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

Lecture 3 (GI)- Exam 2 Flashcards

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
Q
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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25
Q
A
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26
Q

Appendicitis:
* What are the sxs?
* What are the PE?

A

Symptoms
* Abdominal pain
* N/V/D
* Fever

PE findings:
* Know all the signs: Mcburny, obturator, psosas, rovsing, etc

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27
Q

Commonly tested

What are some causes of appendicitis?(4)

A

Know that lymphoid hyperplasia is children

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28
Q

How do you dx appendicitis?

A
  • Ultrasound (pediatrics)
  • CT abdomen with IV contract
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29
Q

Appendicitis treatment: not ruptured
* What is first line?
* What do you need to do perioperativly? Post operative?

A

First-line: appendectomy
* Perioperative antibiotics: Ceftriaxone plus metronidazole
* 0 to 7 days post operative antibiotics-> Less evidence

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30
Q

Appendicitis treatment: ruptured or sepsis
* What is first line?

A

First-line: supportive care plus antibiotics
* Stabilize
* Percutaneous drain
* Antibiotic therapy

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31
Q

Rupture / sepsis:
* What are the empiric IV antibiotics choices? (3)
* What can be added?

A
  • Meropenem or imipenem
  • Piperacillin/tazobactam
  • Ciprofloxacin plus metronidazole
  • ± percutaneous drain
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32
Q

Appendicitis treatment:
* When do you convert the antibiotics?
* When do you f/u?

A
  • 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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33
Q

Antimicrobial prophylaxis:
* What do you do for gastroduodenal surgery?
* What do you do for billary tract surgery?

A
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34
Q

Antimicrobial prophylaxis:
* What do you use for appendectomy?
* What do you use for small intestine surgery?

A
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35
Q

Antimicrobial prophylaxis:
* What do you do for hernia repair?
* What do you do for colorectal surgery?

A
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36
Q

Celiac sprue/disease
* Most common type of what?
* What are other names? (2)
* What is it?

A
  • Most common type of mucosal malabsorption
  • AKA - Nontropical Sprue or Gluten-Sensitive Enteropathy
  • Immunologic intolerance to gluten
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37
Q
A
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38
Q

Celiac Sprue / disease
* Affected persons have waht?
* What is the patho behind this?

A
  • 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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39
Q
A
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40
Q

Celiac disease: Presentation
* What are the sxs? (6)
* What can happen to the skin?
* What can happen to the blood?

A
  • Crampy abdominal pain, diarrhea, flatulence, bloating, weight loss, steatorrhea.
  • Dermatitis Herpetiformis – blistering, pruritic skin rash (Gluten rash)
  • Iron deficiency anemia
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41
Q

Celiac disease
* What are some sxs that can occue due to vitamin deficiency? (4)

A
  • Osteoporosis (vitamin D malabsorption)
  • Peripheral neuropathy (B12 deficiency)
  • Easy bruising (vitamin K malabsorption)
  • Edema (malabsorption of protein)
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42
Q

Celiac disease
* How do you dx it?

A

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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43
Q

Celiac disease
* how do you txt it?

A
  • Strict gluten-free diet for life
  • Correct micronutrient deficiencies
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44
Q

General treatment approach- celiac
* Consultation with who?
* Educate what?
* Lifelong what?

A
  • Consultation with a skilled dietitian
  • Education about the disease
  • Lifelong adherence to a gluten-free diet
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45
Q

General treatment approach- celiac
* What do you need to ID and treat?

A

Identification and treatment of nutritional deficiencies
* Vit A, D, E, B12
* Copper, Zinc
* Carotene
* Folic acid
* Ferritin, iron

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46
Q

General treatment approach- celiac
* Access to what?
* Continuous what?

A

Access to an advocacy group

Continuous long-term follow-up by a multidisciplinary team
* Osteoporosis
* Pneumococcal vaccine

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47
Q

What are some good and bad foods for celiac disease?

A
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48
Q

What is the difference between food allergy and food intolerance?

A
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49
Q

lactose intolerance
* What is lactose?
* How it is broken down? What happens with it?

A

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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50
Q

Lactose intolerance
* What happens when there is a deficency of lactase?

A
  • 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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51
Q

Lactose intolerance
* What are the types (3)

A
  • Congenital lactose intolerance rare (automsomal recessive)
  • MCC = lactase nonpersistence
  • Secondary: Malabsorption syndromes
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52
Q

Lactose intolerance: Lactase nonpersitence
* When is lactase high?
* When does it decrease?
* Race difference?

A
  • High lactase when young
  • Decreases with age; lower when older
  • Caucasians maintain lactase
  • African Americans, American Indians, Asian Americans low lactase
53
Q

Lactose intolerance
* What are the sxs? (3)
* How do you dx it?(3)

A

Symptoms:
* Abdominal pain
* Bloating
* Diarrhea

Diagnosis:
* Clinical, lactose hydrogen breath test, lactose tolerance test

54
Q

Lactose intolerance
* What is the txt?

A
  • Decreasing lactose intake
  • 2 cups of milk or lactase equivalents/day
  • Lactase supplements: One to 3 tablets before dairy containing food
56
Q

Infectious Diarrhea: inflammatory/bloody diarrhea (dysentery)
* What are common sxs? (5)
* What is postive?
* What is required?

A
  • 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
57
Q

Infectious Diarrhea: inflammatory/bloody diarrhea (dysentery)
* What are the common causes?

A

Shigella, Salmonella, Campylobacter, Yersinia, invasive strains of E.coli, Entamoeba histolytica and C. difficile

58
Q

Infectious Diarrhea: Noninflammatory, non-bloody or watery
* Caused by what?
* What type of diarrhea?
* What are the common sxs?

A
  • Milder, caused by viruses or toxins that affect small intestine
  • Large-watery diarrhea
  • Common Symptoms: Nausea, vomiting, cramps
59
Q

Infectious Diarrhea: Noninflammatory, non-bloody or watery
* What are the common causes?

A

Rotavirus, norovirus, astrovirus, enteric viruses, vibriones, enterotoxin-producing E. coli, Giardia lamblia, crystosporidia & agents that cause food-borne gastroenteritis

61
Q

Acute gastroenteritis
* Most are what?
* Patients seeking care should be evaluated for what?

A
  • Most are self limiting and self resolve without specific treatments
  • Patients seeking care should be evaluated for dehydration
62
Q

Acute gastroenteritis
* Further work-up considered for patients with the following? (5)

A
  • 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)
67
Q

Volume repletion: Mild to moderate dehydration
* What is first line?

A

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

68
Q

Volume repletion: Severe
* What is first line?

A

First-line: intravenous replacement therapy

70
Q

Antibiotic therapy: AGE
* Who is antibiotic therapy recommended for? (5)

A
  • Severe diarrhea (enterotoxigenic, cholera)
  • Moderate to severe Travelers diarrhea
  • Enterotoxigenic E.coli
  • Most febrile dysenteric diarrhea
  • Culture-proven bacteria diarrhea
71
Q

Antibiotic therapy: AGE
* What is it not recommended for?

A

Enterohemorrhagic E. coli (EHEC)
* Shiga toxin producing
* E.coli 0157H7

73
Q

Fill in for the txt?

74
Q

Fill in for txt

75
Q

Antibiotic therapy: Salmonella, nontyphi and shigella spp
* Abx not recommended execpt for who?

A

Abx not recommended except for:
* Severe disease
* Age <1 or > 50yrs
* Immunocompromised

Abx treatment increases duration of fecal excretion

76
Q

Vaccine therapy: Rotavirus Vaccine
* What is the type of vaccine?
* What is the route?
* What is the timing of the vaccines?

A

Live attenuated

Oral drops
* Rotateq (2, 4, 6 mo)
* Rotarix (2, 4 mo)
* Last dose before 8 months
* Do not start after 15 weeks

77
Q

Vaccine therapy: Rotovirus
* What is the risk?

A

Intussusception

78
Q

giardiasis
* What is the species? MC what?
* How is it transmitted?

A
  • 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
79
Q

giardiasis
* What is the first line treatment?
* what are the alternatives?

A

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)

80
Q

Clostridium Difficile
* What is the morphology?
* What does it cause?

A
  • Gram positive anaerobic bacilli, spore former
  • Inflammation limited to colon
81
Q

Clostridium Difficile
* What are the risk factors?(5)

A
  • Advanced age
  • Hospitalization
  • Prior or concomitant antibiotics
  • Cancer chemotherapy – immune compromise
  • Gastrointestinal surgery
82
Q

Clostridium Difficile
* What is the initial treatment for mild to moderate?
* What is the treatment for severe?

A

Initial episode mild to moderate:
* Fidaxomicin 200 mg PO BID
* Vancomycin 125mg PO QID

Severe
* Vancomycin 500mg PO/NG QID
* ± metronidazole 500mg IV Q8H

83
Q

C. Diff
* What can you do for recurrent disease?

A
  • Vancomycin tapers
  • Fecal microbiota transplant
84
Q

Rickets / osteomalacia
* What happens to bone? Why does this happen?

A

Bone softening – usually secondary to faulty bone mineralization
* Deficiency or impairment metabolism of vitamin D, calcium or phosphate

85
Q

What is needed for normal bone mineralization?

A

Requires osteoid plus
* Adequate calcium and phosphate
* Alkaline phosphatase

Calcium and phosphate levels regulated by vitamin D and parathyroid hormone

86
Q

Rickets / osteomalacia
* What is the MCC? What are the 3 reasons why?

A

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)

87
Q

Rickets / osteomalacia
* What are the labs?
* What happens on the imaging?

A

Labs
* Low vitamin D
* Low calcium
* Increased alkaline phosphatase

X-rays – decreased bone mineral density / osteopenia

88
Q

Vitamin D replacement: Nutritional deficient Rickets
* What is the MC therapy? (2)
* What is recommended?
* What is the dose?

A

MC therapy
* Vitamin D2 (ergocalciferol)
* Vitamin D3 (cholecalciferol)

Daily therapyrecommended

Elemental calcium 30 to 50 mg/kg/day from dietary sources

89
Q

Fill in for the vitamin D replacement-Said FYI

90
Q

What is the process to get active form of vit D?

91
Q

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?

A
  • 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
92
Q

Vitamin D replacement
* What do you need to monitor and when?
* Imaging?

A

Monitoring: monthly
* Calcium
* Phosphorus
* Alkaline phosphatase
* ± PTH

X-ray every 3 months

94
Q

Fill in covered part

95
Q

Fill in covered part

97
Q

Vitamin B1
* What is the job?
* What are the causes for it to be low?
* What are the sxs?

98
Q

Wernicke’s / Korsakoff syndromes: Chronic alcoholism
* Interferes with what?
* Prevents with what?
* What can decrease thiamine storage?

A
  • Interferes with conversion of thiamine to thiamine pyrophosphate (TPP)
  • Prevents thiamine absorption in the small intestines
  • Cirrhosis may decrease thiamine storage
99
Q

Wernicke’s / Korsakoff syndromes
* What is wernicke’s encephalopathy?
* What is korsakoff syndrome?

A

Wernicke’s encephalopathy
* Acute, reversible

Korsakoff syndrome
* Chronic, irreversible
* Prevention is key

100
Q

Wernicke’s treatment
* What do you need to give?
* Initial replacement should be what?

A

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

101
Q

Wernicke’s treatment
* Give thiamine before what? Why?

A

ALWAYS GIVE BEFORE GLUCOSE
* Glucose needed for severe alcoholism / malnutrition
* Increases thiamine demand and may worsen symptoms

102
Q

Wernicke’s treatment
* What do you need to give after initial replacement

A

Continued replacement recommended for high-risk patients
* 100mg PO daily

103
Q

Wernicke’s treatment

104
Q
A

B2: Casa G; B3: Ds

106
Q
108
Q

Folic acid (vitamin B9) deficiency
* When is there an increase and decrease demend/intake?

A

Increased demand
* Pregnancy

Decreased intake
* > 6-week restrictive diet

109
Q

Folic acid (vitamin B9) deficiency
* What causes decrease in absorption of folic acid?

A

Increased ETOH

Medications
* Phenytoin
* Trimethoprim
* Sulfasalazine
* Methotrexate

110
Q

Folic acid deficiency
* Folic acid is what
* What does a deficiency cause?
* What happens to blood cells?

A

Folic acid is a DNA precursor
* Deficiency = impairment cell division (most apparent in rapidly dividing cells)

Blood cells
* RBC, WBC, and platelets = anemia, pancytopenia

111
Q

Folic acid deficiency
* What happens to oral mucosa?
* Increase levels of what? What does that cause?

A
  • 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)
112
Q

Folic acid deficiency
* impaired closure of what?

A

Impaired closure of fetal neuropore

113
Q

Folic acid deficiency diagnosis and treatment
* What is on CBC and peripheral blood smear

A
  • CBC – low hemoglobin / hematocrit, MCV > 100
  • Peripheral blood smear – large red blood cells
    *
114
Q

Folic acid deficiency diagnosis and treatment
* What happens with vitamin B12 and folate levels?

A

< 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

115
Q

Folic acid deficiency diagnosis and treatment
* What is the txt?

A
  • Folic acid
  • 1 to 5mg PO daily for 2-4 months
117
Q

B12 deficiency
* What is the process of B12 absorption?

A
  • 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
118
Q

Vitamin B12 Deficiency
* What is vitamin b12?
* What happens with deficiency?
* What happens with the blood cells?
* What happens with oral mucosa?

A
  • 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
119
Q

Vitamin B12 Deficiency
* What levels are increased? What does that cause?

A

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)

120
Q

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?

A

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

121
Q

Vitamin B12 diagnosis and treatment

122
Q

Fat soluble vitamins
* What are the causes of deficiency?

A

Decreased absorption
* Poor diet

Fat malabsorption
* Chronic pancreatitis
* Cystic fibrosis

125
Q

Phenylketonuria (PKU)
* Error of what?
* MC form? What does that cause?

A

MC inborn error of metabolism

MC forms autosomal recessive
* Phenylalanine hydroxylase enzyme deficiency
* Tetrahydrobiopterin deficiency

126
Q

Phenylketonuria (PKU)
* What is elevated?
* Metabolized by what?
* Competes for what?
* Decreased what?

A

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

127
Q

Phenylketonuria (PKU)
* Testing part of what?
* What are the sxs?

A

Testing part of the newborn screening

Symptoms
* Musty order of sweat and urine
* Hypopigmentation of skin, hair, eyes
* Developmental delays
* Seizures

128
Q

Phenylketonuria (PKU)
* What is the txt?
* What are some supplements?

A

Treatments:
* Diet low in phenylalanine
* Avoid: foods high in protein (AA precursor)

Supplements:
* Tyrosine
* Tetrahydrobiopterin

Pharm III (14 decks)

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