ICR-Final Flashcards
Greatest challenge swallowing with liquid, coughing immediately after swallowing, often associated with neurological disease (stroke, MS)
Oropharyngeal dysphagia
Treating oropharyngeal dysphagia
Refer to speech pathology for modified barium swallow
Food gets stuck with solids and liquids several seconds after swallowing
Esophageal dysphagia.
Differential for esophageal dysphagia with solids only? With liquids and solids?
Solids only: rings, webs, EoE, peptic stricture, esophageal cancer. Both: diffuse esophageal spasm, scleroderma, achalasia
Where is food typically getting stuck when patients point to the region they think it is getting stuck?
There or lower
Red flags for patients with dysphagia
Food impaction, weight loss, history of heavy tobacco/alcohol use, dysphagia itself is a red flag with heartburn
Patient sitting in waiting room spitting into a cup because they can’t swallow
Food impaction
2 main assessments of esophagus in patients with dysphagia
Barium esophagram (diagnostic only, less invasive) or upper endoscopy (diagnostic & therapeutic = 1st choice)
What pushes you towards doing a barium esophagram over upper endoscopy?
Endoscopy is not available. Patient has too many comorbidities.
When would you consider doing esophageal manometry?
Anatomic evaluation checks out normal and you suspect a motility disorder.
How do you treat this?
Schatzki rings occur near the GE junction and respond well to esophageal dilation.
How do you confirm this diagnosis?
This is eosinophilic esophagitis, note the eosinophilic microabscesses on the esophageal wall and concentric rings. This is diagnosed by biopsy w/15-20 Eos per high power field.
How do patients with EoE typically present first and how do you first manage them?
1st: intermittent dysphagia. Treat w/PPI, then if that doesn’t work you treat with topical steroids.
How do you diagnose and treat this patient?
This patient has an esophageal web, which responds extremely well to esophageal dilation.
What type of dysphagia will this patient present with?
Progressive solid food dysphagia. This is a peptic stricture from long standing GERD that has damaged the mucosal lining of the esophagus.
Which of these is esophageal squamous cell carcinoma and which is esophageal adenocarcinoma? What are associations with each? Where do they typically arise?
Top: SSC, associated w/African American and tobacco/alcohol use. Typically occurs mid esophagus. Bottom: Adenocarcinoma, associated with Barrett esophagus, GERD, older white men. Typically occurs distal esophagus.
What would you expect to see on esophageal manometry in a patient with diffuse esophageal spasm? What about on barium swallow?
Peristalsis and contraction all at the same time. Barium swallow = corkscrew esophagus.
What would you expect to see on esophageal manometry in a patient with achalasia?
No peristalsis and no LES relaxation. ON imaging you would see the bird beak.
List 5 causes of odynophagia
Secondary to mucosal break/ulcer, infection (HSV, CMV, Candida = white plaques), pills (kissing ulcers), caustic agent (diffuse, circumferential injury), radiation
How do ulcerative colitis and Crohn’s disease differ in symptoms, colon involvement, small bowel involvement and perforating/stricture disease?
*
How do you evaluate a patent with IBD?
Labs may show anemia and elevated inflammatory markers. Endoscopy is essential for diagnosis and imaging can help.
Endoscopy findings in ulcerative colitis?
Granular, erythematous and bleeds w/mild trauma
Endoscopy findings in Crohn’s disease?
Edematous mucosa w/linear ulcerations
A patient presents with a burning/gnawing epigastric pain. Physical exam reveals epigastric tenderness. He has a long history of NSAID use for arthritis. How do you evaluate and treat this patient?
He is at risk for peptic ulcer disease. You can “test and treat” by stopping NSAIDs and checking H. pylori status. You could do upper endoscopy or upper GI series. Check CBC to see if BUN is elevated to assess for bleeding. Check AAS (acute abdominal series) if concerned for bleeding.
Patient presents with constant, unrelenting epigastric pain radiating to the back w/nausea and vomiting. Physical exam shows fever, anorexia, nausea, vomiting, tachycardia, tachypnea, hypoactive bowel sounds and marked abdominal tenderness. How do you evaluate this patient?
Acute pancreatitis. Labs: serum amylase and lipase (more specific). RUQ ultrasound if there is gallstone etiology (ALT >3x upper limit) and CT scan to confirm.
Grey-Turner’s and Cullen’s signs
Seen in acute necrotizing pancreatitis.
Most common causes of acute pancreatitis in the US
Gallstones and alcohol
A patient presents with RUQ and epigastric pain that is sudden onset and severe. The pain radiates to the right shoulder/scapula. There is also nausea, vomiting and fever. Physical exam reveals guarding and Murphey’s sign. How do you evaluate this patient?
Acute cholecystitis. CBC shows leukocytosis. Hepatic panel shows AST/ALT elevation and elevated bilirubin. RUQ ultrasound is test of choice.
Thick gallbladder wall and pericholic fluid
Cholecystitis
Where to palpate for acute appendicitis
McBurney’s point or right-sided rectal palpation
Special tests for acute appendicitis
Psoas sign and obturator sign
Appendicitis test of choice
CT in adults, ultrasound in children
A patient presents with abdominal pain, vomiting, obstipation. Physical exam reveals a distended abdomen with diffuse tenderness and rigidity. KUB is shown below. How do you evaluate this patient?
This patient has abdominal obstruction, note the fluid-air levels on the KUB. Further evaluation is done by imaging.
A patient presents with nausea, vomiting, bloody diarrhea and severe abdominal pain out of proportion to the physical exam. How do you evaluate this patient?
Mesenteric ischemia. Lactate levels indicate areas of underperfusion. CT confirms diagnosis with air in bowel or occlusion.
Dull or midline abdominal pain with vaginal bleeding
Endometritis
Lower abdominal pain with nausea, vomiting and peritonitis
Salpingitis (fallopian tube infection)
Lower abdominal pain with nausea, vomiting and peritonitis. Also w/RUQ tenderness.
Fitz-Hugh Curtis Syndrome.
Physical exam for PID
Cervical motion tenderness, discharge and palpable adnexal mass with tubo-ovarian abscess
Evaluation of PID
Pregnancy test, CBC and test for gonorrhea or chlamydia
A patient has variable abdominal symptoms that get worse with stress. Nocturnal symptoms are absent. How do you diagnose this condition?
IBS. Rome III criteria: recurren pain > 3x/month in last 3 months w/2 of following: improvement with defecation, onset w/change in stool frequency, onset w/change in stool form. Symptom onset > 6 months ago.
Acute vs. chronic diarrhea
Acute < 4 weeks, chronic > 4 weeks
Etiologies of acute diarrhea
Infectious or initial presentation of more severe disorder
When does someone need to be seen for acute diarrhea?
Severe abdominal pain, temp > 101.3, blood, 6+ stools/day, immunocompromised, antibiotics in past 3 months
3 categories of chronic diarrhea. How do you evaluate each?
Watery (history, labs, stool studies and endoscopy), inflammatory (go to endoscopy) or fatty (see if it’s small bowel or pancreas by imaging or endoscopy)
Diarrhea red flags
Blood, anemia, waking at night to go, weight loss, immunocompromised
2 types of watery diarrhea. How do you differentiate between the two?
Osmotic (poorly absorbed ion or sugar) or secretory (infection, endocrine, tumors). Differentiate by calculating stool osmotic gap = 290 - 2(Na + K). Secretory if < 50. Osmotic if > 125.
What type of watery diarrhea goes away when the patient does not eat?
Osmotic
4 causes of inflammatory diarrhea
IBD, infection, ischemic colitis, radiation proctitis
4 causes of > 14gm fat in stool per day
Fatty diarrhea caused by celiac, Whipple’s, tropical sprue or pancreatic insufficiency.
7 key clinical clues for diarrhea
New meds, recent illnesses, diet, previous surgeries, travel, FH and psychiatric illness (IBS or laxative abuse)
56 yo man w/profuse water diarrhea after abx therapy. What is your diagnosis.
Note pseudomembranes, classic for C. difficile.
Woman with several years of mushy diarrhea and history of anemia. Diagnosis?
Note scalloping of duodenal folds indicating celiac disease.
82 yo man presents with fatty diarrhea. What is your diagnosis?
Note calcified pancreas. He has chronic pancreatitis causing pancreatic insufficiency.
Low fecal elastase
Pancreatic insufficiency
How is bilirubin produced?
*
3 things that can cause increased unconjugated bilirubin. 2 things that can cause increased conjugated bilirubin.
*
A patient has an indirect bilirubinemia. CBC is normal and hemolysis is ruled out. What is your differential?
1) Crigler-Najjar: seen in infants, absence (I) or decreased (II) UDP glucuronosyltransferase = can’t conjugate bilirubin. 2) Gilbert’s: more common, impaired bilirubin conjugation when fasting or ill w/ mild increase in indirect bilirubin
Physical exam findings in patients with chronic liver disease
Gynecomastia, caput medusa, ascites, spider angiomas and asterixis (can’t keep hands up when holding out)
Test of choice when looking for obstructive jaundice due to biliary obstruction.
RUQ U/S, CT is often adequate.
Painless jaundice
Often cancer
Painful jaundice
Choledocolithiasis
Best marker of liver synthetic function
Prothrombin time. Albumin is also good.
Liver enzymes
AST, ALT, Alk Phos (also in bone, intestine and intestine), GGT (most useful in confirming elevated Alk Phos is coming form liver)
Labs with predominant hepatocellular injury
Elevated AST, ALT
Labs with predominant cholestatic etiology
Elevated Alk Phos, bilirubin
Most abundant portion of blood
Plasma
Buffy coat
Layer of blood that contains leukocytes
What is your preferred value for measuring anemia?
Hgb, it is actually measured. Hct is a calculated number.
Causes of microcytic anemia
“CELTICS”: Chronic disease (late), eHgb (variant Hgb), Lead, Thalassemia, Iron Deficiency, Cancer, Sideroblastic
Causes of normocytic anemia
“CRSHH”: Chronic disease (early), Renal disease (early), Sickle, Hemolysis, Hemorrhage
Causes of macrocytic anemia
B12/Folate deficiency, alcohol, meds, cirrhosis
Most common anemia world wide?
Iron deficiency anemia, commonly seen in kids, women (menstruation) and parasitic infections. *Being a male and iron deficient is never normal.
Protein responsible for iron absorption in the gut. What disease is this associated with?
Ferroportin. Unregulated absorption of iron can cause hemochromatosis, especially in absence of hepcidin, which turns ferroportin off.
Common presentations of iron deficiency anemia in the clinic
PICA (ice chewing) is rare. Pallor, glossitis and koilonychia of the nails are common.
How do you confirm your diagnosis of iron deficiency anemia?
Decreased serum Fe, increased TIBC, decreased ferritin, increased soluble transferrin receptor and decreased hepcidin.
Lab test that is pathogmonic for iron deficiency anemia
Ferritin < 15. Note that ferritin is also an acute phase reactant and can be ramped up when you are ill.
What would you expect to see on peripheral blood smear in a patient with iron deficiency anemia?
Anisocytosis (variable size) poikilocytosis (variable shape) and central pallor
55 year old man presents with fatigue. Labs are Hgb 10, MCV 75, low serum Fe, high TIBC and ferritin of 5. What is your next step?
Colonoscopy and EGD to evaluate for bleeding. Fecal occult blood testing is a screening test and you would never do it.
A 22 year old woman presents with fatigue. Labs show Hgb 5 and peripheral smear is shown below. What do you do next?
Hgb of 5 means that there has been chronic anemia occurring for a very long time. You would give iron therapy then assess for malignancy and heavy menses.
A 56 year old man presents for a routine physical. Labs show Hgb 11.8, MCV 77, creatinine 0.8, ferritin 15, TIBC 400 and low serum iron. In addition to starting iron therapy, what should you do next?
EGD and colonoscopy
Most common anemia in a hospitalized patient?
Anemia of chronic disease. Sometimes normocytic, often microcytic.
Labs that hint towards anemia of chronic disease. What is the underlying cause of anemia of chronic disease?
Normal/low serum iron, normal/low TIBC, normal/high ferritin, high ESR/CRP. Note that hepcidin will be increased, turns off ferroportin and causes anemia due to inability to release Fe from macrophages.
What drugs do you give to a patient with anemia and CKD?
Erythropoietin stimulating agents to get Hgb 10-11 and increase ferritin levels. They also may need IV iron because iron stores are inaccessible.
What would you expect to see on peripheral blood smear in anemia due to CKD? Liver disease?
Echinocytes (Burr cell). Acanthocytes (spur cell) are typically seen in liver disease.
A 62 year old man presents with RA and colon cancer 12 years ago. Labs show Hgb 10, MCV 90, reticulocytes 0.1%, ferritin elevated, Fe normal, TIBC normal and peripheral blood smear is normal. What is your next step?
Make sure he is up to date on all of his GI evaluations. Note that he does not have increased reticulocytes because he likely has anemia of chronic disease.
What thalassemia is coded for with 2 paired genes (4 total)? What thalassemia is coded for with 2 genes total?
4 = alpha thalassemia. 2 = beta thalassemia.
Hgb Barts
You got two defective alpha genes from mom and two defective alpha genes from dad. This causes Hydrops fetalis and is not compatible with life.
Hgb H
Two abnormal genes from one parent and one abnormal alpha gene from dad. This presents like beta-thalassemia major with severe anemia and dependency on transfusions.
B12 pathway
Salivary amylase frees B12 -> B12-RBinder -> B12 split off from RBinder by pancreatic enzyme-> B12-IF forms -> B12-IF absorbed into blood
Surrogate marker for B12 or folate deficiency
Homocysteine. It cannot be converted to methionine without B12 and folate.
Surrogate marker for B12 and not folate
MMA (methylmalonyl CoA). MMA will build up and cause peripheral neuropathy because odd-chain fatty acids are incorporated into myelin sheaths. Note that this can not only happen with B12 deficiency, it can also happen with IF defect and methylmalonyl CoA mutase defects.
What would you expect to see on peripheral blood smear in a patient who has anemia and only eats tea and toast for meals?
Megaloblastic anemia w/hypersegmented neutrophils (> 5 lobes)
Why do people with thyroid disease or diabetes present with anemia?
They are prone to pernicious anemia = destruction of parietal cells = loss of intrinsic factor
A 78 year old woman presents with increased forgetfulness over the past 7 months. Labs show Hgb 7.8, MCV 110, B12 and Folate are low. MMA is high. What is the most likely diagnosis? What do you need to do after you give her B12 supplementation?
B12 deficiency. Follow up with her to make sure she has gotten better. If she hasn’t then you have unmasked a folate deficiency.
What is the clinical spectrum of thalassemia?
Thalassemia trait: asymptomatic. Thalassemia major: transfusion dependent. Thalassemia intermedia is in between.
What is responsible for the condition shown below?
Beta-thalassemia major (beta0/beta0). The child is not making any beta chain whatsoever, the alpha chains pair up and the Hgb is ineffective. The body responds by trying to ramp up erythropoiesis and you get it in the skull bones, sternum and humerus.
How do you treat Cooley’s anemia?
Beta-thalassemia major is treated with bone marrow transplant because the patient’s marrow is not producing any viable globin chains.
What causes hemolysis in people with G6PD?
Stress causes increased demand on glutathione in the RBC. When people have G6PD deficiency, they can’t keep up, the cell accumulates free radicals and lyses.
What would you expect to see on peripheral blood smear in a patient with thalassemia?
Ringed cells
Common geographic locations for G6PD and thalassemia
SE Asia, Middle East and Africa
Common causes of oxidative challenge that can make G6PD deficiency present with anemia
Bactrim (abx with sulfa), dapsone, fava beans, primaquine, sulfa, methylene blue (used to treat methemoglobinemia) and nitrofurantoin.
Primary hemostasis
Endothelial damage -> GpIb on platelet binds to vWF on injured endothelium -> Platelet activated -> Granules secreted and activate nearby platelets to degranulate and aggregate w/fibrinogen crosslinks -> Secondary hemostasis promoted by granule secretion.
Elevated PT makes you think of…
Vitamin K deficiency (II, VII, IX, X, C, S), early liver disease
2 functions of vWF
Binds platelets to injured endothelium, prevents degradation of factor VIII
Most common pathologies with intrinsic pathway
Hemophilia
How do we measure the intrinsic pathway function?
PTT
Tertiary hemostasis
Clot stabilization by thrombin formation
How do we turn off tertiary hemostasis
Fibrinolysis
Superficial mucocutaneous bleeding
Typically with platelet problems
Visceral and joint bleeding
Coagulation cascade
Most common inherited bleeding disorder
AD vWF deficiency. Presents with mucocutaneous bleeding and possible visceral bleeding due to degradation of factor VIII
How do you differentiate hemophilia from vWF deficiency?
Woman is most likely vWF deficiency.
Virchow’s triad
Hypercoaguability (smoking, obesity, pregnancy elderly, malignancy, factor V Leiden, Stasis and Vessel injury
Genetic defects that give you hypercoaguable states
Factor V Leiden mutation, protein C/S deficiency, prothrombin mutation, ATIII deficiency
Coumadin right after you give it
Initially it is prothrombotic because it inhibits Vitamin K activity and decreases protein C & S synthesis. Leave heparin on for several days after starting Coumadin.
Causes of antiphospholipid antibody syndrome that leads to hypercoaguability
Lupus anticoagulant (highest risk), anti-cardiolipin Ab and the beta-2 glycoprotein. If you have all 3 you are at highest risk for thrombosis.
How might B12/folate deficiency cause thrombosis?
Not sure, but hyperhomocysteinemia is a marker for increased risk for clotting. Treating hyperhomocysteinemia does nothing.
Best way to check for protein C and S deficiencies
Genetic, serum levels are not reliable because they get used up.
