Gastric Disorders + Nutrition Flashcards

1
Q

Which of the following will inhibit gastric acid secretion?

a) somatostatin
b) vagal stimulation
c) antral distension
d) histamine
e) calcium

A

a) somatostatin

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2
Q

What is the effect on lesions to the lateral hypothalamus on hunger?

A

leads to loss of appetite (hypophagia)

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3
Q

What are the major nutritional complications of celiac disease?

A

iron deficiency (anemia)

lactose intolerance

osteopenia

vitamin B deficiencies

altered bowel habits

calorie/protein deficiency

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4
Q

What is the clinical workup for carbohydrate malabsorption?

A

breath test with lactose, fructose

lactose intolerance genetic typing

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5
Q

What is the impact of liver blood flow on high extraction drugs? Low extraction drugs?

A

high: sensitive
low: insensitive

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6
Q

What is this?

A

Peutz-Jeghers syndrome

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7
Q

What is adiposity rebound?

A

the inflection point between a declining BMI and an increasing BMI that occurs between age 5 and 7

if rebound occurs earlier, increases risk of being overweight later in live

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8
Q

What are the symptoms of iodine deficiency?

A

goiter (thyroid gland hyperplasia in response to elevated TSH), hypothyroidism

can affect fetuses in utero

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9
Q

What is the only identified factor that increases hunger?

A

ghrelin

levels increase by fasting, fall after a meal

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10
Q

How are smaller sugars (from starches) broken down into monosaccharides?

A

disaccharidases on the brush border

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11
Q

What specific genetic variants predispose patients to obesity?

A

leptin deficiency (chromosome 7)

defective leptin receptor (chromosome 1)

defective pro-opiomelanocortin (chromosome 2)

deficient melanocortin 4 receptor (chromosome 18)

obesity-associated FTO gene

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12
Q

How are proteins absorbed in brush border endothelium?

A

via carrier protein transport and glutathione transport

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13
Q

What are the risk factors for thiamine deficiency?

A

alcoholism, eating disorders, GI surgery

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14
Q

Where is amylin released from? When is it released?

A

co-secreted with insulin from pancreatic islet beta-cells

released in response to nutritional stimuli

inhibits gastric emptying and glucagon secretion, reduces short-term food intake

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15
Q

What are the major complications of autoimmune gastritis?

A

1) hyperplasia of gastrin producing cells and enterochromaffin-like cells
2) development of carcinoid tumors
3) development of epithelial dysplasia followed by adenocarcinoma

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16
Q

What is the pathogenesis of multifocal chronic atrophic gastritis?

A

associated with dietary and environmental risk facters

also associated with H. pylori infection

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17
Q

A patient comes in with stomach pain. He is currently taking omeprazole to help with the pain. You give him a urea breath test that comes back negative. What can you conclude?

a) he definitely does not have an H. pylori infection
b) he definitely has an H. pylori infection
c) he might have an H. pylori infection, but he needs serologic testing
d) he might have an H. pylori infection, but he needs fecal antigen testing

A

c) he might have an H. pylori infection, but he needs serologic testing

PPIs interfere with H. pylori growth, leading to false negatives on non-serologic testing

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18
Q

What are the main mechanisms that protect the luminal surface of epithelial cells from autodigestion?

A

mucus secretion (impermeable to H+)

bicarbonate secretion (neutralizes acid)

intercellular tight junctions

blood flow removes acid and supplies nutrients

muscularis mucosa limits injury

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19
Q

When trying to lose weight, why is exercise less effective as a treatment than dietary restriction?

A

energetically, physical activity and exercise does not burn sufficient calories to cause a significant change in energy balance

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20
Q

What is hunger?

A

biological sensation that initiates eating

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21
Q

Which of the following mechanisms plays an important role in the development of a gastric ulcer in a 32 year old patient with rheumatoid arthritis taking ibuprofen 800 mg three times daily for one month?

a) reduction in blood flow to the gastric mucosa
b) ion trapping and low pKa of ibuprofen
c) excessive production of acid induced by ibuprofen
d) concomitant infection with H. pylori
e) autoimmune damage to gastric epithelium

A

a) reduction in blood flow to the gastric mucosa

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22
Q

How are glucose and galactose transported?

A

active transport via a carrier that also transports Na+ (2 Na/ 1 glucose)

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23
Q

What is the pathogenesis of Whipple’s disease?

A

bacteria enter body via small intestine and spread to other organs through lymphatics and blood

primary abnormality is an immunological deficiency in the host that allows this bacteria to cause disease

involvements: mitral and aortic valve, CNS, mesenteric lymph nodes, lungs, kidneys, small intestine

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24
Q

What are the macroscopic features of appendicitis? Microscopic?

A

macroscopic: dilation of lumen and congested serosal vessels, dilated distal lumen full of purulent material, organ becomes soft and hemorrhagic
microscopic: acute inflammatory features

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25
Q

What is the thermodynamic definition of obesity?

A

an energy imbalance where energy-in exceeds energy-out (ie. more calories consumed than calories expended)

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26
Q

Which of the following statements regarding Helicobacter pylori is not true?

a) transmission of H. pylori mirrors transmission of polio virus
b) H. pylori infection may be a factor in the development of gastric lymphoma
c) postprandial release of gastrin and gastric acid is higher in patients with H. pylori antral gastritis
d) patients infected with H. pylori have an eradication rate of greater than 90% when treated with antibiotics
e) there seems to be “familial clustering” of H. pylori infection

A

c) postprandial release of gastrin and gastric acid is higher in patients with H. pylori antral gastritis

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27
Q

When is CCK released in relation to food intake?

A

released postprandially from I cells in the small intestine

reduces food intake through CCK-1 receptors on the vagus nerve

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28
Q

What is the general process of drug metabolism?

A

broken into two phases

phase I - usually involves oxidation or reduction by CYP enzymes (activates prodrugs, inactivates standard drugs)

Phase II - modifies drug metabolite with water soluble adducts to enable elimination (ex. glucuronidation)

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29
Q

What is the difference between high extraction and low extraction drugs? What are examples of each?

A

high extraction = very efficiently cleared by the liver, low extraction = less efficient

high: morphine, propranolol, lidocaine
low: digoxin, diazepam, pheytoin

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30
Q

What are the complications of appendicitis?

A

perforation, peritonitis, abscess formation, septic thrombophlebitis

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31
Q

What are the dietary risk factors of stomach carcinomas?

A

dried/salted fish, pickeled vegetables, contaminated foods/rices

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32
Q

What are risk factors for iron deficiency?

A

young age, menstruation, pregnancy, blood loss, malabsorptive disorders (ex. celiac disease), bariatric surgery

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33
Q

What are hamartomas?

A

tumor-like malformations characterized by an abnormal mixture and overgrowth of tissue indigenous to the region of the malformation

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34
Q

A patient is given chemotherapy with 5-fluorouracil and irinotecan. After two treatments, the patient had neutropenia. Given that these drugs do not typically cause bone marrow suppression at the doses given to this patient, which of the following factors might have contributed to neutropenia and thrombocytopenia in this case?

a) 5-fluorouracil induced an immune-mediated thrombocytopenia
b) elimination of an active metabolite of irinotecan was impaired in this patient resulting in greater toxicity
c) 5-fluorouracil inhibited the metabolism of irinotecan resulting in greater toxicity
d) the subject has bone marrow infiltration by adenocarcinoma

A

b) elimination of an active metabolite of irinotecan was impaired in this patient resulting in greater toxicity

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35
Q

What is the effect of CCK on hunger?

A

it enhances satiation

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36
Q

Where are the major sites of chronic peptic ulcer?

A

anterior and posterior walls of duodenum

antral and prepyloric regions of stomach

lower end of esophagus

Meckel’s diverticulum with gastric mucosa

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37
Q

What are the characteristics of helicobacter pylori (shape, gram stain, etc.)?

A

curved, motile gram-negative bacterium

requires microaerophilic conditions for growth

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38
Q

What is the average weight of a 1 year old?

A

10 kg

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39
Q

What are the secretory components of oxyntic glands? Where are they found?

A

parietal cell –> secretes HCl

ECL –> secretes histamine

Chief cell –> pepsinogen

some D cells –> somatostatin

located in gastric body and fundus

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40
Q

What is satation?

A

level of fullness during a meal which regulates the amoutn of food consumed

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41
Q

When can BMI be used for children?

A

> 2 years of age

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42
Q

What is the clinical workup for fat malabsorption?

A

fecal fat studies (48-72 hour stool collection, fecal elastase, fecal electrolytes)

vitamin B12 specific testing

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43
Q

What is the mechanism of hypothalamic obesity?

A

ventromedial hypothalamus damage –> hyperphagia –> no response to leptin –> weight gain

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44
Q

What is the effect of ghrelin on hunger?

A

increases hunger

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45
Q

What are the symptoms of celiac disease?

A

diarrhea, steatorrhea, weight loss, development of symptoms related to nutritional deficiency

related to malabsorption

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46
Q

What are the major host defense mechanisms of the mucosal immune system?

A

physical barrier: mucus, epithelial cells, secretory IgA

antimicrobials: trefoil peptides, paneth cell peptides

specialized immune response: antigen uptake, lymphocyte trafficking, effector cells

also indigenous microbiota

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47
Q

What enzyme hydrolyzes starch? Where does it come from? What is the mechanism of hydrolysis?

A

alpha amylase

salivary and pancreatic secretions

attacks interior 1,6 bonds (not at branch points)

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48
Q

What are the risk factors for niacin deficiency?

A

malabsorptive GI disorders, eating disorders, alcoholism, isoniazid use

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49
Q

Which function would NOT be directly affected by inhibition of the Na/K ATPase?

a) absorption of 2-monoglycerides
b) absorption of galactose
c) secretion of bile salts by the liver
d) absorption of amino acids
e) salivary secretion

A

a) absorption of 2-monoglycerides

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50
Q

What is the effect of niacin deficiency?

A

pellagra –> 4 “Ds”: dermatitis, diarrhea, dementia, death

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51
Q

If a patient is diagnosed with menetrier disease, what major complication should you be concerned about?

A

gastric adenocarcinoma

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52
Q

What are the unique characteristics of visceral fat cells?

A

more active lipolysis, extra adrenergic and glucocorticoid receptors, and increased responsiveness to glucocorticoids

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53
Q

What are the major risks associated with gastric carcinoma? Cardia carcinoma?

A

gastric: H. pylori infection, chronic gastritis
cardia: alcohol and tobacco use

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54
Q

What are the clinical features of gastric carcinomas?

A

no specific symptoms, depends on size/location

vomiting if upper GI

anemia from occult blood loss

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55
Q

What are the causative factors relating obesity and insulin resistance to metabolic syndrome?

A

1) FFAs are increased (impairs insulin action)
2) intracellular lipid accumulation
3) circulating cytokines modify insulin action

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56
Q

How is Zollinger Ellison Syndrome diagnosed?

A

measuring fasting serum gastrin (> 1000)

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57
Q

What is the effect of amylin on hunger?

A

enhances satiation

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58
Q

How is helicobacter pylori transmitted?

A

person-to-person contact

oral-oral in industrialized countries, fecal-oral in developing countries

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59
Q

What is early gastric carcinoma?

A

carcinoma confined to the mucosa or mucosa + submucosa of stomach (regardless of lymph metastasis)

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60
Q

Which brain regions are involved in hypothalamic obesity?

A

ventromedial or paraventricular region of the hypothalamus or amygdala

regions responsible for integrating metabolic info on nutrient stores provided by leptin with afferent sensory info on food availability

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61
Q

What is the role of the ileum in absorption?

A

fat (and fat-soluble vitamin) absorption

bile salt recycling

ileocecal valve and ileal “break”

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62
Q

What are the two key factors in developing metabolic syndrome?

A

insulin resistance

obesity

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63
Q

What is the pathophysiology of zollinger-ellison syndrome?

A

islet cell tumors that secrete gastrin –> increases parietal cell mass –> increased acid secretion

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64
Q

What are the gross features of stomach carcinomas?

A

fungiating, ulcerating, nodular, diffuse, or superficial

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65
Q

What controls release of gastrin in the stomach? What is its effect on acid production?

A

G cells produce gastrin

Gastrin –> CCK-B receptor –> GPCR triggers increase of IP3/Ca2+ –> activates the H/K ATPase to release acid into the stomach lumen

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66
Q

What vitamins and minerals do gastric bypass patients need to supplement with either food or oral supplements due to anatomical changes?

A

B vitamins

iron

fat soluble vitamins

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67
Q

What are the functions of IgA?

A

confines bacteria to the mucus layer of the intestinal lumen

binds to invasive pathogens

neutralizes microbial toxins and other inflammatory products

neutralization of antigens and pathogens, uptake of luminal antigens

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68
Q

Where is leptin released from? When is it released?

A

leptin is produced from adipose cells

secreted in response to an increase in fat mass

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69
Q

Why does deposition of fat in lower body segments (buttocks, thigh, hips) reduce the risk for obesity-associated morbidity?

A

lower body fat is associated less with visceral fat and more with subcutaneous fat

visceral fat depot releases adipokines that impact multiple organ systems

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70
Q

What is the effect of vitamin D deficiency?

A

rickets (children), osteomalacia (adults), muscle pain, weakness

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71
Q

What is the inductive vs. effector site of mucosal immunity?

A

inductive site: antigen sampling and presentation

effector site: site of effector immune action

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72
Q

What is the pathophysiology of celiac disease?

A

lack of a specific mucosal peptidase, results in accumulation of gluten or glutamine containing breakdown products and accumulation of toxic peptides

initiates hypersensitivity reactions in the intestinal mucosa

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73
Q

What types of drugs are likely to produce weight gain?

A

psychoactive agents, anti-depressants, anti-diabetic agents, corticosteroids

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74
Q

What are crypt abscesses?

A

collections of neutrophils in the lumen of a gland

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75
Q

What are the effects of vitamin A deficiency?

A

affects function of WBCs, epithelial cells, conjunctiva and cornea of eye

leads to night blindness, bitot spots, and corneal ulceration

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76
Q

How is ectopic fat measured?

A

MRI, magnetic resonance spectroscopy (MRS)

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77
Q

What are major pathologic consequences of obesity?

A

joint immobility and arthralgias (hips, knees, ankles, feet)

GERD and urinary incontinence (increased abdominal pressure)

edema and stasis pigmentation (accumulation of water and hemodynamic changes)

excessive sweating and skin infections

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78
Q

Pancreatitis patients often require pancreatic enzyme supplementation to properly emulsify fats and absorb nutrients. Which nutrients are they at most risk of malabsorbing?

a) B-vitamins, fat soluble vitamins, iron and zinc
b) dietary fats, carbohydrates, fat soluble vitamins, zinc
c) iron, B-vitamins, iodine

A

b) dietary fats, carbohydrates, fat soluble vitamins, zinc

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79
Q

What is the pathogenes if H. pylori associated chronic gastritis?

A

H. pylori can grow in acidic environments due to urease activity that neutralizes the acid

also produces proteins that assist with infection into the gastric mucosa

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80
Q

How is H. plyori diagnosed?

A

serologic testing (IgG antibody)

fecal antigen testing

urea breath test

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81
Q

What are the major characteristics of dietary therapy to treat EoE?

A

typical approach is a hypoallergenic diet that eliminates 6 major allergens

often can be reintroduced gradually

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82
Q

When individuals with obesity reduce their caloric intake, they typically feel hungry which makes long-term weight loss and maintenace difficult. What are the underlying mechanisms that cause them to feel hungrier?

A

calorie reduction and weight loss results in biological adaptation

changes in gut hormones that regulate eating behavior and appetite –> ghrelin rises, GLP-1 and PYY levels fall

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83
Q

How is visceral adipose tissue measured clinically?

A

by measuring waist circumference during the physical exam

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84
Q

A patient with previously well documented duodenal ulcer and gastrointestinal bleeding was treated for H. pylori infection with 14 days of omeprazole 20 mg BiD, amoxicillin 1 gm BiD, clarithromycin 500 mg BiD. He presents with recurrent epigastric pain 2 months after completion of therapy. The best approach to this patient would be:

a) treatment with omeprazole 20 mg BiD, metronidazole 500 mg BiD, clarithromycin 500 mg BiD for 14 days
b) upper gastrointestinal endoscopy
c) carbon labeled urea breath test
d) measure serum IgG antibody to H. pylori
e) omeprazole 20 mg QD for 4 weeks and re-evaluate

A

c) carbon labeled urea breath test

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85
Q

What questions would you ask a patient when taking a history to determine what relevant factors may have contributed to his/her weight gain?

A

when did you start to gain weight?

were there specific life events or factors that played a role (puberty, pregnancy, menopause, smoking cessation, etc)?

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86
Q

What are the clinical features of carcinoid syndrome?

A

paroxysms of flushing, asthma-like attacks, diarrhea, right-sided heart failure (stenosis of tricuspid and pulmonary valves)

can also cause peptic ulcers and malabsorption

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87
Q

What is the effect of cirrhosis on drug pharmacokinetics?

A

reduced hepatocyte mass (impacts low extraction drugs)

reduced portal blood flow (reduced first pass metabolism)

thickened hepatic sinusoidal basement membrane, shunting blood flow (impacts high extraction drugs)

ascites (increased volume of distribution of hydrophilic drugs)

low plasma albumin levels (impacts low extraction drugs)

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88
Q

What is the effect of lesions to the ventromedial hypothalamus on hunber?

A

induces excessive hunger (hyperphagia)

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89
Q

What are the gross findings of celiac disease? Microscopic findings?

A

gross: mucosa with lost ridges and convolutions (becomes flat)
microscopic: shortening and broadening of villi with loss of villi, enterocytes smaller and crowded, increase in intraepithelial lymphocytes, increased inflammation in lamina propria, increased mitotic activity in crypts (elongation of crypts)

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90
Q

What is Gilbert syndrome? What is its effect on drug metabolism?

A

recessive genetic condition that impairs function of UTGA1 gene

leads to impaired conjugation of bilirubin and select drugs (irinotecan, lamotrigine, raloxifene, simvastatin)

requires dose adjustment due to impaired drug elimination

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91
Q

What types of ulcers are associated with pernicious anemia?

A

non-benign ulcers secondary to autoimmune gastritis with achlorhydria

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92
Q

What explains the difference in the time course of azithromycin plasma concentration between patients with and without Roux-en-Y gastric bypass?

a) metabolism of azithromycin is enhanced in post-RYGB subjects
b) oral absorption of azithromycin is impaired after RYGB resulting in lower peak plasma concentration
c) plasma half-life of azithromycin is shorter in post-RYGB subjects
d) distribution of azithromycin to adipose tissue is diminished in post-RYGB subjects

A

b) oral absorption of azithromycin is impaired after RYGB resulting in lower peak plasma concentration

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93
Q

In children, a BMI range of 85-95% is considered:

a) normal
b) overweight
c) obese
d) underweight

A

b) overweight

>95% is obese

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94
Q

What are the effects of vitamin C deficiency?

A

gingivitis, tooth loss, corkscrew hairs, perifollicular hemorrhages, intraarticular hemorrhages, bruising, poor wound healing

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95
Q

What are the complications of diffuse antral chronic gastritis?

A

1) prepyloric and duodenal ulcers
2) gastric lymphoma
3) risk of gastric carcinoma

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96
Q

What is the effect of prostaglandins on acid production in the stomach?

A

prostaglandins activate a GPCR that decreases cAMP levels–> inhibits the H/K ATPase to reduce acid release into the stomach lumen

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97
Q

What is the role of epithelial cells in innate immunity?

A

physical and immune barrier

expression of pattern recognition receptors for the PAMPs on bacteria and viral species

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98
Q

Clearance of drugs by the liver depends on intrinsic metabolic capacity, hepatic blood flow, and the extent to which the drug is bound by plasma proteins. Which statement best describes clearance of a specific drug in advanced cirrhosis?

a) elimination of digoxin in cirrhosis is enhanced by low hepatic blood flow
b) the bioavailability of morphine is enhanced
c) morphine clearance by the liver is impaired because of hypoalbuminemia
d) the bioavailability of oral morphine is lower in cirrhosis

A

b) the bioavailability of morphine is enhanced

cirrhosis leads to reduced portal blood flow, which decreases first pass metabolism and increases bioavailability of high extraction drugs

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99
Q

What is the effect of magnesium deficiency?

A

diarrhea (in Chron’s disease or malabsorptive syndromes)

rare to actually have a true deficiency

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100
Q

What is the general pattern of weight changes in women throughout life?

A

weight status predicted by weight in youth

weight gain during pregnancy is variable

central fat deposition increases after menopause

101
Q

What is the effect of zinc deficiency?

A

impaired growth, skin rashes, hypogonadism/delayed puberty, hair loss, anorexia

102
Q

What is the histology of Peutz-Jegher’s syndrome?

A

branching bundles of smooth musclee derived from muscularis mucosae

branches covered by normal epithelium with a normal lamina propria

paneth cells and endocrine cells at base of crypts

103
Q

Where is GLP-1 released from? When is it released?

A

enteroendocrine L cells in the distal ileum and colon

released after food ingestion in response to nutrient intake

104
Q

How are proteins hydrolyzed in the gut?

A

gastric/pancreatic enzymes breaks downto small peptides –> final hydrolysis by brush border peptidases –> hydrolysis to AA in enterocytes

105
Q

What mutations are associated with Puetz-Jegher’s syndrome?

A

mutation in STK11/LKB1 gene

106
Q

What is the role of the jejunum in absorption?

A

protein, carbohydrate breakdown

absorption

107
Q

Where does visceral fat drain? What is the effect of its drainage?

A

drains into portal venous system

FFAs are secreted onto the liver to stimulate hepatic triglyceride secretion

108
Q

What is the effect of vitamin B12 deficiency?

A

elevated homocysteine and methylmalonic acid levels

megaloblastic anemia, glossitis, myelopathy, neuropathy, neurologic features (ex. parasthesias, ataxia)

109
Q

All of the following are unique properties of the gut associated lymphoid tissue (GALT) except:

a) microfold cells
b) initiates both innate and adaptive immune responses
c) induction of immunological tolerance
d) preferential production of IgA

A

b) initiates both innate and adaptive immune responses

while innate and adaptive immune responses occur in the GALT, these responses also occur in the peripheral immune system so they are not unique to GALT

110
Q

What are the causes/risk factors for vitamin B12 deficiency?

A

uptake requires intrinsic factor

risk factors: advanced age, atrophic gastritis, vegan diet, gastrectomy, bariatric surgery, some medications (metformin, PPIs), pernicious anemia

111
Q

What is the effect of iron deficiency?

A

hypochromic, microcytic anemia (leading to fatigue, SOB, cold intolerance)

pica (consumption of non-food items)

112
Q

What is satiety?

A

level of hunger after a meal is consumed which regulates the frequency of eating

113
Q

What is enterohepatic recirculation?

A

recycling process for drugs that are eliminated through the hepatobiliary tract

involves cleavage of drugs by enzymes and recirculation

114
Q

What is oral tolerance?

A

induction of mucosal and systemic non-responsiveness to luminal antigens

115
Q

Medications used to treat obesity that target receptors in the appetite center typically cause an 8-12% weight loss. Why arent they more effective? What regulatory processes prevent further weight loss?

A

redundant biological systems are in place to maintain appetite regulation

it is fundamental to survival to seek food

hormonal and neuropeptide signals have feedback loops to diminish their effects

116
Q

How is trypsinogen activated?

A

activated to trypsin via enterokinase and by trypsin itself

117
Q

Where does drug absorption predominantly occur? Why?

A

small intestine

due to large surface area, long transit time, pH of gut lumen (weak bases best absorbed here)

118
Q

What are the symptoms of Crohn’s disease?

A

diarrhea, abdominal pain, weight loss, fever, rectal bleeding and perianal fistulae (if colonic involvement)

119
Q

How is pepsinogen activation triggered?

A

by H+ production or by pepsin itself

120
Q

Would a drug with a high first pass metabolism more likely have a low or high bioavailability?

A

low

high first pass metabolism means much of the drug is eliminated before reaching systemic circulation

121
Q

What is the role of the colon in absorption?

A

water, salt, short-chain fat absorption

processing of stool

122
Q

What is the mechanism of H. pylori induced gastritis?

A

H. plyori preferentially damages D cells, leading to decreased somatostatin release and thus increased acid secretion

123
Q

What are the symptoms of appendicitis?

A

lower right quadrant pain, nausea, vomiting, low-grade fever

124
Q

How is chymotrypsinogen activated?

A

activated to chymotrypsin via trypsin

125
Q

What is the etiology/pathogenesis of appendicitis?

A

bacterial infection often precipitated by obstructed appendiceal lumen (leads to increased luminal pressure, vascular compromise, bacterial overgrowth)

126
Q

After how many months should birth weight double? Triple?

A

4-5 months

12 months

127
Q

Which of the following statements might be correct regarding drug absorption after Roux-en-Y gastric bypass?

a) absorption of ibuprofen (pKa = 4.4) will be impaired because of reduced gastric surface area
b) a drug with high first pass metabolism such as atorvastatin will have lower availability after RYGB
c) a drug absorbed mainly through the small intestine such as omeprazole will achieve maximum plasma concentrations following an oral dose more rapidly after RYGB
d) certain prodrugs that require biotransformation in the liver such as enalapril may have reduced activity

A

c) a drug absorbed mainly through the small intestine such as omeprazole will achieve maximum plasma concentrations following an oral dose more rapidly after RYGB

shorter path for the drug to go before it gets absorbed in the small intestine

128
Q

What is the effect of intestinal bypass on peak plasma concentration of drugs?

A

decreases peak plasma concentration (due to lost absorptive surface area)

129
Q

What agent is principally responsible for carcinoid syndrome?

A

serotonin (derived from dietary tryptophan)

130
Q

Which statement best explains how gastric bypass surgery (e.g. Roux-en-Y) might interfere with oral absorption of drugs?

a) a less acidic luminal pH may enhance absorption of drugs that are weak acids
b) bypassing the proximal small intestine may reduce bioavailability for drugs with high first pass metabolism
c) bypassing the proximal small intestine may enhance bioavailability for drugs that are substrates for p-glycoprotein
d) a more acidic luminal pH may enhance absorption of drugs that are weak bases

A

d) a more acidic luminal pH may enhance absorption of drugs that are weak bases

131
Q

What is the morphology of diffuse antral chronic gastritis?

A

acute and chronic nucosal inflammation associated with lymphoid follicles

rarely includes intestinal metaplasia

132
Q

What are the effects of leptin on neurons in the ARC?

A

1) inhibiting neurons that coexpress the orexigenic (increased food intake) hormones NPY and AGRP
2) stimulating neurons that coexpress anorexigenic (reduced food intake) hormones POMC and CART

133
Q

What are the complications of Crohn’s disease?

A

local: subacute intestinal obstruction, perforation and fistula formation, adenocarcinoma
systemic: amyloidosis, ankylosing spondylitis and polyarthritis

134
Q

What is the role of the mouth, esophagus, and stomach in digestion?

A

mechanical processing and release of food and liquid to the small bowel

production of intrinsic factor for vitamin B12

135
Q

What is dumping syndrome?

A

occurs when the contents of the stomach empty too quickly into the small intestine, drawing excess fluid in and causing nausea/cramping/diarrhea

can occur after gastric bypass surgery

136
Q

Where are proteins absorbed?

A

stomach (with pepsin)

small bowel (with pancreatic enzymes, endothelial/brush border enzymes)

137
Q

How does gastric cancer spread?

A

through gastric wall to adjacent organs

lymphatic spread

vascular spread

Krukenberg: metastasis to ovaries

138
Q

What controls release of ACh in the stomach? How does it affect acid production?

A

controlled by Vagus innervation

ACh –> M3 receptor in gastral parietal cell –> GPCR triiggers increase of IP3/Ca2+ –> activates the H/K ATPase to release acid into the stomach lumen

139
Q

A 30 y.o. female was recently diagnosed with celiac disease and has started on a gluten free diet. She reports that she would like to get pregnant and is askign for nutrition advice on what vitamins she needs to take to prepare her body for pregnancy. What do you suggest?

a) prenatal vitamins and a blood work to check CBC and iron panel along with serum folate, B12, and vitamin D
b) prenatal vitamins only as they are a good source of extra vitamins needed in celiac disease
c) digestive enzymes, B-complex, multivitamin, iron supplement

A

a) prenatal vitamins and a blood work to check CBC and iron panel along with serum folate, B12, and vitamin D

140
Q

How does mucus secretion protect the stomach?

A

mucus is relatively impermeable to H+, so acid does not get through the mucus to the surface epithelial cells

141
Q

What are the two major mechanisms of injury in NSAID induced ulcers?

A

1) topical mechanism causing a back diffusion of H+ into the cells (short lasting injury, rapid healing)
2) decreased prostaglandin synthesis has systemic effects that take out the protection mechanisms of gastric mucosa (decreased mucus secretion, bicarbonate secretion, and blood flow)

142
Q

What supplements are important to take after gastric bypass surgery?

A

B-vitamins, vitamin D, calcium, iron

143
Q

What are risk factors for iodine deficiency?

A

living in areas with iodine-poor soil

avoidance of (iodized) salt

144
Q

What is the effect of riboflavin deficiency?

A

weakness, glossitis, angular stomatitis, cheilosis

145
Q

Among the various determinants of obesity, which ones are remedial? How would you counsel a patient?

A

psychosocial or behavioral factors –> counseling

discontinuing any weight-gaining medications

146
Q

What is the effect of peptide YY (PYY) on hunger?

A

enhances satiation

147
Q

What are risk factors for zinc deficiency?

A

malabsroptive disorders, eating disorders, malnutrition, genetic disorder (acrodermatitis enteropathica)

148
Q

A 67 y.o. farmer has a breakfast of eggs, bacon, ham, grits and cheese, fried potatoes, biscuits with syrup, buttermilk, and coffee before beginning a long day in the field. Which of the following hormones is released by the presence of fat and protein in the small intestine and helps to decrease gastric emptying?

a) CCK
b) GIP
c) gastrin
d) motilin
e) secretin

A

a) CCK

149
Q

What is dysbiosis?

A

alterations of intestinal flora away from baseeline/equilibrium

150
Q

What controls release of histamine in the stomach? How does it control acid production?

A

ECL cells release histamine

Histamine –> H2 receptor –> GPCR triggers increase of cAMP –> activates the H/K ATPase to release acid into the stomach lumen

151
Q

What are the microscopic features of chronic peptic ulcers?

A

four recognizable layers:

zone of fibrinopurulent exudates (surface)

zone of necrotic tissue

zone of granulation tissue

zone of fibrous tissue (deep)

152
Q

Where are disaccharidases located?

A

glycocalyx of brush border

153
Q

Why is lipodystrophy (reduction or absence of subcutaneous fat) associated with higher risk of metabolic syndrome?

A

subcutaneous fat depots are important for energy storage

when these are absent, excess energy is stored ectopically in organs (ex. liver)

154
Q

Intestinal epithelial cells serve an immunological function by:

a) initiating innate immune responses
b) serving as a physical barrier that excludes antigens
c) transport and secrete IgA
d) all of the above

A

d) all of the above

Intestinal epithelial cells perform function beyond the absorption of nutrients. They initiate innate immune responses through expression of TLRs, exclud antigens via tight junctions, and transport IgA antibodies from plasma cells in the lamina propria to the lumen of the gut.

155
Q

How do amino acids leave mucosal cells?

A

slowly via facilitated diffusion

156
Q

Where is visceral adipose tissue?

A

adipose tissue within the abdominal cavity, below abdominal muscles, that is comprised of omental and mesenteric adipose tissue + adipose tissue of the retroperitoneal and perinephric regions

157
Q

What is the etiology of Chron’s disease?

A

unknown

genetic predisposition (jewish populations and scandinavian countries)

also related to infections, immunologic, psycho-somatic factors

158
Q

What are the microscopic features of Crohn’s disease?

A

sarcoid type granulomas

fissuring ulcerations

transmural inflammation

submucosal widening with inflammation, fibrosis, lymphangiectasia, and neural hyperplasia

occasional crypt abcesses

159
Q

What are the two main compartments of the gastric mucosa?

A

superficial foveolar compartment –> surface epithelial cell lining

deeper glandular compartment –> variable glands in different gastric regions

160
Q

What differentiates acute and chronic gastritis?

A

acute = active = neutrophils present

chronic = chronic inflammation = lymphocytes and plasma cells

161
Q

What is the function of isomaltase?

A

breaks terminal 1,6 bonds of saccharides (into glucose)

162
Q

What is the pathophysiology of obesity-induced hypertension?

A
  • underlying hemodynamic alterations
  • increase in sympathetic nervous activity
  • insulin resistance, activation of the renin-angiotensin system
163
Q

What is the role of the duodenum in absorption?

A

release of pancreatic enzymes

bicarbonate neutralization

mineral absorption including iron

164
Q

What are the two major functions of the mucosal immune system?

A

1) host defense
2) tolerance to food antigens and commensal bacteria

165
Q

How is H. pylori infection typically acquired?

A

usually acquired at a young age due to poor sanitory conditions (especially contaminated water supply)

166
Q

A 56 year old male undergoes a surgical procedure for a benign pancreatic mass resulting on removal of > 90% of his pancreas. Several months later he complains of ongoing foul-smelling diarrhea which occurs after eating. A 72-hour fecal fat and fecal elastase are sent on a high fat diet. What would you expect to find and why?

a) fecal fat 26 g/day (high), fecal elastase 550 ug/g (normal)
b) fecal fat 4 g/day (normal), fecal elastase 45 ug/g (low)
c) fecal fat 26 g/day (high), fecal elastase 45 ug/g (low)
d) fecal fat 4 g/day (normal), fecal elastase 550 ug/g (normal)

A

c) fecal fat 26 g/day (high), fecal elastase 45 ug/g (low)

fecal fat should be elevated due to decreased pancreatic enzymes (like fecal elastase)

167
Q

What are the major complications of chronic peptic ulcers?

A

perforation, hemorrhage, fibrosis leading to pyloric stenosis, acquired diverticula, rare malignant transformation

168
Q

Describe the mechanism of diarrhea that may be seen in some patients with Zollinger Ellison syndrome.

A

excessive amounts of acid that reach the duodenum can denature pancreatic enzymes resulting in maldigestion of fat and protein with resultant diarrhea

secondary mechanism = direct acid damage to small intestinal epithelium with secretory diarrhea

169
Q

What are the risk factors for folic acid deficiency?

A

alcoholism, malabsorptive GI disorders, bariatric surgery, restrictive diets, certain medications

170
Q

Which one of the following is NOT stimulated by CCK?

a) secretion of bile by the liver
b) secretion of pancreatic HCO3-
c) secretion of pancreatic enzymes
d) relaxation of the sphincter of Oddi
e) contraction of gall bladder smooth muscle

A

a) secretion of bile by the liver

171
Q

What is the classic presentation of a child with celiac disease?

A

poor weight gain, distended abdomen

172
Q

What are the major complications of celiac disease?

A

10-15% develop tumors (lymphomas)

ulcerative jejunoileitis

173
Q

What is the pathogenesis of diffuse antral chronic gastritis?

A

associated with H. pylori infection

174
Q

What are the symptoms of zollinger-ellison syndrome?

A

peptic ulcer (frequently in proximal duodenum)

diarrhea (denaturation of pancreatic enzymes)

175
Q

What is the effect of GLP-1 on hunger?

A

enhances satiation

176
Q

Where is fat absorbed?

A

mouth/stomach: mechanical digestion and mixing

small bowel: enzymes (lipase) and bile facilitate breakdown and absorption

177
Q

What are the clinical manifestations of malabsorption of fat?

A

characteristic diarrhea (foul smelling, floats in toilet, difficult to clear with flushing)

178
Q

What is the effect of intestinal bypass on drug absorption due to pH alterations?

A

impairs absorption of weak acids, enhance absorption of weak bases

179
Q

What is the average daily weight gain in the first 3-4 months? First year? Second year?

A

3-4 months: 20-30 grams

first year: 15-20 grams

second year: 5-10 grams

180
Q

What is the impact of intrinsic hepatic metabolism on high extraction drugs? Low extraction?

A

high: insensitive
low: sensitive
* high extraction drug clearance is driven primarily by blood flow*

181
Q

What types of secretory cells are in pyloric glands?

A

G cells –> gastrin

D cells –> somatostatin

in the antrum of the stomach

182
Q

What is the function of sucrase?

A

breaks down sucrose (into glucose and fructose)

breaks down maltose (into glucose and glucose)

183
Q

What is the usual distribution of carcionma of the stomach?

A

prepyloric region, pyloric antrum, along lesser curvature, and (less commonly) cardia/body

184
Q

What are the three systems for amino acid absorption?

A

1) neutral system I (for neutral amino acids)
2) basic system (for basic amino acids)
3) neutral system II (imino system - for proline, hydroxyproline, sarcosine, and other glycines)

185
Q

Where is the main site of leptin signaling?

A

hypothalamic arcuate nucleus (ARC)

186
Q

What are the diagnostic tests for celiac disease?

A

antigliadin antibodies, antiendomysial antibodies, anti-tissue transglutaminase antibodies

187
Q

What is the gross pathology of Crohn’s disease?

A

discontinuous and serpiginous ulcers

strictures

cobble-stone appearance of involved mucosa

188
Q

What is the impact of protein binding on high extraction drugs? Low extraction drugs?

A

high: insensitive
low: sensitive

189
Q

What is ectopic fat?

A

deposition of fat in non-adipose tissue

major sites: pancreas, skeletal muscle, heart, liver

190
Q

What is the clinical presentation of Whipple’s disease?

A

systemic bacterial disease, predominantly affecting middle-aged males who present with migratory polyarthralgia, steatorrhea, and wasting

symptoms: malaise, weight loss, diarrhea (malabsorption), arthritis

191
Q

What are paneth cells?

A

cells at the base of intestinal crypts that produce antimicrobial peptides

not present in large intestines

192
Q

What is Peutz-Jegher’s syndrome?

A

a dominant hereditary disorder characterized by intestinal polyposis and mucocutaneous melanin pigmentation

polyps most common in small bowel, lobulated or pedunculated

193
Q

What are the risk factors for riboflavin deficiency?

A

alcoholism, eating disorders, cystic fibrosis, celiac disease, malabsorptive disorders

194
Q

What is the effect of intestinal bypass on bioavailability?

A

blunts first pass metabolism –> increases bioavailability

drugs that require longer times for absorption may have decreased bioavailability

195
Q

What are the effects of folic acid deficiency?

A

increase in homocysteine levels

megaloblastic anemia, fatigue, shortness of breath

neural tube defects in fetuses

196
Q

What is the anatomical distribution of Crohn’s disease?

A

ileocecal region most common

colonic disease or both

197
Q

What is the mechanism of injury in gastric H. pylori infection?

A

attaches to the apical membrane of gastric epithelial cells causing direct injury

damage results in an immune response that furthers inflammation and damage

198
Q

What is the effect of obesity on the respiratory system?

A

increases in the mechanical work of breathing leads to ventilatory insufficiency

199
Q

What is the presentation of cystic fibrosis in children?

A

recurrent respiratory infections, poor weight gain, edema, fat malabsorption

200
Q

How are hexoses transported?

A

down a concentration gradient with GLUT transporters

can also be transported against a concentration gradient with a sodium co-transporter

201
Q

What pathology is associated with the histological changes seen on the right?

A

chronic gastritis

superficial plasmacytic infiltrate, lymphoid aggregates

202
Q

What is the waterlow criteria?

A

a scale to assess malnutrition based on changes in weight related to height

203
Q

What is the effect of thiamine deficiency?

A

buildup of lactate and TCA cycle intermediates

manifests as beriberi (dry –> peripheral neuropathy, wet –> neuropathy + heart failure, or cerebral –> Wernicke-Korsakoff)

204
Q

Where are carbohydrates absorbed?

A

upper GI (mostly digested mechanically and with salivary enzymes)

stomach (mechanically)

small bowel (brush border enzymes)

absorbed by diffusion and transport

205
Q

Which statement explains why co-administration of nilotinib with irinotecan might be dangerous?

a) both drugs may independently suppres bone marrow hematopoiesis
b) nilotinib induces UDP-glucuronosyltransferase-1 (UGT1A1) which is required for irinotecan activation
c) nilotinib inhibits UDP-glucouronosyltransferase-1 (UGT1A1) which is required for Phase II metabolism and clearance of irinotecan active metabolites
d) irinotecan inhibits UDP-glucouronosyltransferase-1 (UGT1A1) which is required for Phase II metabolism and clearance of nilotinib

A

c) nilotinib inhibits UDP-glucouronosyltransferase-1 (UGT1A1) which is required for Phase II metabolism and clearance of irinotecan active metabolites

206
Q

What is somatostatinoma syndrome?

A

somatostatin-producing tumors that are rare

symptoms: diabetes, diarrhea, steatorrhea, hypochlorhydria

207
Q

Explain the mechanism of iron deficiency in patients with undiagnosed or uncontrolled celiac disease.

A

patients with celiac disease have villous atrophy in the proximal small bowel, mainly in the duodenum

atrophy impairs absorption

since iron is best absorbed in proximal small bowel (including duodenum), it is affected

208
Q

Where are the neurons of the reward pathways of the brain? What areas receive this information?

A

dopaminergic neurons in the ventral tegmental area and substantia nigra

nucleus accumbens, striatum, orbitofrontal cortex receive and integrate the info

209
Q

When is the peak of diagnosis for inflammatory bowel disease?

A

peaks in late adolescence and early twenties

210
Q

How are endocrine neoplasms of the gut classified?

A

based on embryologic derivation from the site of origin

211
Q

What are M (microfold) cells?

A

cells above germinal centers in the gut lumen that create pockets for antigens

212
Q

What are the clinical manifestations of protein absorption?

A

muscle breakdown, anasarca, irregular bowel habits

213
Q

What is the pathogenesis of autoimmune chronic gastritis?

A

destruction of parietal cells by antibodies directed against parietal cells and intrinsic factor

214
Q

What is the relationship between a sedentary lifestyle and weight gain?

A

restricted physical activity causes weight gain and often leads to overfeeding

215
Q

What is the relationship between the height of children and their parents?

A

girls = [(fathers height - 5 in) + mothers height]/2

boys = [(mothers height + 5 in) + fathers height]/2

216
Q

The gastric zymogen, pepsinogen, is converted to the active enzyme pepsin by:

a) gastric HCl
b) gastrin
c) enterokinase
d) acetylcholine
e) intrinsic factor

A

a) gastric HCl

217
Q

How can risk of NSAID induced ulcers be mitigated?

A

use of oral prostaglandins (misoprostol) with NSAIDs

acid suppression with PPIs

use of selective COX2 NSAIDs

218
Q

What is the effect of somatostatin on acid production in the stomach?

A

Somatostatin binds to GPCR –> blocks increase in cAMP –> inhibits the H/K ATPase to decrease acid release into the stomach lumen

219
Q

What is the function of maltase?

A

breaks terminal 1,4 bonds of saccharides (into glucose)

220
Q

What are the three major components of daily total energy exposure?

A

resting metabolic rate, thermic effect of feeding, energy expenditure of physical activity

221
Q

What is the pathology of autoimmune gastritis?

A

mucosa of the body and fundus of the stomach is selectively affected (antrum spared)

decreased parietal cells, increased lymphocytes and plasma cells in deep mucosa

pseudopyloric and intestinal metaplasia

222
Q

What are the three factors that determine hepatic clearance?

A

intrinsic liver metabolism, liver blood flow, plasma protein binding of the drug

223
Q

What is celiac disease?

A

a malabsorptive disorder, usually starting in childhood, that is due to sensitivity to gluten and/or breakdown products of gluten

leads to mucosal damage

similar pathology can be seen in soybean or cow-milk protein sensitivities

224
Q

Where is PPY released from? When is it released?

A

synthesized and released from endocrine L cells in the distal gut

released in response to food consumption (especially fat), suppressed in the fasted state

225
Q

What characteristics of carcinoids increase likelihood of malignancy?

A

size of origin, size of intramural penetration

226
Q

What is the presentation of inflammatory bowel disease in adolescents?

A

poor growth, growth hormone resistance, pubertal delay

227
Q

A 40 year old male has eosinophilic esophagitis and has started on a six food elimination diet protocol to treat his food allergies where he removes wheat, dairy, eggs, soy, nuts, fish. He likes to exercise regularly and is concerned about having a healthy diet. What macronutrients and micronutrients are you concerned could be lacking from this restricted diet?

a) fiber, calcium, iron, sodium, carbohydrates
b) fiber, protein, vitamin D, B-vitamins
c) fiber, calories, protein, monosaturated fats
d) fiber, calories, proteins, trace minerals

A

b) fiber, protein, vitamin D, B-vitamins

228
Q

What is the pathology of Whipple’s disease?

A

dilated intestine, thick and rigid

thickened mesentery

villous atrophy (variable degree)

numerous macrophages in the lamina propria

229
Q

What is the mechanism of autoimmune gastritis?

A

autoimmune destruction of parietal cells

results in hypochlorhydia, loss of intrinsic factor (and inadequate vitamin B12 absorption leading to pernicious anemia)

230
Q

What is the clinical workup for protein loss or malabsorption?

A

small bowel biopsy

231
Q

What is bioavailability?

A

fraction of an administered dose of unchanged drug that reaches systemic circulation

232
Q

What is first pass metabolism?

A

the phenomenon in which a drug is eliminated before it reaches systemic circulation

233
Q

What dose adjustments should be considered in patients with hepatic cirrhosis?

A

reduced dose for high extraction drugs

monitor free drug concentration for low extraction drugs with high protein bindings

higher loading dose for hydrophilic drugs if ascites

caution for drugs with narrow therapeutic windows

use caution for renally eliminated drugs

234
Q

What is the general relationship between obesity and genetics?

A

multifactorial (genetics + environment)

some genetic syndromes lead to obesity (ex. Prader-Willi)

235
Q

During a patient’s hospitalization following a Roux-en-Y gastric bypass, the patient reported to have increased sensitivity to ethanol following surgery. Which of the following provides the best explanation for this observation?

a) weight loss reduced the volume of distribution for ethanol
b) first pass metabolism of ethanol is lower after surgery
c) time to maximum plasma ethanol concentration is shorter after surgery
d) hepatic metabolism of ethanol is enhanced after surgery

A

c) time to maximum plasma ethanol concentration is shorter after surgery

236
Q

What is the cause of Whipple’s diease?

A

tropheryma whippelii (rod shaped bacterium) infection systemically

237
Q

What factors during pregnancy play a role in newborn body weight and future development of obesity?

A

poor glycemic control, obesity, and excessive weight gain during pregnancy

238
Q

What factors are secreted by adipocytes?

A

leptin

cytokines (IL-6, TNF-alpha)

prothrombotic agents (PAI-1)

angiotensinogen

adiponectin

239
Q

What is menetrier disease?

A

a rare disease associated with excessive secretion of TGF-alpha

causes diffuse hyperplasia of the foveolar epithelium of body and fundus

causes hypoproteinemia

symptoms: weight loss, diarrhea, peripheral edema, icnreased risk of gastric adenocarcinoma

240
Q

What are the major components of management of celiac disease?

A

CELIAC

Consultation with dietitians

Education about the disease

Lifelong adherence to gluten-free diet

Identification and treatment of nutritional deficiencies

Access to an advocacy group

Continuous long-term follow-up by a multidisciplinary team

241
Q

What is the function of lactase?

A

breaks down lactose (into glucose and galactose)

242
Q

What is a normal amount of weight loss in the first few days of life?

A

5-10% of birth weight

243
Q

A 35 y.o. man presents with 3 months of abodminal pain, diarrhea with blood, and weight loss. He is mildly anemic with an elevated C-reactive protein. Endoscopy confirms the clinical suspicion of Crohn’s disease. Each of the following mechanisms have been suggested to play a role in the pathogenesis of this inflammatory bowel disease except:

a) increased intestinal permeability
b) expression of susceptibility genes
c) impaired IgA production
d) impaired innate immunity

A

c) impaired IgA production

  • the precise pathogenesis of IBD is unknown, however contributing factors have been identified*
  • family histories suggests genetic factors that confer susceptibility –> specifically genes related to innate immune responses*
244
Q

What are the clinical manifestations of carbohydrate malabsorption?

A

bloating, darrhea, fatigue

245
Q

What are the risk factors for vitamin C deficiency?

A

alcoholism, restrictive diets, cancer cachexia

246
Q

How is fructose absorbed?

A

through facilitated diffusion down its gradient

specific and saturable

247
Q

What are the causes of hypothalamic obesity? What are the presenting symptoms?

A

causes: trauma, tumor, inflammatory disease, surgery in posterior fossa, increased intracranial pressure
symptoms: 1) headache, vomiting, diminished vision; 2) impaired endocrine function with reproductive effects, diabetes insipidus, and thyroid or adrenal insufficiency; 3) neurologic and physiologic derangements (convulsions, coma, somnolence, hypothermia/hyperthermia)

248
Q

What are the risk factors for vitamin D deficiency?

A

exclusive breast feeding (infants), avoidance of sun exposure, dark skin pigmentation, aging, malabsorptive disorders, obesity