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Pharm III > Lecture 3 (GI)- Exam 2 > Flashcards

Lecture 3 (GI)- Exam 2 Flashcards

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1
Q

Vomiting reflex
* Located where?
* What does it contain?
* What happens with stimulation?

A

Located in medulla oblingata
* Contains muscarinic receptors
* Stimulation = triggers vomiting reflex

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2
Q

Vomiting reflex
* What are the Four primary stimulators of VC?

A
  • Chemoreceptor trigger zone (CTZ)
  • Vestibular system (VS)
  • GI mechanoreceptors
  • Higher brain centers
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3
Q

Vomiting pathophysiology: Chemcoreceptor trigger zone
* Located where?
* Outside what?
* Triggered by what?
* Stimulates what?
* What are the receptors?

A

Receptors: Chem D(2)oN(K1)’t (5)HiT(3)

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4
Q

Vestibular system:
* What is it important for?
* Problems communicated via what?
* Stimulations of what?
* What are the receptors?

A
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5
Q

Higher brain centers (cerebrum)
* Response to what?
* Direct stimulation of what?

A
  • Response to emotional, pain, smell, sight
  • Direct stimulation of vomiting center muscarinic receptors
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6
Q

Gastrointestinal center
* What is resleased?
* Stimulates what? (2)
* What are the receptors?

A
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7
Q

What are the Select Nausea and vomiting etiologies? (10)

A
  • Increased intracranial pressure
  • Vestibular dysfunction
  • Dyspepsia
  • Gastroparesis
  • Infections
  • Medications / chemicals
  • Pregnancy
  • Pain
  • Psychiatric disorder

“I Vow Doctors Get Instant Medical Pregnancy Pain Patches”

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8
Q

Chemotherapy induced nausea and vomiting (CINV)
* What is acute?
* What is delayed?
* What is anticipatory? What is first line?

A

Acute - ≤ 24 hours

Delayed - >24 hours

Anticipatory = prior to chemotherapy
* First-line = benzodiazepines

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9
Q

Chemotherapy induced nausea and vomiting (CINV)
* What is breakthrough?
* What is refractory?

A
  • Breakthrough – despite prophylactic treatment
  • Refractory – no response to therapies
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10
Q

Chemotherapy induced nausea and vomiting (CINV)
* What is the goal?
* What is the treatment?
* What risk?

A

Goal = no nausea or vomiting
* Treatment based on emetogenicity of regimen (higher teh emetogenicity is= longer they are on treatment)
* Low to extremely high risk

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11
Q

Chemotherapy induced nausea and vomiting (CINV)
* How long for moderate emtogenicity? High?

A
  • 48 hours for moderate emetogenicity
  • 72 hours for high emetogenicity
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12
Q

Post operative nausea and vomiting
* How many people get this?
* Who has greater risks? Expand how that will affect medications?

A

30% of patients within 24 hours of anesthesia

Multiple risk factors -: more risk factors = greater risk
* 0 to 1 risk factors = 10 to 20% (lowest risk)-> 1 to 2 antiemetics
* 3 to 5 risk factors = 50 to 80% (highest risk)-> ≥ 2 antiemetics

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13
Q

What are the risk factors of post operative n/v?

A
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14
Q

Post operative nausea and vomiting
* What is the typical regimen?
* What is the rescue therapy?

A

Typical regimen:
* Ondansetron plus
* Dexamethasone
* ± scopolamine (first 3 days if used)

Rescue therapy – different drug class

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15
Q

Antiemetic use during pregnancy
* How many women deal with this?
* What else can a women have?

A
  • 50 to 80% of pregnant women experience nausea
  • 0.3 to 3% will have hyperemesis gravidum
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16
Q

Antiemetic use during pregnancy
* What are some prevention measures? (4)

A
  • Starting prenatal vitamins early
  • Avoiding trigger foods or odors
  • Ginger
  • Small, more frequent meals
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17
Q

Antiemetic use during pregnancy
* What is first line?
* What are the alternatives?
* What ype of support?

A

First-line
* Pyridoxine (B6) ± doxylamine
* Doxylamine = H1 antagonist

Alternatives
* Other H1 receptor antagonists
* Ondansetron

Nutrition support

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18
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A
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19
Q

Antihistamines / anticholinergic agents

A
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20
Q

Antihistamines / anticholinergic agents

A
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21
Q

5Ht3 / NK-1 receptor antagonists

A
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22
Q

5Ht3 / NK-1 receptor antagonists

A
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23
Q

Miscellaneous antiemetics

A
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24
Q

When you give metoclopramine, what can you Coadminsterion with to decrease EPS?

A

Diphenhydramine

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Appendicitis: * What are the sxs? * What are the PE?
Symptoms * Abdominal pain * N/V/D * Fever PE findings: * Know all the signs: Mcburny, obturator, psosas, rovsing, etc
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# Commonly tested What are some causes of appendicitis?(4)
Know that lymphoid hyperplasia is children
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How do you dx appendicitis?
* Ultrasound (pediatrics) * CT abdomen with IV contract
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Appendicitis treatment: not ruptured * What is first line? * What do you need to do perioperativly? Post operative?
First-line: appendectomy * Perioperative antibiotics: Ceftriaxone plus metronidazole * 0 to 7 days post operative antibiotics-> Less evidence
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Appendicitis treatment: ruptured or sepsis * What is first line?
First-line: supportive care plus antibiotics * Stabilize * Percutaneous drain * Antibiotic therapy
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Rupture / sepsis: * What are the empiric IV antibiotics choices? (3) * What can be added?
* Meropenem or imipenem * Piperacillin/tazobactam * Ciprofloxacin plus metronidazole * ± percutaneous drain
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Appendicitis treatment: * When do you convert the antibiotics? * When do you f/u?
* Conversion to oral antibiotics once clinically improved to complete 7 to 10 days course * Follow-up in 6 to 8 weeks for scheduled appendectomy
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Antimicrobial prophylaxis: * What do you do for gastroduodenal surgery? * What do you do for billary tract surgery?
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Antimicrobial prophylaxis: * What do you use for appendectomy? * What do you use for small intestine surgery?
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Antimicrobial prophylaxis: * What do you do for hernia repair? * What do you do for colorectal surgery?
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Celiac sprue/disease * Most common type of what? * What are other names? (2) * What is it?
* Most common type of mucosal malabsorption * AKA - Nontropical Sprue or Gluten-Sensitive Enteropathy * Immunologic intolerance to gluten
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Celiac Sprue / disease * Affected persons have waht? * What is the patho behind this?
* Affected persons have a genetic predisposition * Exposure to gliadin (found in wheat, barley, rye, oats-mentioned oats are safe) evokes a cellular immune response that causes mucosal damage mainly in the proximal intestine.
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Celiac disease: Presentation * What are the sxs? (6) * What can happen to the skin? * What can happen to the blood?
* Crampy abdominal pain, diarrhea, flatulence, bloating, weight loss, steatorrhea. * Dermatitis Herpetiformis – blistering, pruritic skin rash (Gluten rash) * Iron deficiency anemia
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Celiac disease * What are some sxs that can occue due to vitamin deficiency? (4)
* Osteoporosis (vitamin D malabsorption) * Peripheral neuropathy (B12 deficiency) * Easy bruising (vitamin K malabsorption) * Edema (malabsorption of protein)
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Celiac disease * How do you dx it?
EGD w/ Intestinal biopsy TTG (tissue transglutaminase) IgA endomysial antibodies are present Serologic blood tests * Tissue transglutaminase antibodies * Anti-gliadin antibodies (IgA and IgG) * Anti-endomysial antibodies (IgA)
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Celiac disease * how do you txt it?
* Strict gluten-free diet for life * Correct micronutrient deficiencies
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General treatment approach- celiac * Consultation with who? * Educate what? * Lifelong what?
* Consultation with a skilled dietitian * Education about the disease * Lifelong adherence to a gluten-free diet
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General treatment approach- celiac * What do you need to ID and treat?
Identification and treatment of nutritional deficiencies * Vit A, D, E, B12 * Copper, Zinc * Carotene * Folic acid * Ferritin, iron
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General treatment approach- celiac * Access to what? * Continuous what?
Access to an advocacy group Continuous long-term follow-up by a multidisciplinary team * Osteoporosis * Pneumococcal vaccine
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What are some good and bad foods for celiac disease?
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What is the difference between food allergy and food intolerance?
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lactose intolerance * What is lactose? * How it is broken down? What happens with it?
Lactose is a disaccharide made of glucose and galactose Broken down in the small intestine by lactase into monosaccharide molecules * Readily absorbed * Glucose used for energy
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Lactose intolerance * What happens when there is a deficency of lactase?
* Decreased absorption of lactose in small intestine * Stays in the lumen and travels to the colon * Fermented by GI bacterial flora = symptoms
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Lactose intolerance * What are the types (3)
* Congenital lactose intolerance rare (automsomal recessive) * MCC = lactase nonpersistence * Secondary: Malabsorption syndromes
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Lactose intolerance: Lactase nonpersitence * When is lactase high? * When does it decrease? * Race difference?
* High lactase when young * Decreases with age; lower when older * Caucasians maintain lactase * African Americans, American Indians, Asian Americans low lactase
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Lactose intolerance * What are the sxs? (3) * How do you dx it?(3)
Symptoms: * Abdominal pain * Bloating * Diarrhea Diagnosis: * Clinical, lactose hydrogen breath test, lactose tolerance test
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Lactose intolerance * What is the txt?
* Decreasing lactose intake * 2 cups of milk or lactase equivalents/day * Lactase supplements: One to 3 tablets before dairy containing food
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Infectious Diarrhea: inflammatory/bloody diarrhea (dysentery) * What are common sxs? (5) * What is postive? * What is required?
* Frequent bloody, small-volume stools, often with fever, abdominal cramps, tenesmus and fecal urgency * Fecal leukocytes are often positive, * Stool culture required for definitive etiology
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Infectious Diarrhea: inflammatory/bloody diarrhea (dysentery) * What are the common causes?
Shigella, Salmonella, Campylobacter, Yersinia, invasive strains of E.coli, Entamoeba histolytica and C. difficile
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Infectious Diarrhea: Noninflammatory, non-bloody or watery * Caused by what? * What type of diarrhea? * What are the common sxs?
* Milder, caused by viruses or toxins that affect small intestine * Large-watery diarrhea * Common Symptoms: Nausea, vomiting, cramps
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Infectious Diarrhea: Noninflammatory, non-bloody or watery * What are the common causes?
Rotavirus, norovirus, astrovirus, enteric viruses, vibriones, enterotoxin-producing E. coli, Giardia lamblia, crystosporidia & agents that cause food-borne gastroenteritis
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Acute gastroenteritis * Most are what? * Patients seeking care should be evaluated for what?
* Most are self limiting and self resolve without specific treatments * Patients seeking care should be evaluated for dehydration
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Acute gastroenteritis * Further work-up considered for patients with the following? (5)
* **Severe illness** (profuse watery diarrhea, signs of hypovolemia, passage of ≥6 unformed stools per 24 hours, severe abdominal pain, need for hospitalization) * **Features of inflammatory diarrhea** (bloody diarrhea, small volume mucous stools, fever) * **High-risk host features** (eg, age ≥65 years, cardiac disease, immunocompromising condition, inflammatory bowel disease, pregnancy) * **Symptoms persisting for more than one week** * **Public health concerns** (eg, diarrheal illness in food handlers, health care workers, and individuals in day care centers)
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Volume repletion: Mild to moderate dehydration * What is first line?
First-line: oral replacement therapy * Effective, inexpensive, noninvasive, home therapy * Balanced oral rehydration fluids recommended * Glucose, Na, K, H20 * Homemade: ½ tsp salt, 6 teaspoons sugar per 1L H2O
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Volume repletion: Severe * What is first line?
First-line: intravenous replacement therapy
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Antibiotic therapy: AGE * Who is antibiotic therapy recommended for? (5)
* Severe diarrhea (enterotoxigenic, cholera) * Moderate to severe Travelers diarrhea * Enterotoxigenic E.coli * Most febrile dysenteric diarrhea * Culture-proven bacteria diarrhea
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Antibiotic therapy: AGE * What is it not recommended for?
Enterohemorrhagic E. coli (EHEC) * Shiga toxin producing * E.coli 0157H7
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Antibiotic therapy: Salmonella, nontyphi and shigella spp * Abx not recommended execpt for who?
Abx not recommended except for: * Severe disease * Age <1 or > 50yrs * Immunocompromised Abx treatment increases duration of fecal excretion
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Vaccine therapy: Rotavirus Vaccine * What is the type of vaccine? * What is the route? * What is the timing of the vaccines?
Live attenuated Oral drops * Rotateq (2, 4, 6 mo) * Rotarix (2, 4 mo) * Last dose before 8 months * Do not start after 15 weeks
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Vaccine therapy: Rotovirus * What is the risk?
Intussusception
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giardiasis * What is the species? MC what? * How is it transmitted?
* Giardia duodenalis (G. lamblia, G. intestinalis); MC intestinal parasite responsible for diarrhea worldwide * MC intestinal parasite in the US * Ingestion: contaminated water; fresh water; usually history of camping or hiking
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giardiasis * What is the first line treatment? * what are the alternatives?
First-line treatments: * **Tinidazole 2 gm PO x 1 dose** OR * Metronidazole 250 mg PO three times daily x 5 to 7 days Alternatives: * Nitazoxanide (Alinia) * Paromomycin – historically DOC in pregnancy (now we use metro for pregnancy)
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Clostridium Difficile * What is the morphology? * What does it cause?
* Gram positive anaerobic bacilli, spore former * Inflammation limited to colon
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Clostridium Difficile * What are the risk factors?(5)
* Advanced age * Hospitalization * Prior or concomitant antibiotics * Cancer chemotherapy – immune compromise * Gastrointestinal surgery
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Clostridium Difficile * What is the initial treatment for mild to moderate? * What is the treatment for severe?
Initial episode mild to moderate: * Fidaxomicin 200 mg PO BID * Vancomycin 125mg PO QID Severe * Vancomycin 500mg PO/NG QID * ± metronidazole 500mg IV Q8H
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C. Diff * What can you do for recurrent disease?
* Vancomycin tapers * Fecal microbiota transplant
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Rickets / osteomalacia * What happens to bone? Why does this happen?
Bone softening – usually secondary to faulty bone mineralization * Deficiency or impairment metabolism of vitamin D, calcium or phosphate
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What is needed for normal bone mineralization?
Requires osteoid plus * Adequate calcium and phosphate * Alkaline phosphatase Calcium and phosphate levels regulated by vitamin D and parathyroid hormone
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Rickets / osteomalacia * What is the MCC? What are the 3 reasons why?
MCC = vitamin D deficiency Not enough in the body * Poor intake * Intestinal malabsorption * Inadequate UV light exposure Not activated * Liver or kidney disease Medications – phenytoin (metabolized by liver hydroxylases)
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Rickets / osteomalacia * What are the labs? * What happens on the imaging?
Labs * Low vitamin D * Low calcium * Increased alkaline phosphatase X-rays – decreased bone mineral density / osteopenia
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Vitamin D replacement: Nutritional deficient Rickets * What is the MC therapy? (2) * What is recommended? * What is the dose?
MC therapy * Vitamin D2 (ergocalciferol) * Vitamin D3 (cholecalciferol) Daily therapy recommended Elemental calcium 30 to 50 mg/kg/day from dietary sources
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What is the process to get active form of vit D?
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Vitamin D replacement: Liver or kidney disease or mutation of vitamin D metabolism * What do you give? * Dose dependent on what? * What is the dietary source dose?
* Calcitriol [1,25(OH)2D3] required * Dose dependent on age and severity of deficiency * Elemental calcium 30 to 75 mg/kg/day from dietary sources
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Vitamin D replacement * What do you need to monitor and when? * Imaging?
Monitoring: monthly * Calcium * Phosphorus * Alkaline phosphatase * ± PTH X-ray every 3 months
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Vitamin B1 * What is the job? * What are the causes for it to be low? * What are the sxs?
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Wernicke’s / Korsakoff syndromes: Chronic alcoholism * Interferes with what? * Prevents with what? * What can decrease thiamine storage?
* Interferes with conversion of thiamine to thiamine pyrophosphate (TPP) * Prevents thiamine absorption in the small intestines * Cirrhosis may decrease thiamine storage
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Wernicke’s / Korsakoff syndromes * What is wernicke's encephalopathy? * What is korsakoff syndrome?
Wernicke’s encephalopathy * Acute, reversible Korsakoff syndrome * Chronic, irreversible * Prevention is key
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Wernicke’s treatment * What do you need to give? * Initial replacement should be what?
Thiamine 500mg IV Q8H x 2 days; then 250mg IV/IM daily x 5 days * Multiple recommendations exist Initial replacement should be IV or IM
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Wernicke’s treatment * Give thiamine before what? Why?
ALWAYS GIVE BEFORE GLUCOSE * Glucose needed for severe alcoholism / malnutrition * Increases thiamine demand and may worsen symptoms
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Wernicke’s treatment * What do you need to give after initial replacement
Continued replacement recommended for high-risk patients * 100mg PO daily
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Wernicke’s treatment
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## Footnote B2: Casa G; B3: Ds
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## Footnote DRAE
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Folic acid (vitamin B9) deficiency * When is there an increase and decrease demend/intake?
Increased demand * Pregnancy Decreased intake * > 6-week restrictive diet
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Folic acid (vitamin B9) deficiency * What causes decrease in absorption of folic acid?
Increased ETOH Medications * Phenytoin * Trimethoprim * Sulfasalazine * Methotrexate
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Folic acid deficiency * Folic acid is what * What does a deficiency cause? * What happens to blood cells?
Folic acid is a DNA precursor * Deficiency = impairment cell division (most apparent in rapidly dividing cells) Blood cells * RBC, WBC, and platelets = anemia, pancytopenia
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Folic acid deficiency * What happens to oral mucosa? * Increase levels of what? What does that cause?
* Oral mucosa: Old epithelial cells not replaced = glossitis * Increased levels of homocysteine and normal methylmalonic acid * Homocysteine = increased release of proinflammatory cytokines in vasculature and clumping of platelets (atherosclerosis, cardiovascular events)
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Folic acid deficiency * impaired closure of what?
Impaired closure of fetal neuropore
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Folic acid deficiency diagnosis and treatment * What is on CBC and peripheral blood smear
* CBC – low hemoglobin / hematocrit, MCV > 100 * Peripheral blood smear – large red blood cells *
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Folic acid deficiency diagnosis and treatment * What happens with vitamin B12 and folate levels?
< 2 ng/mL = deficiency / > 4ng/mL normal RBC folate levels provide information about folic acid stores and help determine timeline Consider checking methylmalonic acid (MMA) and homocysteine levels * MMA and homocysteine elevated – B12 deficiency * MMA normal, homocysteine elevated – folic acid deficiency
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Folic acid deficiency diagnosis and treatment * What is the txt?
* Folic acid * 1 to 5mg PO daily for 2-4 months 
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B12 deficiency * What is the process of B12 absorption?
* Acid degrades food products -> releases vit B12 * Parietal cells secrete intrinsic factory * B12 binds to intrinsic factor * Intrinsic factor shuttles B12 into cells of the ileum
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Vitamin B12 Deficiency * What is vitamin b12? * What happens with deficiency? * What happens with the blood cells? * What happens with oral mucosa?
* Vitamin B12 (cobalamin) is a DNA precursor * Deficiency = impairment cell division (most apparent in rapidly dividing cells) * Blood cells: RBC, WBC, and platelets = anemia, pancytopenia * Oral mucosa->Old epithelial cells not replaced = glossitis
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Vitamin B12 Deficiency * What levels are increased? What does that cause?
Increased levels of homocysteine and methylmalonic acid * Homocysteine = increased release of proinflammatory cytokines in vasculature and clumping of platelets (atherosclerosis, cardiovascular events) * Methylmalonic acid = damages myelin sheath of nerves, impairment of neurological and muscle function (peripheral neuropathies, paresthesias, impaired proprioception/vibratory sense, dementia, poor balance)
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Vitamin B12 diagnosis and treatment * What can you do for dx? * What is the level for deficiency * when it is between 100-400, what do you need to check? What do the results mean?
Peripheral blood smear ± bone marrow evaluation < 100 pg/mL – deficiency 100 to 400 pg/mL – check methylmalonic acid (MMA) and homocysteine levels * MMA and homocysteine elevated – deficiency * MMA level elevated, homocysteine normal – deficiency
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Vitamin B12 diagnosis and treatment
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Fat soluble vitamins * What are the causes of deficiency?
Decreased absorption * Poor diet Fat malabsorption * Chronic pancreatitis * Cystic fibrosis
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Phenylketonuria (PKU) * Error of what? * MC form? What does that cause?
MC inborn error of metabolism MC forms autosomal recessive * Phenylalanine hydroxylase enzyme deficiency * Tetrahydrobiopterin deficiency
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Phenylketonuria (PKU) * What is elevated? * Metabolized by what? * Competes for what? * Decreased what?
Elevated phenylalanine * Metabolized by different enzymes to phenylacetones – excreted in the urine * Competes for tyrosine and tryptophan to cross BBB * Decreased neurotransmitters in the brain = trouble with brain development / intellectual disability
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Phenylketonuria (PKU) * Testing part of what? * What are the sxs?
Testing part of the newborn screening Symptoms * Musty order of sweat and urine * Hypopigmentation of skin, hair, eyes * Developmental delays * Seizures
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Phenylketonuria (PKU) * What is the txt? * What are some supplements?
Treatments: * Diet low in phenylalanine * Avoid: foods high in protein (AA precursor) Supplements: * Tyrosine * Tetrahydrobiopterin
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Pharm III (14 decks)

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