maldigestion; malabsorption
Extra: complications include anemia (Fe deficiency common; folate, B12 deficiency infrequent), osteoporosis (vit D deficiency, Ca), malnutrition (growth retardation), and risk of cancer (lymphoma, GI malignancies)
alopecia (hair loss) observed in ~1% of recently diagnosed CD in children

Q: what is main tx for celiac disease?
[...]
A: gluten free diet (forever) and fix any complications arising
Extra: most improve in 2 weeks; 1/3 of pts have persistent sx; 5% fail to improve after 2 years (refractory CD is rare)

Q: where is lower GI bleeding usually found?
[...]
A: distal to ileocecal valve (colonic)

Q: where is mid-gut bleeding usually found?
[...]
A: distal to ligament of Treitz and proximal to ileocecal valve (small bowel)

Q: when should you suspect LGIB instead of UGIB?
[...]
A: bright red blood (hematochezia, no hematemesis or coffee ground emesis)

Q: what should you investigate in physical for suspected LGIB?
[...]
A: hemodynamic stability, ab tenderness, masses, digital rectal exam

Q: how to investigate LGIB?
[...]
A: CBC, electrolytes, coagulation (INR, PTT), blood type & screen/x-match

Q: what are common causes of perianal bleeding?
[...]
A: hemorrhoids or fissures

Q: where are most diverticular bleeds found?
[...]
A: sigmoid colon

Q: how to tx diverticular bleed?
[...]
A: endoscopically via clips, injection, cautery, band ligation

Q: what is a common presentation of IBD?
[...]
A: chronic bloody diarrhea; red/maroon blood, clots, mucous

Q: 24M w/ few episodes of painless BRBPR in past month. Assoc w/ harder stools and straining during defecation. Bleeding is small V and apparent on tissue paper; not mixed in w/ stool. Healthy otherwise. DRE reveals small internal hemorrhoids. Recent labs show normal Hb, electrolytes, renal fn, TSH, HbA1c. What is the next most appropriate management step?
[...]
A: conservative therapy and reassurance
Extra: BRBPR = minimal bright red blood per rectum

Q: 74M w/ several painless BRBPR in past 3 months. Assoc w/ looser stools and straining during defecation. Bleeding is small volume and mixed in w/ stool. 20-lb weight loss over last year. No FHx of IBC/CRC. Vital signs stable. DRE reveals small internal hemorrhoids. Recent labs show microcytic anemia. CT shows annular mass in rectosigmoid colon w/ multiple hepatic lesions concerning for metastatic disease. What is next most appropriate management step?
[...]
A: flexible sigmoidoscopy w/ biopsy
Extra: stage 4 cancer; tx attempts likely palliative (very sad case)
BRBPR = minimal bright red blood per rectum

Q: 74M w/ several episodes of painless hematochezia over 2 days. Bleeding is large volume, bright red, and maroon. No FHx IBD/CRC. Vital signs initially demonstrate tachycardia and hypotension, but have normalized after IV saline. DRE reveals maroon clots. Recent labs demonstrate normocytic anemia, Hb down to 110 from 150 one years ago. Prior colonoscopy demonstrated low-risk adenoma, resected, and sigmoid diverticulosis. What is next most appropriate management step?
[...]
A: colonoscopy ± endoscopic hemostasis
Extra: likely bleeding diverticulitis given maroon clots and likely LGIB

Q: what is the most common GI disease requiring acute admission to hospital?
[...]
A: acute pancreatitis (34/100k)

Q: how to dx acute pancreatitis?
[...]
A: upper ab pain; serum amylase or lipase ≥3X upper normal limit; imaging confirmation

Q: how does acute pancreatitis present?
[...]
A: epigastric pain radiating to back (max intensity 10-20 min)

Q: what is the pathophys of acute pancreatitis?
[...]
A: XS trypsin in acinar cells catalyzing conversion of digestive enzymes and activating complement + kinin systems

Q: which duct in this figure is blocked in biliary pancreatitis?
[...]
A: pancreatic duct (6)
Extra: reflux of bile back into PD; obstruction of PD at ampulla from stones; edema resulting from passage of stone

Q: what labs to order to investigate acute pancreatitis?
[...]
A: CBC, liver panel (ALT, AST, bili, ALP), serum Ca, serum TG

Q: what are the following defs?
- mild acute pancreatitis: [...]
- moderately severe acute pancreatitis: [...]
- severe acute pancreatitis: [...]
A: no local or systemic complications and organ failure (transient, corrects w/ fluid lvl normalization); local or systemic complications; transient organ failure (<48 h); local or systemic complications, persistent single or multiple organ failure (>48 h)

Q: what is initial tx in acute pancreatitis?
[...]
A: fluid resuscitation (5-10 mL/kg/h until hr < 120 bpm, MAP btw 65-85 mmHg, urinary o/p > 0.5-1.0 mL/kg/h, Ringer's lactate) and nutrition

Q: what are the 3 main forms of chronic pancreatitis?
1. [...]
2. [...]
3. [...]
A: chronic calcific pancreatitis; chronic obstructive pancreatitis (asymptomatic); chronic autoimmune pancreatitis (steroid-responsive pancreatitis)

Q: what are the major risk factors for chronic pancreatitis?
1. [...]
2. [...]
3. PRSS1 mutation
A: EtOH (5 drinks/day for 5-10 yrs); tobacco (usually >1 PPD)
Extra: PRSS1 mutation leads to premature trypsinogen activation or by failure to inactive trypsin during inflammation process (autosomal dominant w/ high penetration rate)

Q: what are the imaging steps to take to ix chronic pancreatitis?
[...]
A: CT imaging to MRI to endoscopic u/s
Extra: classic finding: pancreatitic duct dilitation, calcification, parenchymal atrophy
other findings: enlarging pancreas, normal pancreas (~7%)
CT can also detect related complications including pseudocysts, portosplenic vein thrombosis, pseudoaneurysm, fistulas

Q: what is mgmt for chronic pancreatitis?
[...]
A: abstain from alcohol + smoking; if stones present consider lithotripsy

Q: what are potential dx for cholestasis w/ dilated bile ducts?
[...]
A: CBD stone, biliary stricture, PSC, worms, malignancy
Extra: PSC = primary sclerosing cholangitis
look for IgM and p-ANCA = perinuclear anti-neutrophil cytoplasmic antibody

Q: what is MRCP?
[...]
A: T2 weighted scan to look at biliary system
Extra: MRCP = MR cholangio-pancreatography
non-invasive and only diagnostic

Q: what does ERCP do?
[...]
A: side-viewing endoscope is inserted into the duodenum and contrast is injected via the ampulla of Vater into the bile ducts
Extra: ERCP = endoscopic retrograde cholangio-pancreatography
Different instruments can then be introduced via the endoscope to cannulate the common bile duct. If necessary, a sphincterotomy of the ampulla of Vater or removal of gallstones from the common bile duct can also be performed.

Q: why should black gallstones cause concern?
[...]
A: b/c it indicates hemolysis and cirrhosis
Extra: risk factors for cholsterol gallstones = 7 Fs
7 Fs: Female, Fertility, Fifty, Family, Fat, Fasting, Pharmacology

Q: when should you rm gallstones?
[...]
A: only when there are sx or complications (use laparoscopic cholecystectomy)

Q: where is IBD related to PSC usually localized to?
[...]
A: caecum (RHS)

Q: why is symptomatic PSC scary?
[...]
A: b/c we have no effective therapy

Q: what is cholangioCA called if found in region 2?
[...]
A: perihilar (pCCA)

Q: how to dx and tx PSC?
[...]
A: MRCP ± EUS for dx; ERCP for tx

Q: how to dx PBC after increase in ALP and u/s?
[...]
A: AMA (present in 95%), ANA, ASMA
Extra: PBC = primary biliary cholangitis

Q: what is tx for PBC?
[...]
A: UDCA 13-15 mg/kg once daily
Extra: do NOT EVER take it w/ PSC b/c clinical trials indicate higher mortality vs placebo
UCDA is a bile acid that inhibits intestinal absorption of cholesterol and reduces hepatic synthesis and secretion of endogenous cholesterol. Can be used to treat primary biliary cholangitis because of its antiapoptotic and immunomodulatory effects. Also used for nonsurgical treatment of cholesterol gallstones.

Q: what are the most common causes of intrahepatic cholestasis?
[...]
A: drugs, viral hepatitis, sepsis (#1 cause in hospitals)
Extra: infiltrative causes include sarcoidosis, amyloidosis, malignancy, and granulomatous hepatitis
congenital causes include biliary atresia, Alagille syndrome, PFIC
pregnancy can also cause intrahepatic cholestasis (3rd trimester, intense pruritis; ALT > ALP; increased bile acids; stillbirth risk; mgmt w/ UCDA and cholestyramine w/ vit K b4 delivery)

Q: what should you immediately think of when you see pruritis and excoriations?
[...]
A: chronic cholestasis
Extra: excoriations = chronic skin-picking or dermatillomania

Q: how to manage pruritis 1st line?
[...]
A: antihistamines and cholestyramine separated from other meds w/ 2 hr window

Q: what is dx and tx pathway for PBC?
[...]
A: AMA; if +ve tx w/ UDCA

Q: what is dx and tx pathway for PSC?
[...]
A: MRCP to dx; if normal, biopsy; no therapy (super scary if symptomatic)

what are the main risk factors for MAFLD?
1. obesity
2. DM
3. dyslipidemia
4. hypertension
Extra: MAFLD = metabolic associated fatty liver disease

Q: what will ALT be in pts w/ MAFLD?
[...]
A: mild w/ ALT < 5xULN
Extra: ensure to screen for chronic liver disease!

Q: how to manage MAFLD?
[...]
A: diet and exercise and avoidance of XS EtOH; statins good if pt has hyperlipidemia

Q: what are common clinical presentations of alcohol related liver disease?
1. [...]
2. [...]
3. [...]
A: steatosis and steatohepatitis; fibrosis progressing to cirrhosis; alcoholic hepatitis

Q: how to tx severe cases of alcoholic hepatitis?
[...]
A: prednisone 40 mg daily and reasses Lille score at day 4 or 7

Q: when to suspect thalassemia for blood and liver ix?
[...]
A: low MCV (<75) and normal ferritin

Q: what is HbE?
[...]
A: thalassemia-like hemoglobinopathy due to beta chain mutation (common in SE Asia)

Q: what is the triad for hemolytic anemia?
[...]
A: anemia, jaundice, splenomegaly (EXCEPT in SCD, no splenomegaly)

Q: why do babies w/ beta thalassemia major present w/ sx ~6 months post-birth and not immediately?
[...]
A: b/c HbF carries O2 for first ~6 months

Q: what counts as acute and chronic fever?
[...]
A: <7 days is acute and >14 days is chronic

Q: what are some anti-pyretics?
[...]
A: acetaminophen (Tylenol), ASA, ibuprofen, corticosteroids

Q: what causes rigors?
[...]
A: PGE2 on peripheral nerves

Q: how to test for mycobacterium species?
[...]
A: by using acid fast stains

Q: how long do bacterial cultures usually take for dx?
[...]
A: 18-48 hr; for mycobacteria: 10 d - 7 wks

Q: what are the 3 breakpnts in MIC?
[...]
A: susceptible, resistant, or intermediate
Extra: MIC = minimum inhibitory concentration

Remarks: order IgM and IgG for active infections
order only IgG for immunity/past exposure

Q: what are the 2 plexi for the enteric NS?
[...]
A: Auerbach's for myenteric plexus and Meissner's for submucosal plexus

Q: how many contractions/min would you expect to see in small intestine?
[...]
A: 8/min

Q: what are the 2 chemicals directly involved in peristalsis?
[...]
A: ACh for contraction and NO for relaxation; 5-HT to coordinate peristalsis

Q: which cells (other than muscle and motor neurons) would you expect to see damaged if peristalsis didn't work?
[...]
A: enterochromaffin cells

Q: what is the main diff btw splanchic mechanoreceptors and vagal+pelvic mechanoreceptors?
[...]
A: splanchic encode mainly noxious events whereas the other 2 encode mainly physiological events

Q: how would you expect pain to present btw visceral vs parietal peritoneum
[...]
A: visceral is dull and poorly localized whereas parietal is more intense and precisely located

Q: what stimuli can stomachs feel and not feel?
[...]
A: can feel distention & contraction but not cutting or burning

Q: what is hyperalgesia?
[...]
A: exaggerated algesic response to noxious stimulus

Q: what is allodynia?
[...]
A: innocuous stimulus perceived as noxious stimulus

what should you immediately suspect if ALT is in the "1000s club"?
1. viral, drugs, WD
2. pregnancy
3. AI
4. ischemia

Q: what condition should you check for if you see increased INR w/ suspected liver disease?
[...]
A: check for encephalopathy b/c it could indicate ALF
Extra: ALF = acute liver failure

Q: how does alcohol use affect drug toxicity w/ acetaminophen?
[...]
A: EtOH causes increased activity of CYP2E1 and decreases glutathione activity, which leads to more NAPQI (toxic) and thus liver injury

Q: what tests would you order if you suspect AI liver disease?
[...]
A: ANA, ASMA, IgG
Extra: ASMA found in the majority of cases of severe hepatocellular hepatitis

Q: what to suspect if HBsAg is -ve, anti-HBs is +ve, and anti-HBc is -ve?
[...]
A: the person is vaccinated against HBV

Q: what to suspect if HBsAg is -ve, anti-HBs is +ve, and anti-HBc is +ve?
[...]
A: the person has had past infection
Extra: HBc: core of HBV; must have seen live virus to be +ve

Q: what to suspect if HBsAg is +ve, anti-HBs is -ve, and anti-HBc is +ve?
[...]
A: the person has acute or chronic HBV infection
Extra: HBc: core of HBV; must have seen live virus to be +ve
HBs: "shield" (immunity)

Q: what to suspect if HBsAg is +ve, anti-HBs is -ve, and anti-HBc IgM is +ve?
[...]
A: the person has acute HBV infection
Extra: HBc: core of HBV; must have seen live virus to be +ve
HBs: "shield" (immunity)

Q: what to suspect if HBsAg is +ve, anti-HBs is -ve, and anti-HBc IgG is +ve?
[...]
A: the person has chronic HBV infection
Extra: HBc: core of HBV; must have seen live virus to be +ve
HBs: "shield" (immunity)

Q: what does person have if anti-HAV is +ve?
[...]
A: acute HAV infection

Q: what should you expect in pre-hepatic jaundice w/ increased bili production?
[...]
A: hemolysis, ineffective erythropoiesis, hematoma

Q: what should you expect in pre-hepatic jaundice w/ decreased hepatic bili uptake?
[...]
A: sepsis and drugs

Q: what is next step in ddx formulation in cases of hepatic jaundice?
[...]
A: go to the elevated liver enzymes scheme (investigate w/ liver panel)

Q: 78M w/ hx of alcoholism. What is his Hb and MCV likely going to be?
[...]
A: Hb low and MCV high (macrocytic)

Q: what does anti-HBc +ve indicate?
[...]
A: exposure to HBV (IgM = acute, total = active/cleared infection)

Q: what does HBsAg +ve indicate?
[...]
A: acute OR chronic HBV infection

Q: where is HBV common?
[...]
A: South Africa and SE Asia (also in territories + Greenland)

Q: what sx does EBV have (mono)?
[...]
A: sore throat, mild hep w/ self-limited jaundice

Q: what are sx of CMV?
[...]
A: fever, malaise, cholestatic hepatitis

Q: in which phases do we tx chronic HBV?
[...]
A: if HBVDNA elevated and there is evidence of liver inflamm/fibrosis (phase 2 or 4)

Q: what is a helpful tx for pts w/ MAFLD?
[...]
A: statins and fibrates

Q: who should we avoid prescribing Tylenol in pts w/ liver disease?
[...]
A: pts actively misusing alcohol

Q: what should you suspect if you see hepatitis, cirrhosis, HCC, joint arthritis, bronze skin, and diabetes?
[...]
A: hemachromatosis

Q: how to screen for HH?
[...]
A: transferrin saturation ≥ 45% and ferritin > 1000 ng/mL fasting

Q: how to manage HH?
[...]
A: phlebotomy (500 mL every 1-2 weeks until ferritin < 50 g/L)

Q: how to test for WD?
[...]
A: check for low ceruloplasmin
Extra: can check for KF rings on slit lamp exam, raised 24 h urine copper (>40 ug/day)

Q: what is tx for A1AT deficiency?
[...]
A: avoid smoking and alcohol (no effective tx)

Q: how might ischemia arise in ALF?
[...]
A: shock liver and Budd-Chiari syndrome

Q: which pathway does PTT and PT/INR measure?
[...]
A: PTT measures intrinsic whereas PT/INR measures extrinsic
Extra: PTT = play table tennis = inside = intrinsic
PT = play tennis = outside = extrinsic

Q: what does thrombin time measure?
[...]
A: conversion of fibrinogen to fibrin

Q: what are clinical features of thrombocytopenia?
[...]
A: prolonged bleeding after trauma and petechial rash

Q: who is mostly affected in (1) acute and (2) chronic ITP?
[...]
A: acute is usually children whereas chronic is usually adults
Extra: ITP = immune thrombocytopenic purpura
low platelets

Q: how to tx ITP?
[...]
A: supportive care and (if severe bleeding) steroids + IVIG

Q: what does PT assess?
[...]
A: F7 and common pathway factors (5, 10, 2, fibrinogen)

Q: what does a long PT w/ sufficient vit K indicate?
[...]
A: congenital clotting factor deficiency (F7 deficiency), liver disease

Q: what does a long PT w/ insufficient vit K indicate?
[...]
A: vit K antagonist (e.g., Warfarin)

how might one be deficient in vitamin K?
1. dietary deficiency (lack of green veggies)
2. high doses of vit A and E
3. fat malabsorption
4. acquired deficiency (Abx, warfarin)
5. impared gut flora

Q: what does aPTT measure?
[...]
A: time it takes to produce fibrin polymers after adding phospholipids

Q: where is VWF synthesized?
[...]
A: vascular endothelium and bone marrow megakaryocytes

Q: how to dx VWD?
[...]
A: check for reductions in VWF activity and VWF antigen, low F8

Q: how to manage VWD?
[...]
A: DDAVP to increase plasma conc of VWF; VWF concentrates; use meds to promote hemostasis
Extra: DDAVP = synthetic vasopressin (antidiuretic hormone) analog used for a number of conditions, including central diabetes insipidus, nocturnal enuresis, von Willebrand disease types 1 and 2, and mild hemophilia A.

Q: which chromosome would be affected if someone has hemophilia?
[...]
A: X chromosome
Extra: thus, men are more likely to be hemophilic than women

Q: how to manage hemophilia?
[...]
A: prev bleeding, LT mngmt of joint and muscle damage
Extra: can give desmopressin (DDAVP) for hemophilia A

Q: how to tx hemophilia A?
[...]
A: DDAVP to increase F8 lvls from baseline

Q: what are sx of Gilbert syndrome?
[...]
A: hemolysis, ineffective erythropoiesis, sepsis
Extra: Inherited metabolic disease in which the intrahepatic conjugation of bilirubin and glucuronic acid is impaired. Often presents as mild jaundice during times of stress (e.g. sickness, overexertion, dehydration, etc.) and causes unconjugated hyperbilirubinemia. Most cases are asymptomatic or mild and do not require treatment.

Q: why should you order GGT alongside ALP, AST, and ALT?
[...]
A: to rule out bone src when you suspect the disease is liver or cholestatic related

Q: how to dx PBC?
[...]
A: increased AMA, IgM, and ALT

Q: how to dx PSC?
[...]
A: increased ALP, GGT; MRCP

Q: how to check for cirrhosis?
[...]
A: use FibroScan
Extra: An ultrasonographic technique that determines liver stiffness. Used as diagnostic tool for early diagnosis of liver fibrosis and progression to liver cirrhosis.
fibroscan = transient elastography
CSPH = clinically significant portal htn
TE ≤ 15 kPa and platelets ≥ 150 rules out CSPH
TE ≥ 25 kPa rules in CSPH

Q: when is cholecystectomy indicated?
[...]
A: blockage of bile ducts (e.g., relating to pancreatitis, cholecystitis, biliatresia)

Q: what are sx of hepatic insufficiency on physical?
[...]
A: jaundice, muscle wasting, ascites, metabolic bone disease, Terry's nails, bruising, edema

Q: what are sx of hyperestrogenism on physical for stigmata of chronic liver disease?
[...]
A: gynecomastia, altered hair dist'n, spider nevi, palmar erythema, testicular atrophy

Q: what are sx of portal hypertension on physical for stigmata of chronic liver disease?
[...]
A: encephalopathy, varices, splenomegaly, caput medusae, ascites, clubbing, edema

Q: A 47 year old female presents to the ER with a 5 day history of nausea, abdominal pain, and bloody diarrhea. Previously well with baseline normal bowel habit and no prior GI bleeding. No constitutional symptoms. No family history of IBD or CRC. Medication(s): Clindamycin for recent dental procedure. Allergies: Penicillin. The abdomen is quite tender to palpation. DRE reveals blood-stained stool.
- HGB 112 (Low)
- WBC 28.6 (Very high)
- PLT 554 (High)
What is most likely ddx?
[...]
A: infectious colitis
Extra: notice very high WBC count and recent Abx use

Q: A 57 year old obese male presents to the family medicine clinic for a prescheduled periodic visit. On review of systems, the patient admits to a 1 year history of intermittent bright red blood per rectum (BRBPR). There is no associated pain with the bleeding, and it is small in volume and typically seen in the toilet and/or on the tissue with wiping. Normal bowel movements otherwise. They were never concerned about this as they presumed the bleeding was due to hemorrhoids. There has been no significant unintentional weight loss, night sweats, or unexplained fevers. What is most appropriate next step?
[...]
A: DRE

Q: what happens in DIC?
[...]
A: both thrombosis AND bleeding (b/c of coag factors being used up in one part of body so other parts can't form clots)
Extra: decreased platelets and fibrinogen; massive TF activation
increased PT and PTT (reflects low circulating coagulation factors)
increased D-dimer (fibrin degradation product)

Q: what should you immediately suspect if you see thrombocytopenia, elevated D-dimer, increased PT and aPTT, and low fibrinogen?
[...]
A: DIC

Q: A previously healthy 38-year-old woman is brought to the emergency department by her husband because of left-sided weakness for the past 4 hours. As she was getting dressed this morning, she was suddenly unable to button up her shirt. When she showed her husband, he noticed that she was confused. She has a 3-year history of diabetes mellitus, for which she takes metformin. She had a knee operation 1 month ago. Her temperature is 38.9°C (102°F), pulse is 98/min, respirations are 17/min, and blood pressure is 138/85 mm Hg. She is confused and oriented only to person. Neurologic examination shows diminished muscle strength on the left side. There are scattered petechiae over the chest, arms, and legs. A peripheral smear shows numerous schistocytes. Further evaluation is most likely to show which finding in the serum test?
[...]
A: decreased ADAMTS13 activity in serum
Extra: This patient has the classic constellation of findings found in thrombotic thrombocytopenic purpura (TTP): neurologic abnormalities (likely TIA or stroke, confusion), fever, impaired renal function (increased BUN and creatinine), microangiopathic hemolytic anemia (decreased hemoglobin, elevated LDH and indirect bilirubin, schistocytes), and thrombocytopenia.

Q: what is the classic pentad in TTP?
[...]
A: neurological sx, fever, renal fn impairment, MAHA, thrombocytopenia
Extra: Nasty Fever Ruined My Tubes: neurological, fever, renal fn impairment, MAHA, thrombocytopenia

Q: what is diff btw acute and chronic diarrhea?
[...]
A: acute is <3 wks whereas chronic is >3 months

Q: what is ix for acute diarrhea?
[...]
A: CBC, stools, sigmoidoscopy

Q: how to tx mild/moderate CDI?
[...]
A: 1st line vancomycin; 2nd line fidaxomicin and metronidazole

Q: how to tx severe CDI?
[...]
A: vancomycin or fidaxomicin

Q: large V diarrhea in the small bowel; what is likely ddx?
[...]
A: celiac disease

Q: small V bloody diarrhea in the large bowel; what is likely ddx?
[...]
A: ulcerative colitis

Q: what is on ddx for high PTT, normal PT, and bleeding?
[...]
A: VWD, deficiency in F8, F9, F11
Extra: [$] \frac{10a}{5a} = \frac{2a}{1a} [/$]

Q: what is inheritance pattern of F8 deficiency and VWD?
[...]
A: F8 deficiency is X-linked whereas VWD is autosomal dominant

Q: what are ddx for high PTT, normal PT, no bleeding?
[...]
A: APL, F12 deficiency, HMWK deficiency, PK deficiency
Extra: HMWK = high molecular weight kininogen
PK = pre-kallikrein

Q: what are clinical features of APL?
[...]
A: arterial/venous thrombosis
Extra: APL = antiphospholipid syndrome

Q: what does high PTT, high PT, +ve D-dimer, and low fibrinogen indicate?
[...]
A: DIC w/ low platelets and schistocytes

Q: what does high PTT, high PT, +ve D-dimer, and high fibrinogen indicate?
[...]
A: liver disease w/ coagulopathy w/o DIC

Q: what is PBC?
[...]
A: granulomatous inflamm of small intrahepatic bile ducts
Extra: look for AMA and IgM

Q: what is PSC?
[...]
A: hardening of tissue and inflamm of bile ducts (both intra and extrahepatic)

Q: what is on ddx w/ spherocytes on PBS?
[...]
A: hereditary spherocytosis, AIHA, hemolytic transfusion rxn

Q: when is ERCP contraindicated in cholestatic causes of liver disease?
[...]
A: if common bile duct not dilated

Q: what type of bacterium is C. difficile?
[...]
A: anaerobic G+ bacilli
Extra: spore-forming
observed as part of intestinal flora in newborns (85%)
5-15% healthy adults are colonized w/ C. diff

Q: what is ix for C. diff?
[...]
A: liquid stools: NAAT (e.g., PCR), toxin A + B (ELISA), cultures
Extra: prevention: soap + water > alcohol
1st line: vancomycin 125 mg PO QID x10-14 days
2nd line: fidaxomicin 200 mg PO BID x10 days or metranidazole 500 mg PO TID x10-14 days

Q: what should you think when you see Rouleaux formation?
[...]
A: multiple myeloma
Extra: CRAB: hypercalcemia, renal, anemia, bone pain
A type of macrocytic anemia characterized by large, nucleated red blood cell precursors that contain uncondensed chromatin. Caused by inhibition of DNA synthesis (e.g., from vitamin B12 or folic acid deficiency) that results in G2 cell cycle arrest, which leads to relatively immature nuclei compared to the cytoplasm. Associated with hypersegmented neutrophils.

Q: what is dx if you see spherocytes and have +ve DAT?
[...]
A: AIHA (cold or warm)

Q: what is dx if you see spherocytes and have -ve DAT?
[...]
A: hereditary spherocytosis

Q: what is dx if you see schistocytes and decreased platelets?
[...]
A: MAHA (DIC, HUS, TTP)

Q: what does macrocytic anemia w/ hypersegmented neutrophils suggest if B12 and folate lvls are normal?
[...]
A: megaloblastic anemia
Extra: A type of macrocytic anemia characterized by large, nucleated red blood cell precursors that contain uncondensed chromatin. Caused by inhibition of DNA synthesis (e.g., from vitamin B12 or folic acid deficiency) that results in G2 cell cycle arrest, which leads to relatively immature nuclei compared to the cytoplasm. Associated with hypersegmented neutrophils.

Q: 75M w/ s/p chemoradiation for lung cancer presents w/ pancytopenia (HgB 73). RI < 2% (0.2%) and MCV 85 fl. Ferritin, transferrin sat, folate, B12, TFT, CMP all normal. Bone marrow biopsy (below) + high EPO. What is dx?
[...]
A: aplastic anemia

Q: what molecules to check for hemolysis w/ RI > 2%?
[...]
A: increased LDH, decreased haptoglobin, increased bili
Extra: haptoglobin wants to bind all free Hb
look for spleen or liver disease

Q: how to differentiate btw warm and cold AIHA after +ve DAT (Coombs+)?
[...]
A: warm has +ve IgG and complement whereas cold is just +ve complement (-ve IgG)

Q: 35M Mediterannean man has increased LDH and decreased haptoglobin. He has eaten fava beans for lunch. He is -ve on the DAT and his PBS shows bite cells and Heinz bodies. What is likely ddx?
[...]
A: G6PD deficiency
Extra: G6PD deficiency is x-linked recessive. G6PD is rate-limited enzyme of pentose phosphate pathway, which yields NADPH, which is essential for converting oxidized glutathione back to its reduced form. Reduced glutathione is capable of neutralizing reactive oxygen species (ROS) and free radicals and therefore protecting RBCs from oxidative damage. In the absence of reduced glutathione (e.g., due to G6PD deficiency), RBCs become susceptible to oxidative stress that can damage erythrocyte membranes, resulting in intravascular and extravascular hemolysis.

Q: 35M African has -ve DAT and has schistocytes and helmet cells in the PBS. What is likely ddx?
[...]
A: MAHA (any of DIC, TTP, HUS, HELLP, mechanical valve)

Q: 44F w/ PMHx of Budd-Chiari syndrome and dark urine in morning presents w/ Hg of 105. RI is 2.5%, LDH is high, haptoglobin low, and indirect bili high. DAT is -ve and the PBS is unrevealing. Flow cytometry is +ve. What is likely ddx?
[...]
A: PNH
Extra: paroxysmal nocturnal hemoglobinuria (sometimes can see spherocytes)

Q: in which hep B stages is ALT measurably high?
[...]
A: stage 2 and 4 (immune clearance + reactivation)

Q: in which hep B stage does HBsAg turn -ve and anti-HBs is +ve?
[...]
A: stage 4 to 5 (natural immunity)

Q: in which hep B stage does HBeAg turn -ve and anti-HBe is +ve?
[...]
A: from stage 2 (immune clearance) to stage 3 (inactive residual)

Q: 55 year old female originally from Vietnam presents with lymphoma. The oncologist want to start chemotherapy with Rituximab (anti-CD20). Pt is in stage 5 of HBV infection. What is tx?
[...]
A: start lamivudine/entecavir/tenofovir and frequently observe ALT, HBsAg, HBVDNA

Q: Pt has celiac disease and begins a gluten-free diet. 3 months later, patient returns to clinic, and although her GI symptoms have dramatically improved, her skin lesions have persisted. How to manage her dermatitis herpeteformis?
[...]
A: prescribe dapsone
Extra: Improvement in dermatitis herpetiformis (DH) following withdrawal of gluten from diet intake can be considerably delayed (6-12 months) compared to the gastrointestinal manifestations of Celiac disease. In these cases, treatment with sulfones (such as Dapsone) in addition to gluten avoidance may be necessary to achieve rapid control.

Q: Given pt clinical presentation and strong family history, you suspect a diagnosis of Celiac disease. In addition to anti-tissue transglutaminase antibodies (tTG), which other test is required to screen for Celiac disease?
[...]
A: IgA levels

Q: what are some common meds to prevent or stop bleeding in VWD?
[...]
A: desmopressin, replacement therapy w/ VWF concentrates, antifibrinolytic drugs

Q: which factors are deficient in hemophilia A and B?
[...]
A: A: F8; B: F9

Q: what are the 2 most common causes of acute pancreatitis?
[...]
A: alcohol and gallstones (blocking sphincter of Oddi; most common cause)

Q: what should you immediately think if you see grey Turner's sign, Cullen's sign, nausea, and vomiting?
[...]
A: acute pancreatitis

Q: what is diff in sx btw HUS and TTP?
[...]
A: HUS has no fever AND has shiga toxin + normal ADAMTS13

Q: how to tx HUS?
[...]
A: supportive care and hemodialysis

Q: how to tx HELLP syndrome?
[...]
A: delivery of baby

Q: how to tx DIC?
[...]
A: platelet transfusion if plt ≤ 50, frozen plasma if aPTT ≥ 1.5 ULN, cryoprecipitate if fibrinogen < 1.5 g/L

Q: why might you see bleeding diseases w/ cirrhosis?
[...]
A: b/c all clotting factors except F3 and VWF are synthesized by the liver

Q: what initial ix to take for jaundice?
[...]
A: CBC w/ bili; ALT, AST, ALP, GGT; albumin, INR

Q: what ix to take for unconjugated bili in jaundice?
[...]
A: hemolytic anemia tests (DAT, haptoglobin, LDH, retic, PBS, enzyme studies)

Q: what ix to take for conjugated bili in jaundice?
[...]
A: hepatocellular ix (viral, AIH tests, ceruloplasmin, etc.)

Q: what is tx for physiological jaundice of the newborn?
[...]
A: phototherapy

Q: what is the Rome IV criteria for IBS?
[...]
A: recurrent ab pain ≥1 day/wk in last 3 months assoc with ≥2 of: change in stool frequency, change in stool form, defecation-related changes

Q: how to tx IBS?
[...]
A: 20-35 g of fibre daily & FODMAPs diet
Extra: FODMAPs = diet low in fermentable oligo- di- monosaccharides and polyols

Q: what are common osmotic laxatives to manage constipation?
[...]
A: milk of magnesia, PEG, lactulose

Q: how do stimulant laxatives work?
[...]
A: by stimulating motility thru PG release

Q: which receptors do pro-motility laxatives modulate?
[...]
A: 5-HT_4 receptors

Q: how to tx diarrhea?
[...]
A: cholestyramine, mu receptor agonists

Q: how do mu receptor agonists work to manage diarrhea?
[...]
A: by decreasing ACh release and stimulating NO release (decreases peristalsis and fluid+electrolyte secretion)

Q: An 83-year-old woman presents to the emergency department for abdominal pain. She was in her usual state of health until approximately 8 hours ago, when she began experiencing a crampy pain in the left lower quadrant of her abdomen. Since the onset of her symptoms, she has vomited twice and has not had a bowel movement. Physical examination reveals a temperature of 38.3°C (100.9°F), pulse of 109/min, and blood pressure of 122/70 mm Hg. Abdominal examination is significant for left lower quadrant tenderness with guarding. Rectal examination is notable for rectal tenderness. A complete blood count reveals a WBC count of 14.1/mm3, hemoglobin level of 13.1 g/dL, and platelet count of 200/mm3. What is the most likely dx?
[...]
A: diverticulitis

Q: A 45-year-old man presents to his primary care physician for recurrent, burning chest pain after meals. His pain worsens when he reclines and improves with over-the-counter antacid tablets. He also reports a sour taste in his mouth and a persistent cough for the past 6 months. He has smoked two packs of cigarettes daily for the past 20 years. His temperature is 37.0°C (98.6°F), pulse is 91/min, and blood pressure is 142/90 mm Hg. He is 175 cm (69 in) tall and weighs 135 kg (298 lb). His physical examination is unremarkable. What is the most likely diagnosis?
[...]
A: GERD

Q: A 25-year-old woman presents to her primary care physician for recurrent abdominal pain. She describes having daily episodes of crampy, lower abdominal pain and diarrhea for the past 6 months. Her diarrhea has occasionally been bloody, and she has experienced an unintentional weight loss of 4.5 kg (10 lb) over the past 3 months. She adds that she had a subjective fever several nights last week. Physical examination reveals a temperature of 37.8°C (100.1°F), pulse of 96/min, and blood pressure of 108/66 mm Hg. She appears thin but is in no acute distress. An abdominal examination reveals diffuse tenderness, and a rectal examination is significant for frank blood. What is the most likely diagnosis?
[...]
A: IBS, likely ulcerative colitis

Q: A 14-year-old girl presents to her pediatrician with abdominal bloating and pain, watery diarrhea, and a blistering rash that has persisted for the past week. The rash is distributed across her elbows and knees. She also notes that over the past week she has unintentionally lost 2.3 kg (5 lb) and seems to bruise easily. She denies any fever, chills, recent camping trips, travel, or change in diet. Physical exam is notable for short stature and delayed puberty. She is at the 40th percentile for height and Tanner Stage I for breast development, and she has not had her first menstrual period. Her abdomen is slightly distended and diffusely tender to palpation. Peritoneal signs are absent. On her lower right leg is a golf ball–size hematoma. Labs are negative for fecal leukocytes and blood. What is the most likely diagnosis?
[...]
A: celiac disease

Q: what lvls of VWF activity and antigen is the cutoff threshold for low VWF?
[...]
A: 30%

Q: Suppose a patient has hx of easy bruising and prolonged bleeding after wisdom teeth extraction. The pt's brother had prolonged bleeding after tonsillectomy and his mother has a hx of easy bruising and menorrhagia. PT, platelets, closure times, and thrombin time are normal. Factor VIII is low. What is the most likely dx?
[...]
A: hemophilia A (followed by VWD)
Extra: A = F8 deficiency, B = F9 deficiency, C = F11 deficiency (C is acquired and very rare)

Q: Pt has normal platelets, normal PT, prolonged aPTT, normal TT, and normal fibrinogen level. What is the most likely bleeding disorder?
[...]
A: hemophilia or VWD

Q: how is the inhibition of platelets by aspirin different than that of other NSAIDs?
[...]
A: aspirin irreversibly binds COX (5-7 days until regeneration) whereas NSAIDs bind reverisbly

Q: Pt has hx of mucocutaneous bleeding, normal platelet count, prolonged closure time, and normal PTT. What is most likely dx?
[...]
A: VWD

Q: Pt has hx of joint and soft tissue bleeding, normal platelet count, prolonged PTT, and normal closure time w/o FHx of hemophilia. What is most likely dx?
[...]
A: F8 deficiency

Q: how to tx ITP?
[...]
A: steroids (prednisone) then rituxumab or TPO-RAs then splenectomy

Q: what are sx of DVT?
[...]
A: leg pain, cramping & heaviness, swelling, discoloration

Q: what are common sx of pulmonary embolism?
[...]
A: pleuritic chest pain, coughing, hypotense, tachycardic, pleural rub

Q: what is Virchow's triad for risk factors of VTE?
[...]
A: hemostasis, hypercoagulable state, issue w/ vessel wall

Q: how to test for pulmonary embolism?
pre-test prob unlikely: [...]
pre-test prob likely: [...]
A: D-dimer to rule out; CTPA or u/s
Extra: CTPA = CT pulmonary angiography

Q: which clotting factors does vitamin K inhibit?
[...]
A: 10, 9, 7, 2, C, S
Extra: 1972 Canada-Soviet meeting (coumadin/Warfarin anticoagulants)

Q: how to tx VTE for the long term?
[...]
A: IV heparin or LMWH for 3 mo then reassess

Q: how to how to stop bleeding due to heparin OD?
[...]
A: give protamine

Q: what is sarcoidosis?
[...]
A: idiopathic, chronic inflammatory disease characterized by the formation of noncaseating granulomas

Q: what are common non-cirrhotic, pre-hepatic causes of portal hypertension?
[...]
A: portal vein thrombosis, splenic vein thrombosis, splenomegaly

Q: what are common non-cirrhotic, intra-hepatic, pre-sinusoidal causes of portal hypertension?
[...]
A: schistosomiasis, PBC, sarcoidosis, NRH, BCS

Q: what is the arrow pointing towards?
[...]
A: abscess
Extra: presents as fever and RUQ pain
GNB/anaerobes can cause biliary strictures and diverticulitis
amoebas can cause colitis

Q: what is this arrow pointing towards?
[...]
A: hemangioma (benign vascular tumour)

Q: how often should you get a colonoscopy, sigmoidoscopy, and FIT?
colonoscopy: [...]
sigmoidoscopy: [...]
FIT: [...]
A: 10 years from 50-75 y/o; 5 years from 50-75 y/o; 2 years from 50-75 y/o
Extra: FIT = fecal immunochemical test

Q: what is the arrow pointing towards?
[...]
A: focal nodular hyperplasia
Extra: Focal nodular hyperplasia is a benign, indolent tumor of the liver that is most commonly seen in women of reproductive age. Typically asymptomatic but can cause nonspecific upper abdominal symptoms when large. Typically appears on imaging as a solitary intraparenchymal mass < 5 cm in size, with or without a central scar. Histopathologic features include benign hepatocytes arranged in nodules separated by fibrous septa that contain aberrant blood vessels.

Q: what are common methods to ix HCC?
[...]
A: u/s, CT, MRI with APHE and PVWO

Q: what are 3 ways to tx liver cancer?
[...]
A: surgical resection, ablation, liver transplant
Extra: 5-year survival 70% for resection and ablation (BCLC stage 0 or A)
5-year recurrence: 70% for resection, >70% for ablation, 10-20% for liver transplant (BCLC stage A or B)

Q: what do TACE and TARE stand for?
[...]
A: TACE = transarterial chemoembolization; TARE = transarterial radioembolization

Q: what is 1st line chemo for HCC?
[...]
A: atezolizumab + bevacizumab OR tremelimumab + durvalumab

Header: what drugs should we use for 1st line palliative care in CCA?

Q: what HVPG counts as CSPH?
[...]
A: HVPG ≥ 10 mmHg

Q: what is primary prophylaxis of variceal bleeding due to portal htn?
[...]
A: carvedilol (beta-blocker) OR banding if intolerant (if recurrent, TIPS)

Q: what are common IV therapies for variceal hemorrhage (emergency!)?
[...]
A: normal saline, ceftriaxone (abx), octreotide, PPI

Q: what does TIPS do?
[...]
A: creates a path for blood to move from portal vein to hepatic vein to decrease portal htn
Extra: TIPS = transjugular intrahepatic portosystemic shunt

Q: what is the primary prophylaxis for gastric varices?
[...]
A: cyanoacrylate (crazy glue) and NSBB to prevent decompensation
Extra: NSBB = non-selective beta blockers

Q: what is a hallmark of PHG on endoscope?
[...]
A: mosaic pattern
Extra: PHG = portal hypertensive gastropathy
GAVE = gastric antral vascular ectasia

Q: what is a hallmark of GAVE on endoscope?
[...]
A: watermelon stomach
Extra: PHG = portal hypertensive gastropathy
GAVE = gastric antral vascular ectasia

Extra 1: BCS = Budd-Chiari syndrome
RHF = right heart failure
transudate = SAAG ≥ 11
exudate = SAAG < 11

Q: how to tx ascites?
[...]
A: Na+ restriction, diuretics, AVOID NSAID

Q: how to manage SBP?
[...]
A: cephalosporin x5 days and IV albumin
Extra: SBP = spontaneous bacterial paritonitis

Q: how to manage hepatic encephalopathy?
[...]
A: lactulose po or enema
Extra: Improves hepatic encephalopathy by decreasing absorption of ammonia in the bowel: lactulose is converted to lactic acid by intestinal flora → acidification in the gut leads to conversion of ammonia (NH3) to ammonium (NH4+) → ammonium is excreted in the feces → decreased blood ammonia concentration → laxative effect

Q: what does the MELD score do?
[...]
A: predict survival after TIPS and used for liver transplant allocation

Q: for which conditions is a liver transplant primarily given to in Canada?
[...]
A: 95% for cirrhosis, 5% for ALF

Q: how to rule out SBP in cases of hepatic encephalopathy?
[...]
A: paracentesis

Q: how to rule out UTI in cases of hepatic encephalopathy?
[...]
A: urinalysis and urine culture

Q: what is rx for ascites?
[...]
A: dual diuretics (spironolactone & furosemide), midodrine, iv albumin

Q: Endoscopy reveals large varices with red markings and severe portal hypertensive gastropathy but no ulcers. How to manage the patient?
[...]
A: banding of varices until obliterated, nadolol (NSBB), abx x7 days
Extra: nadolol is a nonselective beta blocker (both β1 and β2 receptors) without intrinsic sympathomimetic activity

Q: Patient has mild confusion and asterixis. He is afebrile and vital signs are stable. Blood and urine cultures are negative. US shows ascites. He has poor urine output which does not respond to IV albumin challenge. Other than LT assessment and midodrine po, octreotide sc, and albumin IV, what should you do?
[...]
A: give lactulose and order a diagnostic paracentesis
Extra: Lactulose - For hepatic encephalopathy
Midodrine po, octreotide sc, albumin IV - For hepatorenal syndrome
Liver transplant assessment - Many programs require 6 months of abstinence. This would need to be first presentation of alcoholic hepatitis to be considered for LT in some centres (e.g. exceptional pathway for LT in Alberta).
Diagnostic paracentesis should be performed to rule out spontaneous bacterial peritonititis (SBP) as cause of HE and HRS
Note: Platelets and fresh frozen plasma do not need to be given before the paracentisis.
Protein restriction - NEVER PROTEIN RESTRICT CIRRHOTIC PATIENTS

Q: given albumin is 25 g/L and fluid albumin is 5 g/L, what is the grade of ascites?
[...]
A: high b/c 25-5=20 g/L > 11 g/L

Q: given ascites, what PMN count to dx SBP?
[...]
A: PMN >250x10^6/L
Extra: polymorphonuclear leukocyte = PMN

Q: what is dx if DAT is +ve?
[...]
A: cold agglutinin disease
Extra: IgM: "mayhem"
warm agglutinin has IgG and C3 whereas cold is C3 and IgM

Q: Pt has episodic jaundice w/ fasting and illness. The labs return an increased indirect bili with normal LFTs, Hb, and haptoglobin. What is the dx?
[...]
A: Gilbert syndrome
Extra: Gilbert b/c it was caused by instigating factors (fasting and illness)

Q: Pt has high ANA, ASMA, and IgG. What is the next step for ix?
[...]
A: do liver biopsy to check for AIH
Extra: rx: steroids

Q: Pt presents with fever, RUQ pain, and Murphy's sign. What is the dx?
[...]
A: acute cholecystitis

Q: Pt presents with fever, RUQ pain, and jaundice. What is the likely ddx?
[...]
A: acute cholangitis

Q: what platelet cnt is classified as thrombocytosis?
[...]
A: >400x10^9/L

Q: what causes reactive thrombocytosis?
[...]
A: overproduction of pro-inflamm cytokines (IL-1, 6, 11) or TPO

Q: what causes autonomous thrombocytosis?
[...]
A: overproduction of platelets by clonal/neoplastic megakaryocytes

Q: what are sx of thrombocytosis?
[...]
A: vasomotor sx, thrombosis, excessive bleeding

Q: how to ix autonomous thrombocytosis?
[...]
A: peripheral blood testing for presence of JAK-2 mutation, bone marrow biopsy

Q: Pt has a sustained platelet count >450x10^9/L and a bone marrow biopsy showing megakaryocytic proliferation. They do not have PF, PMF, CML, MDS, or myeloid neoplasm. A JAK2 mutation is present and there is no evidence of reactive thrombocytosis. What is the dx?
[...]
A: essential thrombocythemia

Q: how to manage chronic essential thrombocythemia other than lifestyle changes?
[...]
A: ASA and platelet-lowering agents

Q: Pt present with increased red cell mass and elevated hemoglobin levels. They also have a JAK2 gene mutation, splenomegaly, and low EPO. What is the dx?
[...]
A: polycythemia vera
Extra: 98% of patients with polcythemia vera have a mutation in the JAK2 gene (gain of function) → ↑ tyrosine kinase activity → EPO-independent proliferation of the myeloid cell lines → ↑ blood cell mass (erythrocytosis, thrombocytosis, and granulocytosis) → hyperviscosity and slow blood flow → ↑ risk of thrombosis and poor oxygenation.

Q: Pt presents with swelling, pain, redness, and increased warmth in their legs for ~7 days prior to seeing you, the physician. The physical exam reveals edema and dilated superficial leg veins. What is the most likely ddx?
[...]
A: DVT

Q: when to suspect DVT w/ Well's score?
[...]
A: DVT likely if score ≥2 whereas unlikely if ≤1

Q: Pt present with dyspnea, pleuritic chest pain, cough, and palpitations. The physical exam reveals tachypnea, tachycardia, hypotension, and arrythmia. What is the most likely ddx?
[...]
A: pulmonary embolism

Q: what dx imaging modality to use when CTPA is contraindicated in cases of suspected PE?
[...]
A: ventilation perfusion scanning
Extra: CTPA = CT pulmonary angiography; contraindicated in renal insufficiency, contrast allergy, radiation exposure in pregnancy and young pts

Q: what are rx for prophylaxis of VTE?
[...]
A: low dose heparin, LMWH, warfarin, DOACs

Q: what are tx in acute VTE?
[...]
A: immediately administer anticoagulants, give thrombolytic tx (e.g., rTPA), or insert vena cava filter

Q: what are the major components of the the DASH score for VTE?
[...]
A: D-dimer abnormal (2 pts), age > 50 (1 pt), male (1 pt), hormone-assoc VTE (-2 pt)

Q: what is the therapeutic INR range for heparin?
[...]
A: 1.5-2.5

Q: how long does it take for Warfarin to show therapeutic effects?
[...]
A: 4-5 days

Q: how to manage Warfarin induced bleeding after stopping it?
[...]
A: replace vitamin K and give factor replacement

Q: what does colicky pain usually indicate?
[...]
A: an issue w/ a hollow organ

Q: what are common ddx for RUQ pain?
[...]
A: biliary colic, bile duct-related, hepatitis, PUD, ulcer, pancreatitis, cancer

Q: what are common causes of LLQ pain?
[...]
A: diverticulitis, perforated colon, CRC, small bowel obstruction, IBD

Q: what are common causes of RLQ pain?
[...]
A: appendicitis, caecal diverticulitis, perforated colon, CRC, IBD

Q: 28F presents w/ 24h hx of central abdominal pain w/ nausea. There is no vomiting and she had a C-section 3 years ago and is otherwise healthy. The patient is afebrile and is tender in the RLQ w/ voluntary guarding. She is not distended and there are no palpable masses. WBC and electrolytes are normal and u/s reveals a distended blind structure in the pelvis. How should she be managed?
[...]
A: IV abx and laparoscopic appendectomy w/in 6 h of presentation for acute appendicitis

Q: what is a volvulus?
[...]
A: twisted bowel on the mesentery causing intestinal obstruction
Extra: Volvulus is defined as the twisting of a loop of bowel on its mesentery and is one of the most common causes of intestinal obstruction. The sigmoid colon, and less frequently, the cecum, are the common sites of volvulus in adults. Patients typically show features of bowel obstruction (abdominal pain, distension, bilious vomiting) or of bowel ischemia and gangrene (tachycardia, hypotension, hematochezia, peritonitis) in severe cases. The whirl sign and a grossly dilated loop of bowel on an abdominal CT scan establish the diagnosis of volvulus in adults. Sigmoid volvulus without peritonitis is initially managed with endoscopic detorsion, followed by a semi-elective surgery (sigmoid colectomy). Sigmoid volvulus with peritonitis, and all cases of cecal volvulus, require emergency surgery. Endoscopic detorsion should not be attempted in a patient with cecal volvulus because of the high risk of perforation.

Q: Pt presents w/ abdominal pain out of proportion to the physical findings and has bloody diarrhea. The physical exam reveals distention, nausea, and vomiting mimicking an obstructive pattern. What is the most common ddx?
[...]
A: ischemic bowel
Extra: check using CT and resect necrotized bowel; put pt on broad spectrum abx and heparinize the pt

Q: what is the fn of M cells in GALT?
[...]
A: engulf ag by micropinocytosis (no lysosomal enzymes)
Extra: GALT = gut associated lymphoid tissue

Q: what is the fn of IgA in the gut?
[...]
A: neutralize ag, prevent macromolecular uptake, inhibit bacterial adherence and colonization

Q: where is protein absorbed in the small bowel?
[...]
A: jejunum and ileum
Extra: duodenum: Fe
jejunum: folate, protein
ileum: B12, bile salts, protein

Q: what drives fluid reabsorption and secretion in the gut?
[...]
A: absorption driven by Na+/glucose transporter; secretion driven by chloride

Q: You are working in Nigeria and a cholera outbreak is occurring. A health care worker asks your advice for a rehydration formula. In addition to water, what do you suggest?
[...]
A: adding sodium w/ glucose

Q: what is guarding on the physical exam?
[...]
A: involuntary tensing of the abdominal wall muscles in response to pain or anticipated pain

Q: which are the 2 most common painless LGIBs?
[...]
A: diverticular bleed and angiodysplasia

Q: how would RBCs show on a PBC w/ a reduced MCHC on the CBC?
[...]
A: RBCs would be hypochromic
Extra: MCHC = mean corpuscular hb concentration

Q: what is the most common way for NSAIDs to cause PUD?
[...]
A: through the inhibition of PG production

Q: squamous cell carcinoma is usually found in the [proximal/distal] esophagus
A: proximal

Q: adenocarcinoma is usually found in the [proximal/distal] esophagus
A: distal

Q: other than bone marrow transplant, how can we tx ppl w/ aplastic anemia?
[...]
A: immunosuppression
Extra: cyclosporin, antithymocyte globulin (ATG), tacrolimus, alemtuzumab

Q: 62F presents w/ progressive motor dysphagia, present for 2 years. She has significant heartburn, treated with a PPI. She has no weight loss, no early staiety, and her appetite is generally good. On review of systems, she describes finger pain/change in colour in cold weather, and has pain in the joints of her hands and feet. She feels dyspnea when she walks upstairs. On examination, she appears to have mild enlargement bilaterally of her thyroid gland. She has thickening and swelling of her digits, as well as crackles bilaterally on chest examination. She had a gastroscopy with no abnormalities evident. What test would you do next to reveal a dx?
[...]
A: esophageal manometry

Q: would you expect any HbA in SCD upon Hb electrophoresis?
[...]
A: NOPE
Extra: answer: B

Q: what is the mechanism of clindamycin?
[...]
A: disruption of protein synthesis
Extra: Mechanism of action: binds to 50S subunit → blockage of peptide translocation (transpeptidation) → inhibition of peptide chain elongation → inhibition of bacterial protein synthesis (bacteriostatic effect)
Used to treat anaerobes, such as Clostridium perfringens, Bacteroides spp. (clindamycin is less effective against Bacteroides than other anaerobic species), group A streptococcus, G+ aerobes

Q: which test is the best non-invasive method to prove H. pylori has been eradicated?
[...]
A: stool antigen test

Q: 35M w/ a longstanding hx of alcohol misuse is admitted w/ severe acute pancreatitis. He was initially managed w/ fluid resuscitation, nasoenteric feeding, sedation, and analgesia. 96h after admission, his condition deteriorates. Which ix would you now use?
[...]
A: CT scan of the abdomen and pelvis w/ contrast

which lab finding is most consistent w/ anemia of chronic disease (increased/normal/decreased)?
Fe: decreased
ferritin: normal
TIBC: decreased
transferrin sat: decreased
retic count: low

Q: 32F had large post-partum hemorrhage and is placed on oral iron. She is health y w/ no medical problems but is found to be fatigued more than usual. Her Hb is 75 g/L, MCV 76, WBC 8.0, platelets 200, and ferritin 7. What would you do based on Choosing Wisely Canada recommendations?
[...]
A: no transfusion and continue oral iron

Q: what clinical condition does this pt most likely have?
[...]
A: iron deficiency (koilonchia; scooped nails)

Q: what does biliary colic refer to?
[...]
A: intense, dull discomfort in RUG that is usually constant and not colicky (think symptomatic gallstones)

Q: what is the diff btw type I, II, and III VWD?
[...]
A: type I is quantitative, II is qualitative, and III is absence of VWF

Q: which common bacteria need to be treated?
[...]
A: clostridium and shigella

Q: which common abx inhibit cell wall synthesis in gram +ve aerobic bacteria?
[...]
A: penicillin, amoxicillin, vancomycin

Q: which major abx inhibits nucleic acid synthesis in anaerobic bacteria?
[...]
A: metronidazoles

Q: what type of bacteria are staph, strep, and enterococcus?
[...]
A: G+ aerobic cocci

Q: what type of bacteria are E. coli, yersinia, salmonella, shigella, klebsiella, pseduomonas, and diptheria?
[...]
A: G- aerobic rods (baccili)

Q: why might you find target cells in disesases like thalassemia, liver disease, asplenia?
[...]
A: b/c they have XS cell membrane compared to cell volume due to lack of Hb

Q: what are Heinz bodies?
[...]
A: clumps of denatured Hb
Extra: the bright pink is a Heinz body; most commonly found in G6PD deficiency

Q: how to differentiate btw diverticular bleed and angiodysplasia (both are painless)?
[...]
A: diverticular bleeds have lots of blood whereas angiodysplasia has slow trickle

Q: how does parietal (somatic) abdominal pain present like?
[...]
A: sharp, well-localized, persistent pain made worse by mvmt

Q: what are common causes of obstructed appendix?
[...]
A: fecalith, lymphoid hyperplasia, fibrosis, neoplasia

Q: what is Rovsing's sign?
[...]
A: RLQ pain w/ palpation of LLQ (dx: appendicitis)

Q: what are common impersonators of appendicits?
[...]
A: PID, ruptured ovarian cyst, ectopic pregnancy, Crohn's disease, diverticulitis
Extra: PID = pelvic inflammatory disease

Q: what is the etiology of diverticulosis?
[...]
A: low fire diet

Q: Pt presents w/ fever and LLQ pain. DRE is normal and WBC is elevated. What is the next most appropriate ix?
[...]
A: CT scan to check for diverticulitis

Q: what happens if there is a "major" adverse rxn to drug? what about "moderate"?
major: [...]
moderate: [...]
A: discontinuation of drug; back box warning

Q: what are the 2 major types of adverse drug rxns?
[...]
A: class effect and idiosyncratic rxn

Q: what occurs in type 1 hypersensitivity (allergy)?
[...]
A: asthma, anaphylaxis, angioedema, urticaria, hypotension

Q: Pt presents w/ anemia and bruising due to hemolysis of RBC, WBC, and platelets. What type of hypersensitivity is this?
[...]
A: type II

Q: Pt presents w/ serum sickness and drug fever. What type of hypersensitivity is this?
[...]
A: type III

Q: how do cyclovir antivirals work?
[...]
A: by inhibiting viral DNA polymerase and chain termination
Extra: ACV = acyclovir

Q: how does remdesivir work against ssRNA coronavirus?
[...]
A: by targeting RNA-dependent RNA polymerase and competing for incorporation in growing RNA strand

Q: how to tx Candida infections?
[...]
A: rx of echinocandins (disrupts cell membrane & causes pore formation)
Extra: inhibits synthesis of β-glucan, a component of the fungal cell wall

Q: what drug class is used to tx athlete's foot?
[...]
A: terbinafine

Q: which 2 common drugs are used to tx aspergillus?
[...]
A: voriconazole and isavuconazole
Extra: Aspergillus is a genus of fungi found ubiquitously in the environment. Transmitted via airborne exposure to mold spores. Risk factors for infection include destructive pulmonary pathology (e.g., COPD) and immunosuppression. Can cause invasive aspergillosis, allergic bronchopulmonary aspergillosis, and aspergilloma.

Q: what types of bacterial infection should you suspect from undercooked chicken?
[...]
A: campylobacter and salmonella
Extra: both campylobacter and salmonella can cause bloody diarrhea; salmonella also causes watery diarrhea

Q: what types of bacterial infection should you suspect from undercooked hamburger?
[...]
A: E. coli (ETEC, EIEC, or EHEC)
Extra: ETEC: watery diarrhea / travelers' diarrhea
EIEC and EHEC: bloody diarrhea (HUS)

Q: what types of bacterial infection should you suspect from recent abx use?
[...]
A: C. diff
Extra: watery diarrhea; tx using vancomycin or fidaxomycin (if not available use metranidazole)
complications include pseudomembranous colitis and megacolon

Q: how do beta-lactam antibacterials such as penicillins, cephalosporins, carbapenems, and monobactams work?
[...]
A: by inhibiting formation of bacterial cell walls

Q: how do beta-lactam antibacterials such as aminoglycosides, macolides, lincosamides, tetracyclines, and oxazolidinone work?
[...]
A: by inhibiting protein synthesis via inhibition of ribosomal subunits

Q: what type of bacteria are Staph. auereus, Staphylococcus, Streptococcus, and Enterococcus?
[...]
A: G+ cocci

Q: what type of bacteria are Bacillus (spore forming), Clostridium (spore forming), Listeria (non-spore forming), and Corynebacterium (non-spore forming)?
[...]
A: G+ bacilli

Q: what type of bateria is Staphylococcus aureus?
[...]
A: G+, facultative anaerobic cocci (non-motile and no spores)

Q: what type of polyps are these?
[...]
A: adenomatous polps

Q: what type of tumour was this?
[...]
A: gastric adenocarcinoma, heaped up margins arranged in glands

Q: what type of tumour is this?
[...]
A: gastric adenocarcinoma, diffuse type

Q: what does left shift refer to?
[...]
A: increased release of immature neutrophils into circulation (increased band cells)
Extra: right shift is vice versa

Q: what are common peritonitic signs?
[...]
A: rigidity, guarding, tenderness, immnocompromised

Q: Pt eats undercooked chicken. What are the 2 most common bacterial infections?
[...]
A: salmonella nad campylobacter

Q: Pt presents with bloody diarrhea after 72h of eating contaminated chicken. What is the most likely bacterial infection?
[...]
A: campylobacter or salmonella

Q: what is tx travellers' diarrhea?
[...]
A: no tx recommended for ETEC (enterotoxigenic E. coli)

Q: Pt presents with HUS and bloody diarrhea after eating undercooked hamburger. What is the most likely bacterial infection?
[...]
A: EIEC (enteroinvasive E. coli) or EHEC (enterohemorragic E. coli)

Q: how to tx acute severe colitis?
[...]
A: abdominal colectomy end ileostomy

Q: when to decide to do surgical resection in acute colitis?
[...]
A: if there is clinical deterioration after giving steroids and IV support

Q: what happens in restorative proctocolectomy?
[...]
A: removal of colon or rectum w/ anastamosis of small bowel to anal canal (gold standard tx for ulcerative colitis)

Q: what propn of pts w/ Crohn's disease require surgery by 20 y/o? By 30 y/o?
[...]
A: >75% by 20, 90% by 30

Q: what are limitations to treating Crohn's disease surgically?
[...]
A: resection is not curative due to recurrence
Extra: surgery for Crohn's when there is loss of response to medical therapy or complications from the disease (e.g., obstruction, perforation, fistulization, bleeding)

Q: what increases likelihood of surgery for Crohn's disease?
[...]
A: smoking (almost guaranteed), stricturing, large bowel diseases

Q: what is IBD?
[...]
A: chronic idiopathic immune-mediated disease of GI tract

Q: what are common sx of ulcerative colitis?
[...]
A: tenesmus, abdo cramping, diarrhea, chronic pain

Q: how to tx acute severe UC?
days 0-3: [...]
days 4-7: [...]
non-responders: consult surgery for proctocolectomy
A: IV corticosteroids; infliximab
Extra: UC = ulcerative colitis
infliximab is an anti-human tumor necrosis factor alpha (TNF-α) monoclonal antibody

Q: what are common biologics for IBD?
[...]
A: TNF antagonists, anti-integrins, anti-interluekins

Q: what are 2 traditional immunosuppressants for IBD?
[...]
A: azathioprine and methotrexate

Q: how to manage hemorrhoids, anal fissures, or other related anal problems?
[...]
A: increased dietary fiber, metamucil, avoid sitting/straining on toilet for prolonged periods

Q: what is the fn of hemorrhoids?
[...]
A: helps w/ continence and act as vascular cushions

Q: what is the etiology of enlarged/symptomatic hemorroids?
[...]
A: predisposition and increased intra-adbo pressure

Q: what are the main diffs btw internal and external hemorrhoids?
[...]
A: internal is proximal to dentate line, has columnar epithelium, and uses visceral innervation whereas external is distal, squamous, and somatic

Q: what are common sx of internal hemorrhoids?
[...]
A: bleeding (drips/squirts), prolapse/protrusion, ache or discharge, rarely pain

Q: what are common sx of external hemorrhoids?
[...]
A: pain, swelling, thrombosis, pruritis, lumps/tags

Q: how to tx refractory hemorrhoids?
[...]
A: rubber band ligation (sclerotherapy) or surgical hemorrhoidectomy
Extra: excisional hemorrhoidectomy is very effective, has low recurrence, but is uncomfortable for the pt post-op for a few weeks while the damage heals

Q: 30M has 2 week hx of excrutiating pain around the anus. The pain was most intense during and after a bowel movement, and a small amount of blood was found upon wiping his anus. There is no PHx. What is the tx?
[...]
A: increased dietary fiber, metamucil, sitz baths, dilitiazam ointment 2% tid

Q: what is the classic triad for anal fissures?
[...]
A: sentinal tag, hypertrophic anal papilla, exposed fibers of internal sphincter

Extra 1: tx is fistulotomy, staged fistula repair, fistula plug, advancement flap, and seton

Q: 21M has hx of recurrent infections requiring draining at the upper end of his natal cleft. There is now a constantly draining, foul odour from his rectal area. He is otherwise healthy. What is the dx?
[...]
A: pilonidal disease
Extra: tx is usually excision or debridement of chronically infected tissue

Q: how does eating FODMAP exaggerate IBS?
[...]
A: poorly digested and fermented leading to increased luminal water (diarrhea) and increased gas production
Extra: FODMAP = fermentable, oligo-, di-, mono-saccharides and polyols

Q: for how long should you use ABHRs and how long should you hand wash?
ABHR: [...]
hand wash: [...]
A: at least 15 s; 15-30 s (length of the happy birthday song)

Q: what PPE to use for contact and droplet precautions?
[...]
A: gown, gloves, glasses

Q: what to wear w/ airborne precautions?
[...]
A: N95 (room should have door closed and have -ve air pressure)

Q: what disease does Listeria monocytogenes cause?
[...]
A: meningitis and sepsis

Q: what disease does the pathogenic species of the Neisseria family cause?
[...]
A: meningitis, sepsis

Extra 1: AXR insensitive for ascites b/c it needs min 500 mL to be detected
AXR signs: medial displacement of ascending and descending colon, separation of adjacent loops, loss of definition of liver and/or spleen edge

Extra 1: Typical presentation: 53M w/ progressive abdominal distention, pain, and early satiety. He has hx of severe gallstone pancreatitis 6 weeks prior. Physical exam reveals a tender epigastrium and RUQ. RUQ has a central bulge, ill-defined borders, and is dull to percussion.

Q: what is the dx?
[...]
A: small bowel obstruction (lots of air fluid lvls)
Extra: etiology: adhesion (65-75%), hernia, tumour, stricture (IBD)

Q: what is likely dx?
[...]
A: sigmoid volvulus causing large bowel obstruction

Q: what are predisopsing factors for sigmoid volvulus?
[...]
A: chronic constipation, megacolon, excessively mobile colon

Q: what is likely source of large volume diarrhea?
[...]
A: small bowel or right colon (usually painless and not very frequent)

Q: what is likely source of small volume diarrhea?
[...]
A: left colon (painful and frequent)

Q: what is the main diff btw secretory and osmotic diarrhea?
[...]
A: secretory continues despite fasting whereas osmotic does

Q: which organs might be affected if you see steatorrhea?
[...]
A: hepatobiliary organs, pancreas
Extra: steatorrhea is usually large volume (bulky), pale, greasy, non-bloody, foul smelling/floating

Q: Pt presents w/ iron deficiency anemia, muscle atrophy, edema, vitamin A deficiencies, and IBS-like features (borborygmi, flatulence, abdo distension). What is the most likely cause of diarrhea?
[...]
A: malabsorptive

Q: how does dysmotility diarrhea present?
[...]
A: watery diarrhea and steatorrhea

Q: 58F presents w/ watery diarrhea persistent over the past year. She has 4 loose BM/day w/ urgency and it awakes her at night. She has no weight loss, used NSAIDs for past 8 months for arthritis, and had a cholecystecomy in the past. She is negative for C. diff and her labs are normal (includign CBC, CRP, TSH, lytes, creatinine, B12, anti-tTG). What is the most likely diagnosis?
[...]
A: microscopic colitis