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Exam 1 Flashcards

1
Q

What are the three subdisciplines of nutritional genomics?

A
  1. Nutrigenetics
  2. Nutrigenomics
  3. Nutritional epigenetics
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2
Q

Nutrigenetics refers to:

A

Functional changes in the nucleic acid code that influences a persons response to nutrients. Variation creates more or less function, may be associated with geographic ancestry

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3
Q

What are some examples of Nutrigenetics?

A

1.) Newborn screening for high levels of vitality indicating PKU (recessive disorder of phenylalanine hydroxylase gene)

2.) altering folate levels in the diet of a person with MTHFR gene alterations

3.) mutation in the HFE gene hemachromatosis) requiring limited consumption of red meat, animal fat, vitamin C, alcohol

4.) lactose intolerant people (LCT gene)

5.) celiac disease

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4
Q

SNP (single nucleotide polymorphism): necessary or sufficient?

A

• necessary: required, always present but is not the only requirement for condition

• sufficient: the individual SNP/variant is the actual cause of the condition

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5
Q

An SNP in the CTP-1A gene (carnitine palmitoyl transferase 1A) leads to what?

A

Difficulty with fatty acid metabolism, not enough fat stores requiring more consistent feeds in newborns

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6
Q

What is nutrigenomics?

A

Environment – gene interactions that may be managed in order to prevent diet related disease (example: Saccone P450 family and the response to nutrients)

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7
Q

What are some applications of nutrigenomics?

A

• smoking cessation
• omega-3 fats to reduce gene expression of inflammatory cytokines

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8
Q

What is the technology used in nutrigenomics?

A

• exome sequencing
• deep sequencing (NGS)
• bioinformatic analysis

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9
Q

What is nutritional epigenetics?

A

Changes in gene expression that do not involve changes in the nucleotide sequence that can be passed down through generations based off of dietary considerations of the ancestry.

mech: methylation of DNA (cytosines) and acetylation of proteins (histones)

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10
Q

How do we detect acetylation from nutritional epigenetics?

A

antibody directed against the protein modification

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11
Q

How do we detect methylation in nutritional epigenetics?

A

Bisulfate treatment converts unmethylated cytosines (but not methylated cytosines) into uracil

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12
Q

What is an epimutation?

A

The changes that are epigenetic are more readily changed (mutated) they are the genetic base pairs — hongerwinter 1944-1945

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13
Q

What cells make up the intestinal tract?

A

1.) non-hematopoietic, epithelial (enterocytes, paneth cells, goblet cells)

2.) hemopoietic cells (macrophage, dendritic cell, T cells)

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14
Q

What is a part of the central organization of the immune system?

A

Blood, spleen, lymph nodes, liver

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15
Q

What is the surface and barrier organization of the immune system?

A
  • skin: cornified epithelium, ducts of exocrine glands
  • mucosal: mucins, respiratory tract, gastrointestinal tract, genital tract, eye conjunctiva
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16
Q

What is the primary site for antigen entry into the body?

A

GALT: gut associated lymphoid tissue, where there is a large reservoir of lymphocytes

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17
Q

Central immune system functions have a tendency toward what cell types and immune reactions?

A
  • Th1 cells (cytotoxic)
  • complement mediation (inflammatory)
  • IgG, IgM
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18
Q

Surface immune system functions have a tendency toward what?

A
  • Th2 helper cells (humoral)
  • agglutination antibodies (reconstruction)
  • IGA, IGE
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19
Q

What is the mucosal immune system responsible for?

A

• immediate identification and elimination of invading cells
• grooming and supporting commensal bacteria
• maintain luminal compartment distinct from body compartment
• cross talk via metabolic products and pattern recognition receptors (TLR, NOD)
• tolerance versus hypersensitivity

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20
Q

What is the metabolic output of the microbiota?

A

• fatty acids in retina and lens
• bone density
• vascularization of the gut
• bio reactor provides biotin, vitamin K, digestion of complex fiber to generate butyric acid

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21
Q

What are the physical and chemical barriers of the G.I. tract?

A

• single layer epithelial cells, tight junction
• mucus that covers the epithelial barrier
• peristalsis driving unidirectional movement
• low pH of the stomach (<3)
• detergents, bile acids, lysozymes, defenses, cathelicidin, trefoil proteins

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22
Q

Deficiencies in MUC-2 result in what?

A

Colitis

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23
Q

Deficiencies in MUC-6 result in what?

A

H. Pylori, Crohn’s disease

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24
Q

What is the mucous layer in the G.I. tract made of?

A

Glycocalyx, thickest in the colon with a thick layer attached to the epithelia, and a loose layer in the mucus

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25
Q

What is the principal regulator of the mucus layer of the G.I. tract?

A

INF-gamma

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26
Q

What are enterocytes?

A

• Absorptive cells that support paracellular and transcellular transportation of nutrients, electrolytes, and water
• make up the epithelial barrier, highly regulated, selective permeability, tight junctions

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27
Q

What is the most prolifically replicating cell of the body?

A

Enterocytes

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28
Q

What are the physical barriers of the G.I. tract?

A

• tight junctions between epithelial cell
• mucus layer provided by the goblet cells
• trefoil proteins, rapid plug of breached barrier
• apical surface with dense micro villi, layer of filamentous brush border glycocalyx

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29
Q

What types of antibodies are in the G.I. tract and what do they do?

A

1.) neutralizing antibodies: natural antibodies IgM, IgG from B1 cell, and toxins, cap receptors

2.) aggregating antibodies: IgA, most abundant antibody produced, non-complement fixing, protease resistant, binds and renders antigen too large to pass through the epithelial wall

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30
Q

What prevents spreading of intercellular pathogens in the G.I. tract?

A

• interferons, IFN- Alpha, beta
• increase MHC class I expression and induce cell mediated toxicity

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31
Q

How are epithelial cells responsible for direct killing in the G.I. tract?

A

• anti-microbial peptides: defensins
• bacterial permeability increasing proteins (BPI)

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32
Q

How are phagocytic cells responsible for direct killing in the G.I. tract?

A

• macrophages and neutrophils
• defensins- aka neutrophils
• complement (pro-inflammatory)
• lysosome reactive oxygen species, ROS
• reactive nitrogen species, RNS

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33
Q

What are defensins?

A

Poly-cysteinyl cationic peptides created by paneth cells (and stores in granules) in the GI crypts that permeabilize membranes

  • alpha-defensins: expressed by neutrophils, NK cells, Paneth cells, epithelial cells
  • beta-defensins: expressed by epithelial cells
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34
Q

What is responsible for expulsion of pathogens in the G.I. tract?

A

• IgE
• vasoactive substances (eosinophils) like leukotrienes, prostaglandins, and histamines
• mucus
• smooth muscle contraction, directional flow (peristalsis)

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35
Q

How does the GI tract create nutrient deprivation to starve pathogens?

A

• chelation
• lactoferrin: Fe
• Calprotectin: Ca
• lipocalin: lipids
• indoleamine 2,3-dioxygenase: tryptophan

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36
Q

How do bacteria and viruses cross the epithelial barrier of the G.I. tract?

A

M cells, however there are macrophages on the basolateral side to engulf the microbes

~ how vaccination typically works

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37
Q

What are the two barriers to pathogens in the G.I. tract?

A
  1. Lamina propria containing macrophages and lymphocytes
  2. Epithelium containing enterocytes with tight junctions
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38
Q

The majority of intra-epithelial lymphocytes express what?

A

CD8, recognize MHC class I antigen

• alpha-beta: thymus derived T cell receptor, common
• delta-gamma: non-thymic derived, combination capacity

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39
Q

What are the physical components of the barrier system of the G.I. tract?

A

• villus
• crypts
• peyers patch

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40
Q

What anatomical feature is responsible for the education of lymphocytes?

A

Peyer’s patches

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41
Q

Gut tropism is linked to what vitamin?

A

Vitamin A

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42
Q

Epidermal skin tropism is linked to what vitamin?

A

Vitamin D

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43
Q

What is essential for diapedesis, or entry within the cell layers of the GI tract?

A

Alpha4beta7 — MAdCAM binding of the lymphocyte and endothelial cell, respectively

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44
Q

What innate properties suppress inflammation?

A

• IL-10
• TGF-beta
• sIL-1R

~ these are challenged by inflammatory properties such as LPS and NF-kB

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45
Q

What are the principle pathogen recognition receptors?

A

• TLR2: highly expressed on epithelial cells, proximal colon, senses G+, and lipoteichoic acid
• TLR4, CD14: express at higher levels in the colon, senses G-, and LPS
• NOD2: expressed by epithelial cells in the ilium, paneth cells, senses muramyl dipeptide and ssRNA

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46
Q

What are the predominant T cells in the lamina propria?

A

CD4+ recognizing MHC class II antigen

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47
Q

Th1

A

• cytokines: IFN-gamma, TNF-alpha, IL12
• fxn: defense to intracellular pathogens

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48
Q

Th2

A

• cytokines: IL10, 13, 5, 4
• fxn: defense to helminths

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49
Q

Th17

A

• cytokines: IL17, 21, 22
• fxn: defense to extracellular bacteria and parasites

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50
Q

Treg

A

• cytokines: IL10
• fxn: regulate tolerance

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51
Q

What is the role for eosinophils in the G.I. tract?

A

Positioned in lymphoid and intestinal mucosa (With high density in the caecum) which allows for rapid recruitment, localization by Beta7 integrins on endothelial cells, in order to alter the balance of Th1:Th2 (recruit more Th1)

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52
Q

What do eosinophils and mast cells secrete to involve muscular action of the G.I. tract?

A

• substance P
• histamine
• serotonin

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53
Q

What are the microbes that are normally present in the mouth?

A

• Firmicutes (lactobacilli), G+
• bacteroidetes, G-
• proteobacteria, G-
• actinobacteria, G+
• spirochetes
• fusobacteria

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54
Q

What bacteria protects against dental carries and periodontitis by producing hydrogen peroxide which inhibits the growth of other bacteria?

A

Facultative anaerobe streptococci

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55
Q

What are the four phyla in the stomach?

A

• stomach has sparse microflora (10^4)
• proteobacteria, firmicutes, actinobacteria, and bacteroidetes

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56
Q

What are the bacteria found in the duodenum/jejunum?

A
  • bacilli, streptococcus, actinobacteria, cornibacteria
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57
Q

What are the bacteria found in the colon/rectum?

A

Firmicutes, bacteroidetes, methanobrevibacter

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58
Q

Bacterial distribution between the epithelium versus the lumen of the G.I. tract

A
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59
Q

What are the reasons for bacterial overgrowth?

A

• decreased peristalsis
• aberrant pH (too high, PPI?)
• anatomical abnormalities
• disturbance in normal microbiome-change in population

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60
Q

What are the symptoms of SIBO, small intestine bacterial overgrowth?

A
  • inflammation in response to bacteria/endotoxin relates to damage of epithelium—>
  • chronic diarrhea/weight loss
  • abdominal discomfort/bloating/gas
  • malabsorption of nutrients (A, D, E, B12, iron)
  • greasy, bulky, smelly stools
  • anemia
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61
Q

What disorders are associated with SIBO?

A

• chronic pancreatic insufficiency
• IBS
• narcotic use, or post radiation
• hypothyroidism
• diabetes
• scleroderma

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62
Q

What are the ways to diagnose SIBO?

A
  1. Therapeutic trials of antibiotics
  2. Small bowel aspiration and culture
  3. Breath testing for methane and hydrogen
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63
Q

What is the treatment for SIBO?

A

• antibiotics: ciprofloxacin, metronidazole, neomycin, rifaximin, tetracyclines

rifa: inhibits bacterial DNA dependent RNA polymerase

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64
Q

What is a non-antibiotic way of treating SIBO?

A

Elemental diet for 14 days, simple nutrients taken up in the proximal section of the small intestine leading to starvation of bacteria

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65
Q

What is the difference in lower G.I. bacteria from vaginally delivered versus cesarean section infants?

A

• vaginal: bacteroides spp.
• C-section: clostridium spp.

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66
Q

What is the common microbiota of formula fed infants compared to breast fed?

A

• formula: Higher counts of bacteroides, clostridium, and enterobacteria
• breast: anaerobes such as staphylococcus, enterococcus, lactobacilli, enterobacteria; especially bifidobacteria

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67
Q

What are the benefits of the G.I. Microbiome?

A

• fermentation of indigestible food
• synthesis of essential vitamins
• removal of toxic compounds
• strengthening the mucosal barrier
• stimulate and regulate the development of immune tissues
• prevent establishment and infection of alien microbes by out-competing

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68
Q

What is clostridioides difficile (c. Diff)?

A

An infection with normal flora typically following broad spectrum antibiotic use. Most commonly seen in hospitalized patients.

Symptoms include: 3+ loose, foul smelling stools for 1-2 days with no blood, fever, abdominal pain, dehydration

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69
Q

What can C.diff lead to?

A

Pseudomembranous colitis: severe complication leading to perforation of the colon, toxic megacolon, and death
~ white yellow plaques composed of fibrin, inflammatory cells, and cellular debris

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70
Q

What are the toxins found in C.diff?

A

• Toxin A and B (TcdA and TcdB) which inactivate the host cell Rho GTPases leading to formation of pseudomembranes (from hyperstimulation of immune system— neutrophils). They can also drive cytoskeletal disruption and apoptosis of colon epithelial cells

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71
Q

What does clostridioides difficile look like?

A

• gram-positive, endospores/spore forming, bacilli, obligate anaerobe, motile

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72
Q

What is the treatment of C.diff?

A
  1. Discontinue offending antibiotic, rehydrate
  2. Administer abx: formerly metronidazole, vancomycin (G+), fidaxomicin (macrolide, low absorption)
  3. Potential for fecal transplant, especially in recurring cases
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73
Q

What should not be done in the case of C.diff?

A
  1. Don’t use antidiarrheal meds (this can slow down the removal of bacteria)
  2. Don’t treat asymptomatic carriers
  3. Remember, diarrhea has other infectious causes
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74
Q

What are the ways you can test for C.diff infections?

A

• PCR, molecular (same day, sensitive)
• antigen detection (one hour, not specific enough)
• toxin testing (ELISA assay, pair with other tests, same day)
• stool culture (slow turnaround, highly sensitive)

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75
Q

What are the four quadrants of the abdomen?

A

• RUQ
• RLQ
• LUQ
• LLQ

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76
Q

What are the nine regions of the abdomen?

A

• right hypochondriac region
• epigastric region
• left hypochondriac region
• right lumbar region
• umbilical region
• left lumbar region
• right iliac region
• hypogastric region
• left iliac region

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77
Q

What are the contents of the right upper quadrant of the abdomen?

A
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78
Q

What are the contents of the left upper quadrant of the abdomen?

A
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79
Q

What are the contents of the right lower quadrant of the abdomen?

A
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80
Q

What are the contents of the left lower quadrant of the abdomen?

A
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81
Q

What are the fascial layers of the abdomen in order?

A
  1. Skin
  2. Campers fascia
  3. Scarpa fascia
  4. Superficial investing fascia
  5. External oblique
  6. Intermediate investing fascia
  7. Internal oblique
  8. Deep investing fascia
  9. Transversus abdominis
  10. Transversalis fascia
  11. Extraperitoneal fat
  12. Parietal peritoneum
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82
Q

What is mesentery?

A

• double layer of peritoneum that wrap around and connect organs to posterior body wall
• continuous reflections of parietal and visceral peritoneum
• allows intraperitoneal organs to be highly mobile

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83
Q

What are the intraperitoneal organs?

A

• fully encased by peritoneum
• small intestine, stomach, gallbladder

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84
Q

What are the retroperitoneal organs?

A

• organs that sit behind the peritoneum fixed to the posterior wall
• kidney, aorta

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85
Q

What are the secondarily retroperitoneal organs?

A

• they become intraperitoneal but are pushed against the posterior abdominal wall during development
• pancreas, ascending and descending colon

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86
Q

What are the peritoneal ligaments?

A

• double layer of peritoneum that connects an organ to another organ
• hypogastric ligament, gastrosplenic ligament, splenorenal ligament

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87
Q

What is the greater omentum?

A

Four layers of peritoneum that attaches to the stomach and proximal duodenum and then to the transverse colon

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88
Q

What is the lesser omentum?

A

• double layer of peritoneum that connects the stomach and duodenum to the liver
• hepatoduodenal ligament and hepatogastric ligament

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89
Q

What is the epiploic (omental) foramen?

A

• communication between the greater sac and the lesser sac
• also allows for fluid and infection to spread

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90
Q

What is ascites?

A

• excess fluid in the peritoneal cavity; commonly in the inferior peritoneal cavity, paracolic gutter, or hepatorenal
• can be caused by mechanical injury, or portal hypertension

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91
Q

What arteries come off of the celiac trunk off of the descending aorta?

A
  1. Splenic artery
  2. Proper hepatic artery
  3. Right gastric artery
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92
Q

What makes up the foregut?

A

• stomach
• liver
• gallbladder
• proximal duodenum
• pancreas
• spleen

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93
Q

What attaches the liver to the anterior wall of the body?

A

Falciform ligament

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94
Q

What is the purpose of the gastric folds (rugae)?

A

Increase surface area in order to increase absorption of nutrients

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95
Q

What is the innervation of the stomach?

A

Parasympathetic: anterior and posterior vagal trunks

Sympathetic: celiac plexus: T6-T9 segments of spinal cord via greater splanchnic nerve

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96
Q

What is congenital hypertrophic pyloric stenosis?

A

• thickening of the smooth muscle in the pylorus which inhibits food from exiting the stomach (resistive gastric emptying)
• surgical fix

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97
Q

What are the purposes of the liver?

A

• filters blood from portal system
• secretes bile
• stores glycogen

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98
Q

What does the portal triad consist of?

A

• common bile duct (bile from liver)
• proper hepatic artery (blood to liver)
• portal vein (blood from intestines)
All contained in the hepatoduodenal ligament

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99
Q

What happens in cirrhosis?

A

Hepatocytes are replaced by fat and fibrous tissue. Liver becomes firm and circulation becomes impeded

— alcoholic cirrhosis is a common cause of hypertension

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100
Q

Which artery supplies the gallbladder?

A

Cystic artery <— hepatic artery proper <— common hepatic artery

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101
Q

What is the foregut composed of and what is it supplied by?

A

• composed of: esophagus, stomach, part of duodenum, liver, gallbladder

• supplied by: celiac artery

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102
Q

What is the midgut composed of and what is it supplied by?

A

• composed of: remainder of small and large bowel up to splenic flexure

• supplied by: superior mesenteric artery

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103
Q

What is the hindgut composed of and what is it supplied by?

A

• composed of: remainder of large bowel to superior part of anal canal

• supplied by: inferior mesenteric artery

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104
Q

What composes the vitteline duct (an embryonic structure providing communication from the yolk sac to the midgut during fetal development)?

A
  1. Omphaloenteric duct
  2. Omphalomesenteric duct
  3. Yolk sac
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105
Q

What is a congenital ilio/Meckel’s diverticulum?

A

Omphaloenteric duct can persist (blind sac, fibrous, fistula)

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106
Q

What is the cloaca?

A

• part of the hindgut
• separated by the choacal membrane to form the urogenital sinus and the anorectum

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107
Q

What is the pectinate line?

A

• Where ectoderm meets endoderm and visceral mesoderm from the hind gut
• delineated change in neurovasculature

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108
Q

Jejunum vs. ileum

A
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109
Q

What is the cecum?

A

• first part of the large intestine
• lower right quadrant of the abdomen
• common site of bowel obstruction

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110
Q

What is the tenia coli?

A

Vestigial longitudinal muscle on the colon

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111
Q

What is diverticulitis?

A

• small outpouching in the mucosa of the colon
• often occur near teniae- where vessels enter the bowel because it is a weak spot
• get filled with food bits and become inflamed

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112
Q

What are the branches of the superior mesenteric artery?

A

• ileal and jejunal
• iliocolic
• appendicular
• right colic
• middle colic

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113
Q

What are the branches of the inferior mesenteric artery?

A

• left colic
• sigmoid
• superior rectal

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114
Q

What are the three major arterial anastomoses in the bowel?

A

• pancreaticoduodenal: celiac trunk to superior mesenteric artery

• marginal artery: superior mesenteric artery to inferior mesenteric artery

• rectal artery: inferior mesenteric artery to internal iliac arteries

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115
Q

What artery is commonly poorly developed in patients, leading to increase chance of ischemia of the splenic flexure?

A

Marginal artery

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116
Q

What is the sympathetic innervation for the gastric system (T5-L2)?

A

• lower thoracic splanchnic nerves (greater, lesser, least)
• lumbar splanchnic nerves

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117
Q

What is the enteric innervation of the gastric system?

A

• submucosal plexus: epithelial cells and smooth muscle of the mucosa

• myenteric plexus: smooth muscle of the gut tube walls

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118
Q

What is the parasympathetic innervation of the gastric system?

A

• Vagus: foregut, midgut

• pelvic splanchnic nerves (S2-S4): hindgut

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119
Q

What are the sensory innervations of the gastric system?

A

• pain: travels with sympathetic pathways

• reflex: travels with parasympathetic pathways

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120
Q

Sympathetic contributions to aortic plexus of autonomic nerves

A
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121
Q

Where does the cross-talk for referred pain occur?

A

In the dorsal horn

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122
Q

What is the rule of 2’s?

A

• Meckel’s diverticulum: 2% of people, within 2 feet of ileocecal Junction, 2 inches long

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123
Q

What are the four parts of the duodenum?

A
  1. Superior
  2. Descending
  3. Inferior
  4. Ascending
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124
Q

Which part of the duodenum is intraperitoneal?

A

The proximal part of the superior duodenum (the rest is retroperitoneal)

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125
Q

Which part of the duodenum houses the major duodenal papilla?

A

The descending part— this is the opening for the hepatopancreatic ampulla; combined bile and main pancreatic duct

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126
Q

Anterior duodenal lymphatic vessels drain into what?

A

Pancreaticoduodenal lymph nodes and the pyloric lymph nodes

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127
Q

The posterior duodenal lymphatic vessels drain into what?

A

Superior mesenteric lymph nodes

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128
Q

Duodenal stenosis and atresia

A

• stenosis: incomplete degeneration of the epithelial plug
• atresia: usually in the second or third segments of the duodenum

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129
Q

What type of organ is the pancreas?

A

• accessory digestive gland
• secondarily retroperitoneal

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130
Q

The main pancreatic duct joins with the bile duct to form what?

A

The hepatopancreatic ampulla (of Vater) which drains into the duodenum via the major duodenal papilla

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131
Q

What are the innervations of the pancreas?

A

• vagus
• celiac ganglion— splanchnic nerves

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132
Q

Annular pancreas

A

• a congenital anomaly that consists of a ring of pancreatic tissue partially or completely encircling the descending portion of the duodenum, and can obstruct the duodenum
• anomalous bifid ventral pancreatic bud- half rotates normally, half remains ventral
• dorsal and ventral sections fuse leading to a ring around the descending duodenum
• more common in females, down syndrome, cardiac defects, intestinal malrotation

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133
Q

What are the veins that drain into the hepatic portal vein?

A
  1. Splenic
  2. Superior mesenteric
  3. Inferior mesenteric
  4. Pancreatic
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134
Q

What vein drains blood directly into the liver?

A

Paraumbilical

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135
Q

What are the porto-caval venous anastomoses?

A
  1. Left gastric —> esophageal —> azygous
  2. Superior rectal—> middle and inferior rectal
  3. paraumbilical —> epigastric
  4. Colic —> communicating veins of Retzius —> retroperitoneal veins —> IVC

bold is portal

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136
Q

What conditions are caused by portal hypertension?

A
  1. Esophageal varices
  2. Caput medusae
  3. Ascites
  4. Hemorrhoids
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137
Q

What layers overlie the kidneys?

A

• perirenal fat
• Renal fascia
• pararenal fat

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138
Q

What is nutcracker syndrome?

A

• the left renal vein passes over the aorta and under the superior mesenteric artery— downward traction or aneurysm in the SMA can compress the vein
• symptoms: left flank pain, left ovarian/testicular pain

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139
Q

What is SMA syndrome?

A

Compression of the third part of the duodenum by the superior mesenteric artery— similar to nutcracker syndrome

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140
Q

Where do the gonadal (ovarian/testicular) veins drain?

A

Left: drains into the left renal vein
Right: drains into the inferior vena cava

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141
Q

Thoracic splanchnic nerves

A

Greater thoracic: T5-9
Lesser thoracic: T10-11
Lease thoracic : T12

~ synapse in pre-aortic ganglia: celiac, superior mantric, aorticorenal

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142
Q

Sympathetic Lumbar and sacral splanchnics:

A

• lumbar: L1-L4 sympathetic trunk ganglia
• sacral: S1-S2 sympathetic trunk ganglia

~ actual nerve fibers are from spinal cord levels L1 and L2, synapse in the inferior mesenteric and superior hypogastric pre-aortic ganglia

~ short preganglionic fiber, long postganglionic fiber

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143
Q

Parasympathetic innervation of the G.I. system

A

• vagus nerve
• pelvic splanchnics (craniosacral origin)
• long preganglionic fiber, short postganglionic fiber

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144
Q

Pelvic splanchnic nerves:

A

• S2-S4
• parasympathetic
• exit anterior rami, synapse on walls of the target organs (NO interaction with sympathetic trunk)

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145
Q

Major autonomic plexuses

A

Celiac, superior mesenteric, aorticorenal, renal, inferior mesenteric, superior hypogastric

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146
Q

What is the innervation of the esophagus?

A
  • sympathetic: postsynaptic directly from T1-T4
  • parasympathetic: upper 1/3 from the recurrent laryngal, lower 2/3 from the vagus nerve

~ vagal trunks: anterior= left, posterior= right

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147
Q

Innervation of the stomach

A

• sympathetic: synapse in the celiac ganglia
• parasympathetic: gastric branches of the vagal trunks

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148
Q

Innervation of the small intestine

A

• sympathetic: synapse in celiac, superior mesenteric ganglia
• parasympathetic: vagal fibers passed through celiac and SM plexus to synapse in the organ wall

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149
Q

Innervation of the colon

A

innervation changes at the left colic Flexure
* sympathetic: superior mesenteric before the flexure, inferior mesenteric after
* Vagus before, pelvic splanchnic after

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150
Q

Myenteric plexus (Auerbach’s)

A

Embedded within the G.I. tract, it is within the longitudinal muscle layer and it coordinates peristaltic contractions

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151
Q

Submucosal plexus (Meissner’s)

A

• embedded within the G.I. tract, it is within the submucosal layer
• controls local secretions, blood flow, immune activity, absorption
• most prominent in the small intestine, not found in the superior stomach or esophagus

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152
Q

What is unique about the innervation of the suprarenal gland?

A

• sympathetic fibers do not synapse in the pre-aortic ganglia, they synapse directly in the medulla —> adrenal gland acts as the ganglion

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153
Q

Pelvic viscera innervations:

A

• sympathetic: from superior hypogastric plexus, lumbar and sacral splanchnics
• parasympathetic: pelvic splanchnics

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154
Q

What are the sympathetic functions of the G.I. tract?

A

• digestive: decreased peristalsis and blood flow, contracts internal anal sphincter
• liver/gallbladder: promotes breakdown of glycogen for energy
• genito/urinary: slow urine production, contracts internal sphincter of the bladder, controls ejaculation

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155
Q

What are the functions of the parasympathetic system in the G.I. tract?

A
  • stomach and intestines: increase peristalsis, digestive secretions/enzymes
  • descending colon/rectum: relaxation of the internal anal sphincter
  • bladder: contracts bladder wall, relaxes internal urinary sphincter
  • glands: stimulates fluids secretion
  • erectile tissue: promote visa dilation, increase blood flow lead to an erection
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156
Q

What are the components of DEE, daily energy expenditure?

A

Basal metabolism, physical activity, thermal effective food

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157
Q

What are the factors that affect your basal metabolic rate?

A

• gender
• body temperature (increases with fever)
• environmental temperature (increases in cold temperature)
• thyroid hormone (increases with hyperthyroidism)
• reproduction (increases with pregnancy/lactation)
• age (decreases as age increases)

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158
Q

Comparing DEE and REE (daily energy, resting energy expenditure)

A
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159
Q

How is metabolism measured?

A

1.) direct calorimetry (gold standard)
2.) indirect calorimetry via respiratory quotient
3.) Resting energy expenditure calculator (Harris Benedict equation)

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160
Q

What are the constant numbers representing kcal/L for oxygen and CO2?

A

• O2: 4.751 kcal/L
• CO2: 6.253 kcal/L

~ these are used to determine basal metabolic rate in 24 hour period

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161
Q

What are the four metabolic states?

A
  • fed: lasts 2 to 4 hours after a meal (primarily uses glucose, storage of glucose)
  • fasted: overnight without eating (primarily breaks down protein, proteolysis)
  • starved: prolonged fasting (primarily uses fatty acids from adipose tissue, ketones, preserves gluconeogenesis for RBCs)
  • hypercatabolic: trauma, sepsis, not related to meals (protein breakdown, fatty acid oxidation, not storing any intake)
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162
Q

What does insulin do?

A

Insulin regulates storage pathways in the feds state. It is released from pancreatic beta cells and is directly responsive to the concentration of glucose in the blood. it inhibits glucagon

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163
Q

What type of receptor is the insulin receptor?

A

transmembrane tyrosine kinase

• rapid kinase effects (activation of PP1 via PKB/Akt, and inhibition of GSK3)
• sustained transcription effects via Ras/Raf/MAPK/ and Erk1/2

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164
Q

What happens to glucagon levels with high protein intake?

A

They increase. There is less insulin available

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165
Q

After eating a carbohydrate rich meal, what biosynthetic pathways are inhibited?

A

ones that produce glucose

  • glycogenolysis
  • gluconeogenesis
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166
Q

After eating a carbohydrate rich meal, what metabolic pathways are activated?

A

ones that store glucose

• fatty acid biosynthesis
• cholesterol biosynthesis
• protein synthesis
• glycogenogenesis

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167
Q

What is the brains response to feeding?

A

Oxidizes glucose to CO2 and makes ATP through oxidative phosphorylation

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168
Q

What are the red blood cells response to feeding?

A

Ferment glucose to lactate — no flexibility

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169
Q

What are the white adipose cells responses to feeding?

A

Convert glucose to citrate for fatty acid synthesis; ferment glucose to glycerol-3- phosphate, the backbone for triacylglycerol synthesis

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170
Q

What is the skeletal/cardiac muscles response to feeding?

A

Skeletal: Glycolysis, fatty acid beta oxidation, glycogenogenesis (storing glucose as glycogen), and protein synthesis

Cardiac: fatty acid beta oxidation, oxidation of glucose and lactate to CO2, glycogenogenesis

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171
Q

How do the cells of the G.I. tract respond to feeding?

A

• intestinal epithelial cells: convert glutamine, glutamate, aspartate from the diet into alpha–KG

• colonocytes: use short chain fatty acids produced by gut bacteria

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172
Q

In the feds state, what do gut epithelial cells use as their primary fuel?

A

Glutamine, aspartate, glutamate from the diet to create acetyl CoA/pyruvate

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173
Q

Low carbohydrates in the blood promote the release of what?

A

Glucagon, a major regulator of hepatic fuel mobilization, from pancreatic alpha cells (activates AMP-K)

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174
Q

What type of receptor is a glucagon receptor?

A

seven transmembrane domain heterotrimeric G protein coupled receptor

• ligand binding causes activation of adenylate cyclase, production of cAMP, and activation of PKA in low blood glucose states (PP1 inhibits PKA in fed states)

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175
Q

What are the two ways the liver increases production and exportation of glucose?

A
  1. Glycogenolysis using hepatic glycogen stores
  2. Gluconeogenesis using carbon skeletons from amino acids, lactate, and glycerol to produce glucose
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176
Q

Where does the ATP to power gluconeogenesis in the liver come from?

A

• FAD2H and NADH reduced by fatty acid beta oxidation

~ the acetyl CoA produced by FA beta oxidation is a substrate for ketone body synthesis

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177
Q

What are used as fuel for skeletal muscles in a fasted state?

A

Branched chain amino acids via proteolysis

(prolonged state = ketone bodies)

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178
Q

What amino acids from proteolysis are used for gluconeogenesis in the liver?

A

Alanine and glutamine

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179
Q

In the fasted state, what does cardiac muscle use for energy?

A

FA beta oxidation (glycolysis decreases)

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180
Q

What do gut epithelial cells use as major fuel in the fastest state?

A

Glutamine (from the blood, not the lumen of the gut)

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181
Q

What are the responses to prolonged fasting/starvation?

A
  • lipolysis of adipose, liver increases its production of ketone bodies to be used by the brain
  • cardiac muscle continues to use fatty acids
  • skeletal muscle breakdown decreases to preserve muscle mass, the liver decreases gluconeogenesis
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182
Q

Starvation is characterized by what?

A

Increased mobilization of fatty acids from adipose tissue. The liver converts these FA to ketone bodies

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183
Q

During what metabolic state is the urea cycle most active?

A

In the fasting state, when the primary energy source is proteolysis

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184
Q

What is hypercatabolism?

A

The rapid mobilization of stored fuels to provide energy for wound repair and immune system function. Characterized by sustained muscle and organ protein breakdown. This can occur after surgery, trauma, burns, or sepsis.

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185
Q

What are the organ responses to hypercatabolism?

A

• initial spike of catecholamines followed by low amounts
• spike of glucagon with slow decrease
• gradual spike of cortisol followed by maintenance of high levels

~ these allow for the increase of proteolysis, gluconeogenesis, and lipolysis

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186
Q

Patients recovering from illness typically have what type of nitrogen balance?

A

Negative— excreting more nitrogen in the urine than they are intaking. This is not good and hinders recovery

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187
Q

What is refeeding syndrome?

A

A period of fasting/malnutrition that creates lipids/protein/insulin suppression followed by an increase in intake (glucose) leading to intracellular shifts of phosphate, potassium, magnesium which causes hypophosphatemia, hypokalemia, hypomagnesmia

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188
Q

In refeeding syndrome, the rapid increase increase in glycolysis can cause a functional deficiency of what vitamin?

A

Thiamine, leading to Wernicke-Korsakoff syndrome symptoms

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189
Q

Muscles required for closing the mouth:

A

Temporalis, masseter, medial pterygoid

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190
Q

Muscles responsible for opening mouth

A

Lateral pterygoid, mylehyoid, geniohyoid, anterior belly of digastric

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191
Q

What muscles are required for lateral movement of the mandible?

A

• pterygoids, temporalis

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192
Q

What provides motor innervation to the tongue?

A

Cranial nerve 10, cranial nerve 12

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193
Q

What provides taste (special sensory) innervation to the tongue?

A

• anterior 2/3: cranial nerve 7 via chorda tympani

• posterior 1/3: cranial nerve 9 (glossopharyngeal)

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194
Q

What nerve provides innervation to the pharynx constrictor muscles?

A

Vagus (CN 10)

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195
Q

What provides innervation to the esophagus?

A

• parasympathetic: upper= recurrent laryngeal, lower= esophageal plexus (vagus)

• sympathetic: cervical and thoracic sympathetic trunk

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196
Q

What are the main dietary carbohydrates?

A

• fructose
• lactose (galactose plus glucose)
• sucrose (fructose plus glucose)
• amylose (alpha 1,4 bonds)
• amylopectin (alpha 1,6 and 1,4 bonds)

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197
Q

What polysaccharide is most similar to glycogen?

A

Amylopectin

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198
Q

What are the dietary disaccharides?

A

• lactose (galactose plus glucose; beta 1,4)
• sucrose (fructose plus glucose; alpha 1,2)
• trehalose (glucose plus glucose; alpha 1,1)

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199
Q

What type of enzyme is amylase?

A

It is an Endoglycosidase, it cuts Alpha 1,4 bonds in polysaccharides. It’s activity is highest in the duodenum

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200
Q

What are the disaccharidases of the brush border?

A
  1. Glucoamylase
  2. Sucrase/ Isomaltase complex
  3. Trehalase
  4. Beta-glycosidase complex
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201
Q

What type of enzyme is glucoamylase/maltase?

A

an exoglycosidase that cleaves alpha 1,4 bonds of maltose to form 2 molecules of glucose. It cuts off the non-reducing ends of starch. It’s activity is highest in the ileum

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202
Q

What does the sucrase – isomaltase complex do?

A

~ it has two extracellular domains. It’s activity is highest in the jejunum

  1. Sucrase cut sucrose into glucose and fructose
  2. Isomaltase cuts the alpha 1,6 bond in isomaltose
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203
Q

What is the catalytic site, and substrate of trehalase?

A

Trehalose. Two glucose units bonded through the number one carbon. It is found in insects, algae, mushrooms and other fungi

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204
Q

What is the beta-glycosidase complex?

A

• a glycophosphatidylinositol (GPI) glycan anchored protein with high activity in the jejunum with two catalytic domains:

  1. Glucosyl ceramide: cuts glucose and galactose from glucosylceramide and galactosylceramide (gluco/galacto-cerebrosidase)
  2. Lactase: splits the beta 1,4 bond in lactose to make galactose and glucose
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205
Q

Primary lactase deficiency:

A

Loss of lactase activity with age

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206
Q

Secondary lactase deficiency:

A

Loss of lactase from damage to intestinal mucosa

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207
Q

Congenital lactase deficiency:

A

Non-functional lactase enzyme inherited from parents (rare)

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208
Q

Metabolic fates of carbohydrates as a diagram

A
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209
Q

What is fructose?

A

A naturally occurring monosaccharide that is only found in honey (it can also be produced by sucrase acting on sucrose to produce glucose and fructose)

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210
Q

Our body can convert linoleic (omega 6) and linolenic (omega 3) acids into what?

A

Prostaglandins, where PGE3 is less inflammatory, produced by fish oil and linolenic acid

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211
Q

What do trans fats do in the body?

A

They are more of a liquid state than cis fatty acids, they can inhibit the desaturases responsible for generating arachidonic acid and eicosapentanoic acid (which eventually become PGE2, and PGE3). Therefore, they are pro-inflammatory. They can also cross the placenta

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212
Q

What is the breakdown of dietary triacylglycerol?

A

Oral: TG — bile salts—> free FA + 2-MG — nascent chylomicron —> MANY TG reformed — lymph —> into the blood as a chylomicron

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213
Q

What hormones promote the secretion of bile and lipase into the lumen of a gut?

A

Secretin and cholecystokinin

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214
Q

Triacylglycerol reacting with a pancreatic lipase leads to what?

A

Two fatty acids and two monoacylglycerol (2-MG)

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215
Q

What two molecules must a nascent chylomicron receive from HDL in the blood in order to become mature?

A

• ApoC2
• ApoE

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216
Q

What is abetalipoproteinemia?

A

An inherited disorder of the microsomal triglyceride transfer protein that results in failure to assemble B apoproteins (therefore chylomicrons in the intestine and VLDL in the liver)

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217
Q

What is an extracellular lipase in the capillary beds of muscle and adipose tissue?

A

Lipoproteinlipase. It is activated by ApoC2

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218
Q

Lipoproteins in the blood: smallest to largest

A

HDL < LDL < IDL < VLDL < chylomicron

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219
Q

Lipoproteins information table:

A
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220
Q

What does low pH do to protein in the gut?

A

Denatures proteins, and activates pepsinogen

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221
Q

What digests tripeptide, dipeptides, and amino acids in the gut?

A

Luminal proteases

222
Q

What digests tripeptides and dipeptides into amino acids?

A

Intracellular peptidases

223
Q

Which enzyme can independently cleave itself to form the active version?

A

Pepsinogen can cleave itself to form pepsin protease

224
Q

What determines the specificity of the Endopeptidase cleavage spot?

A

The N-terminal amino acid (the one to the left / just prior to where the cut would happen)

225
Q

Where does Trypsin cut peptide bonds?

A

Where the carbonyl (N-terminal side) is provided by an arginine or lysine

226
Q

Where do exopeptidase cut?

A

They they cut single amino acids from the end of peptide chains

227
Q

Luminal proteases and their N-terminal carbonyl amino acid requirement (image/picture)

A
228
Q

What is Hartnup disease?

A

Inherited mutations in the SLC6A9 transporter (B^o)in the kidney. This results in symptoms of pellagra because tryptophan is not absorbed and cannot be synthesized to make niacin

229
Q

What causes cystinuria?

A

Inherited mutations in the SLC7A9 (B^o+) or SLC3A1 (rBAT) transporters. The body cannot uptake cysteine, leading to kidney stones

230
Q

What is another way amino acids can be transported across the cellular membrane?

A

Reacting with glutathione

231
Q

What complex activates protein synthesis and inhibits autophagy?

A

MTORC1

232
Q

Activation of AMPK inhibits what cellular energy mechanism?

A

It inhibits protein synthesis and promotes autophagy. It also alters metabolism in order to get more energy; it integrates protein metabolism with lipid and carbohydrate metabolism

233
Q

What are the three key cofactors for enzymes in amino acid metabolism?

A
  1. PLP: transamination, deamination, carbon chain transfers. ~ without it can lead to seizures, diarrhea, anemia, EEG abnormalities
  2. FH4/tetrahydrofolate: one carbon transfers ~ without it can lead to megaloblastic anemia
  3. BH4/tetrahydrobiopterin: ring hydroxylations ~ without it can lead to seizures, developmental delays
234
Q

Explain the cutaneous area of the oral cavity

A

• stratified squamous epithelium that is keratinized
• stratum basal, stratum spinosum, granulosum, corneum
• hair follicles, sebaceous glands, melanin in basal cells

235
Q

At what point is there a transition in stratified squamous epithelium from keratinized to parakeritinized?

A

Mucocutaneous junction of the lip. Parakeratinized does not have granulosum, only has basal, spinosum, stratum superficiale

236
Q

What is the red margin?

A

The Vermillion part of the lip. Epithelium of red margin is thicker than that of the cutaneous area. It is keratinized and red color is due to deep penetration of lamina propria papillae into the epithelium that contains blood vessels. It has meissners corpuscles, which allows high sensitivity to light touch

237
Q

What type of cells line the ventral (underside) surface of the tongue?

A

Stratified squamous non-keratinized epithelium. Mixed glands beneath epithelium

238
Q

What type of cells line the dorsal surface (top) of the tongue?

A

Mucosa which is stratified squamous keratinized epithelium, and the supporting wall is made of skeletal muscle in three planes

Nerve supply: anterior 2/3 by cranial nerve 5 and 7, posterior 1/3 by cranial nerves 9 and 10

239
Q

What does a tastebuds look like?

A
240
Q

What tongue papillae have taste buds?

A
  1. Fungiform
  2. Circumvallate
  3. Foliate

(Filiform, the most common kind, do not have taste)

241
Q

What are the taste buds that are mushroom/Club shaped?

A

Fungiform papillae

• reddish tint due to underlying vascularization
• supplied by cranial nerve 7
• towards tip of tongue

242
Q

Circumvallate papillae

A

• adjacent to sulcus terminalis
• 7 to 12 total, surrounded by deep trench
• taste buds are numerous in the sides of these papillae
• supplied by cranial nerve 9
• serous gland of von Ebner empty into the trenches

243
Q

Foliate papillae

A

• vertical folds of non-keratinized epithelium
• found on the sides/back of the tongue, usually bilaterally symmetrical
• numerous tastebuds present
• serous glands drain into the folds

244
Q

What type of glands are salivary glands?

A

• exocrine (they have ducts)
• major: carotid, submandibular, sublingual

245
Q

What is the difference between a serous and a mucus gland?

A
  • serous: darkly stained cytoplasm, secretes proteins
  • mucous: lightly stand, foamy cytoplasm, secretes glycoprotein (water)
246
Q

Explain the parotid gland

A

• prominent connective tissue capsule with separating lobes/lobules
• adipose cells and tissue is common
• striated and intercalated ducts prominent
• acini almost 100% serous)

247
Q

Explain the submandibular gland

A
  • connective tissue capsule present but not easily visible
  • striated ducts well defined
  • intercalated ducts are scarce
  • acini are 10- 25% mucus,so the MAJORITY is serous
248
Q

Explain the sublingual gland

A

• connective tissue capsule is indistinct
• excretory ducts prominent
• striated/intercalated not prevalent/not existent
• acini are 75% mucus with serous demilunes

249
Q

Classification graph of the major salivary glands

A
250
Q

Layout of tubular structures in the G.I. system

A

• mucosa: epithelium, basement membrane, lamina propria, muscularis mucosa
• submucosa: connective tissue
• supporting wall: smooth or skeletal muscle, bone, cartilage
• adventitia/serosa: CT that connects to other structures OR connective tissue covered by mesothelium

251
Q

Esophagus layers

A
  1. Mucosa: stratified squamous epithelium, non-keratinized
  2. Submucosa: mucus gland in the middle 1/3, submucosal nerves, larger blood vessels, lymphatics
  3. Muscularis externa (supporting wall): skeletal muscle transitions to smooth muscle, myenteric nerves
  4. Adventitia: ~no mesothelium
252
Q

What regulates movement between functional regions in the G.I. system?

A

Sphincters, including:
• upper and lower esophageal
• pylorus
• sphincter of Oddi
• ileocecal valve
• internal and external anal

253
Q

What is the purpose of the muscularis mucosa in the G.I. tract?

A

Gently agitates the mucosal surface and glands leading to the expulsion of contents of the crypts and enhances contact between epithelium and luminal contents

254
Q

What is the most important spot for absorption in the G.I. tract?

A

The submucosa containing the blood vessels and lymph

255
Q

Skeletal versus smooth muscle in the esophagus versus the rectum

A

Esophagus: starts out with skeletal muscle in the first 1/3 and then transitions to smooth muscle in the distal 2/3

Rectum: starts out with smooth muscle and then transitions into skeletal muscle for the external anal sphincter

256
Q

What is produced by the mechanical digestion of food?

A

Chyme

257
Q

How was water transported in the G.I. tract?

A

Paracellular and transcellular (between and through)

258
Q

What area of the G.I. tract is most important for the reabsorption of water/secretions?

A

The small intestine

259
Q

What is the motility of different areas of the G.I. tract?

A

• esophagus: 10 seconds
• stomach: 4 to 5 hours
• small intestine: 2 to 3 hours
• large intestine: 30 to 40 hours

260
Q

What anti-constipation drugs affect motility?

A

Bulk laxatives and contract cathartics

261
Q

What anti-constipation medication affects water balance?

A

Osmotic cathartics

262
Q

How are secretion and motility systems controlled?

A
  1. Parietal cells via cAMP and IP3
  2. Smooth muscle contraction via MLCK and MLCP
263
Q

What determines smooth muscle tone?

A

The degree of phosphorylation of myosin II

• activation of myosin light chain kinase (MLCK) —> contraction
• activation of MLC phosphatase (MLCP) —> relaxation

264
Q

What is the primary activator of myosin light chain kinase (MLCK)?

A

Intracellular calcium (ACh, M3 receptors)

265
Q

What are the primary activators of MLC phosphatase (MLCP)?

A

Cyclic nucleotides (cAMP from VIP and cGMP from NO)

266
Q

What are short loop reflexes?

A

Reflexes within the gut (myenteric and submucosal plexi) that are not signals to the brain

267
Q

What nerve controls the long loop reflexes from the G.I. system to the CNS?

A

Vagus nerve to the nucleus of the solitary tract

268
Q

Endocrine versus paracrine versus neuronal versus contact dependent

A
269
Q

What are the paracrine (gut —> blood —> other gut) G.I. hormones?

A

• cholecystokinin
• gastrin
• motilin
• secretin
• somatostatin

270
Q

What are the hormone endocrine inhibitors of the G.I. tract?

A

Central:
• CCK
• CART
• CRH
• NE
• POMC

Peripheral:
• CCK
• glucose/AA/FFA
• insulin
• leptin
• PYY

271
Q

What are the hormone endocrine stimulants of the G.I. system?

A

Central:
• NPY
• orexin A
• cannabinoids

Peripheral:
• Ghrelin
• cortisol

272
Q

The highest concentration of the human micro biome is where?

A

The mucus layer of the large intestine

273
Q

What can be absorbed in the mouth?

A

• small molecules that are uncharged at a pH around 6.3
• glucose via sodium glucose symporter
• very small particles (<1um) including viruses and some chemotherapeutic drugs can be taken up by endocytosis which can lead to mucositis

274
Q

What are the functions of saliva?

A
  1. Taste (food must be dissolved in saliva to enter the taste pore)
  2. Digestion (amylase, lipase, chewing)
  3. Protection (diffusion/buffering of toxins, lubrication, anti-microbial, remilitarization and cleansing of teeth)
275
Q

How does saliva prevent leaching of calcium phosphate from the teeth?

A
  • it increases the pH of the mouth to 6.3 due to secretion of bicarbonate in the saliva (due to lactic acid from blood/fermentation of carbohydrates by bacteria, the mouth would be a pH of 2 to 4 without saliva)
  • saliva contains potassium, calcium, magnesium, and phosphate which decreases demineralization of enamel
276
Q

What is the two-step process for saliva secretion?

A
  1. Production in acinar cells sodium potassium ATPase and and NKCC1 and chloride channel encourage flow of chloride, then sodium paracellularly, then H2O transcellularly into the mouth
  2. Modification by duct cells where sodium potassium ATPase and sodium/bicarbonate symporter direct NaCl into the duct lumen and water follows
277
Q

What are the control mechanisms of saliva from the autonomic nervous system?

A

• parasympathetic, M3: watery secretion
• sympathetic, beta: viscous secretion

~ paracrine/endocrine regulation is controlled by aldosterone

278
Q

Xerostomia

A

• perceived/actual dry mouth
• consequences: tooth decay, infection, bad breath, decreased appetite, speech difficult difficulties, dysphasia

279
Q

What drug classes commonly caused dry mouth?

A
  1. Anti-muscarinic (including antihistamines, TCA, antipsychotics)
  2. Cardiac glycosides
  3. Diuretics (loop/NKCC2)
  4. Aldosterone receptor blockers
  5. Statins
280
Q

What is a parasympathomimetic that can be used to treat xerostomia?

A

Pilocarpine (side effects include bradycardia, hypotension, bronchoconstriction so it is reserved for extreme cases)

281
Q

What is the medullary swallowing center nucleus that is a pattern generator for the esophagus?

A

Nucleus ambiguus: afferent input via vagus nerve, efferent via glossopharyngeal nerve

282
Q

What are the three phases of swallowing (deglutition)?

A
  1. Oral: initiation of swallowing reflex- nucleus ambiguus
  2. Pharyngeal: protection of the airway Where choking in neuroMSK disorders occurs
  3. Esophageal: initiation of peristalsis, skeletal muscle control of top 1/3, smooth muscle (ENS) control of lower 2/3
283
Q

Describe primary peristalsis

A

• a long loop reflex, fixed action pattern
• circular muscles contract upstream of the bolus and relax downstream, longitudinal muscles relax upstream of the bolus and contract downstream

284
Q

What is the neural control of primary peristalsis?

A

• central pattern generator and the nucleus ambiguus —> striated muscle
• central pattern generator—> DMN—> enteric nervous system—> smooth muscle

285
Q

What do enteric neurons release to allow contraction of circular and longitudinal muscles?

A

Acetylcholine

286
Q

What allows for the relaxation of circular and longitudinal muscles?

A

Vasoactive intestinal polypeptide (VIP), nitric oxide (NO) from enteric neurons

287
Q

What is secondary peristalsis?

A

Reserved for the failure of primary peristalsis, in the smooth muscle section only a short loop reflex can cause contraction of muscle immediately above the obstruction and relaxation of the muscle below the obstruction — any region moderately above the obstruction is unaffected

288
Q

What are factors that can reduce esophageal tone?

A

Chocolate, peppermint, caffeine, alcohol, fatty meals, progesterone, isoproterenol, secretin, VIP, NO, neurotensin, PGE1, cholecystokinin

289
Q

What factors can increase esophageal tone?

A

Protein meal, acetylcholine, phenylephrine, serotonin, gastrin, pancreatic polypeptide, substance P, motilin, neuropeptide Y

290
Q

What are the contents of a fine needle aspiration of a pleomorphic adenoma?

A

• epithelioid cells
• chondroid cells
• single cells

291
Q

Pleomorphic adenoma (benign mixed tumor)

A

• the most common salivary gland tumor, predominantly in adults
• presents as a painless, slow growing, firm and mass located in the parotid gland
• potential for reoccurrence/risk of malignant transformation in long-standing cases

292
Q

Histopathology of pleomorphic adenoma

A

Gross path: well circumscribed, encapsulated, lobulated, 4 to 6 cm

Histology: duct-like structures, myxoid areas, cartilaginous regions. Cells include epithelial, myoepithelial, mesenchymal differentiation

293
Q

What is the treatment for pleomorphic adenoma?

A

Surgical excision, careful to avoid facial nerve

294
Q

Warthin tumor

A

• benign tumor of old smokers, 10% of the time bilateral, parotid gland
• “motor oil” on smear
• three components: cystic background, oncocytes and lymphocyte stroma

295
Q

Histopathology of Warthin tumor

A

• histology: Papillae covered with columnar oncocytes with lymphoid stoma

296
Q

Mucoepidermoid tumor

A

• most common malignant salivary gland tumor characterized by a t(11;19) translocation resulting in a CRTC1-MAML2
• typically affects the parotid gland
• grading level: based off the proportion of cystic versus solid growth, cellular atypia, and mitotic activity

297
Q

Histopathology of mucoepidermidoid carcinoma

A

• gross: may be cystic, may appear encapsulated, often infiltrates microscopically
• microscopic: essential for diagnosis, squamous cells, mucus secreting cells, and intermediate cells

298
Q

What is the growing pattern of mucoepidermoid carcinoma?

A

• growing in nests composed of squamous cells as well as clear vacuolated cells containing mucin and intermediate cells

299
Q

Adenoid cystic carcinoma

A
  • malignant tumor effecting the parotid and submandibular glands (50% in minor salary glands), typically seen in middle-aged adults.
  • presents as slow growing, firm, and often painful mass
  • spreads via perineural invasion by ourselves which can lead to pain and nerve paralysis
  • death typically occurs via lung, bone, liver metastasis
300
Q

Histopathology of an adenoid cystic carcinoma

A
  • gross: infiltrative poorly encapsulated, calcifications
  • microscopic: basal cells with scant cytoplasm forming a classic cribiform pattern(Swiss cheese) and hyaline material with pseudocystic spaces
301
Q

Sialadenitis

A

Inflammation of the salivary glands due to bacterial infections (staph aureus), viral infections (mumps, HIV), or auto immune diseases (Sjogrens)

302
Q

What causes salivary gland calcified stones/Sialoliths?

A

Dehydration, reduced salivary flow, and increased calcium concentration in saliva. Obstruction leading to infection can occur (staph aureus, strep viridans)

303
Q

What are the mucus extravasation diseases?

A
  • mucous dissects out of the glandsand into surrounding tissues creating false cysts with no lining
  • mucocele: lip and minor salivary gland cyst from trauma or duct obstruction
  • ranula: under tongue/floor of the submucosal duct damaged (becomes plunging ranula if it dissect through mylohyoid into neck)
304
Q

Thyroglossal duct cyst

A

• Cyst lined by squamous epithelium +/- columnar epithelium at the midline/base of the tongue to the thyroid which can contribute to thyroid carcinomas

305
Q

Branchial cleft cyst

A

• cyst of the lateral neck, from the second pouch seen in children and young adults. Squamous/columnar or denuded epithelium with lymphoid tissue in the wall

306
Q

Paraganglioma/carotid body tumor

A

• extraadrenal paraganglioma at the bifurcation of the carotid artery (lyre sign)

307
Q

Lumps of the neck and where you would find them image:

A
308
Q

Head and neck paraganglioma

A
  • Zellballen
  • Synptophysin and chromogranin +
309
Q

Oral leukoplakia

A

• clinical diagnosis meaning white patch or plaque that can’t be diagnosed clinically as something specific (candida, lichen planus, denture irritation)
• hyper keratosis causes the white appearance and 5 to 25% are dysplastic

310
Q

What can you see on biopsy for leukoplakia?

A
  • hyperkeratosis
  • squamous cell hyperplasia
  • low-grade dysplasia
  • high-grade dysplasia
  • squamous cell carcinoma
311
Q

Oral squamous cell carcinoma

A

• most common oral cancer, typically seen in middle age/older men
• 50% occur on the tongue, or floor of the mouth
• associated: tobacco, alcohol, P 53 mutation, less HPV related in the mouth/oral cavity

312
Q

Erythroplakia

A

• red velvety plaque/lesion sometimes eroded
• lacks keratinization, increased vasculature, inflation in submucosa
• very high risk of dysplasia

313
Q

What are the two microscopic features of a keratinizing squamous cell carcinoma (both oral and esophageal)?

A

• keratin pearls/whorls
• tram tracks (intercellular bridges of the spinosum)

314
Q

HPV related non-keratinizing squamous cell carcinoma

A

• seen at the base of the tongues, in the tonsillar crypts, young/middle-aged men
• presents as an enlarged neck lymph node
• often seen in a non-smoker/non-drinker
• up to 80% are associated with HPV, most commonly HPV 16

315
Q

Histopathology of HPV associated non-keratinizing squamous cell carcinoma

A

• basaloid tumor cells in a nested pattern without keratinization
• lymphocytes present in the tumor

316
Q

HPV associated esophageal squamous cell adenocarcinoma

A
  • High risk HPV type 16
  • detected in tumors by in situ hybridization or by IHC stain that detects over expression of P16 (a surrogate marker for HPV upregulated by E7 overexpression
  • HPV negative oral pharyngeal cancer shows p53 over expression
317
Q

What is a squamous papilloma?

A

• benign tumor, typically associated with HPV type 6, and 11
• can involve any squamous mucosa in the upper G.I. tract

318
Q

What is recurrent respiratory papillomatosis?

A

• recurrent juvenile laryngal papillomas, may regress at puberty
• infected in utero or at birth
• may require multiple surgeries, morbidity is from repeat surgical or laser removal resulting in fibrosis/scar

319
Q

Local cord nodules/polyps

A

• non-neoplastic, stromal reactive process related to inflammation and or trauma
• clinical symptom is typically hoarseness and change in voice

320
Q

Sinusitis/nasal polyps

A

• allergic sinusitis: most common nasal polyps have stromal edema/inflammation. Recurrent rhinitis results in mucosal protrusion/polypoid mucosa. eosinophils

• infection: mucocele abscess and emypema

• fungal infection: typically immuno suppressed patients/diabetic patients. Considered a medical/surgical emergency

321
Q

Schneiderian polyps/papillomas

A
  • seen in adults, arising from the sinonasal mucosa composed of squamous or columnar epithelial proliferation
  • if inverted type arising from lateral nasal wall, there is more of a chance for malignant transformation
322
Q

Nasopharyngeal angiofibroma

A

• benign but locally aggressive neoplasm of vascular and fibrous tissue
• typically CNN young adolescent males and before the age of 25
• symptoms: persistent nasal obstruction and epistaxis

323
Q

Epstein Barr related nasopharynx carcinoma

A

• common in EBV related endemic areas (Africa-children, south China-adults)
• three patterns of nasopharyngeal carcinoma:
1. Keratinizing squamous cell carcinoma
2. Non-keratinizing squamous cell carcinoma
3. Undifferentiated carcinoma (EBV RELATED)

324
Q

Eosinophilic esophagitis (EoE)

A

• repetitive feeling of food being stuck beneath the sternum with substernal discomfort, not choking but 100% of people have dysphagia
• IgE/Th2 mediated
• more common in men than women
• Tx: dietary modification, cortical steroid, dilatation for structure

325
Q

What is seen on endoscopy for EoE?

A

• trachealization of the esophagus (fixed white rings secondary to fibrosis, made of linear thick mucosa and white exudate)
• crepe paper appearance
• Typically seen in the middle, with strictures

326
Q

EoE histopathology

A

• eosinophilic microabscesses
• basal cell hyperplasia of squamous mucosa

327
Q

What are the three most common infectious esophagitis causes?

A
  1. Candida
  2. Herpes
  3. Cytomegalovirus

~ seen in immunocompromised pts, HIV, chemo, elderly

328
Q

Other than infection, what can cause esophagitis?

A
  1. Ingestion of corrosives (lye)
  2. Pill esophagitis from NSAIDs, antibiotics, iron pills, alendronate
  3. Iatrogenic from chemo, radiation, GVHD
  4. Bullous pemphigoid, Epidermolysis bullosa
  5. Crohn’s disease
329
Q

What is the number one G.I. complaint at the clinical setting?

A

Gastro esophageal reflux disease (GERD)

330
Q

What are the risk factors and symptoms of GERD?

A

• risk factors: anything that decreases lower esophageal sphincter tone
• symptoms: heartburn, pain, esophageal spasm, morning hoarseness, sore throat, bad breath

331
Q

What is seen histologically in GERD?

A
  • non-specific damage to the squamous mucosa
  • scant eosinophils, ulcers, erosions, +/- neutrophils
  • lymphocytes in a squiggle shape
  • lamina propria papillae elongation
332
Q

What is Barrett’s esophagus?

A

• intestinal metaplasia in the tubular esophagus (columnar metaplasia with goblet cells) which changes the appearance from white, shiny to bright red on endoscopy “salmon colored”

333
Q

Where does Barrett’s esophagus occur?

A

The lower 1/3 of the esophagus (gastric cardia intestinal metaplasia is not considered Barrett’s)

334
Q

95% of adenocarcinomas (esophageal cancer) are associated with what?

A

GERD/Barrett esophagus

~ stepwise accumulation of genetic mutations typically EGFR amplification

335
Q

What are the treatments for esophageal adenocarcinoma?

A
  1. Endoscopic mucosal resection (early tumors and dysplasia)
  2. Neoadjuvant chemo radiation prior to resection for higher stage tumors
336
Q

What histopathology is typically seen in patients who have had neoadjuvant chemoradiation for esophageal adenocarcinoma?

A
  1. Dissecting pools of mucin within the muscle layers of the wall, no malignant cells present
  2. Rare, highly atypical enlarged treated to moles floating with an a pool of mucin
337
Q

Squamous cell carcinoma of the esophagus

A

• seen in the middle 1/3 of the esophagus, typically causing strictures with associated symptoms of dysphasia and odynophagia (pain) and obstruction
• risk factors: alcohol, tobacco, scalding hot beverages, esophageal injury, achalasia, tylosis, Plummer-Vinson syndrome

338
Q

Mallory-Weiss syndrome

A

• longitudinal mucosa laceration in the distal esophagus and proximal stomach caused by increased abdominal pressure
• traditionally associated with severe vomiting, history of heavy alcohol use is a classic cause
• 50% are iatrogenic from therapeutic dilation, varies treatment, endoscopy, intubation

339
Q

Mallory- Weiss syndrome versus Boerhaave syndrome

A

• MWS: longitudinal mucosa laceration
• Boerhaave: deep transmural tears extending into mediastium (pneumomediastinum)

340
Q

What are esophageal rings (Schatzki’s rings)?

A

• mucosal ring shaped thickening in the lower esophagus causing dysphasia, treated by endoscopic dilatation
• can be secondary to reflux disease or hiatal hernia

341
Q

What is a Zenker diverticulum?

A

• above upper esophageal sphincter the mucosa and some mucosa protrude through a defect in the cricopharyngeal muscle
• accumulated food can compress the anti-esophagus causing dysphasia and halitosis (bad breath) from degenerating food

342
Q

What happens at the Gastroesophageal junction?

A

The lining goes from stratified squamous epithelium (non-keratinized) to simple columnar epithelium

343
Q

What happens at the Gastroesophageal junction?

A

The lining goes from stratified squamous epithelium (non-keratinized) to simple columnar epithelium

344
Q

Rugae vs gastric pits

A
  • Rugae: larger structure of the fundic region of the stomach. Inner surface folds that allow for distention and absorption. Folds of mucosa with with submucosal core
  • gastric pits:smaller structure located throughout the stomach, tubules that empty gastric glands. Deeper in the pylorus, folds of epithelium with lamina propria core (they are entirely of the mucosal layer)
345
Q

Stomach Cardia: picture

A
346
Q

Layers of the stomach and the cells that make them up

A
  1. Mucosa: simple columnar epithelium, includes gastric pits and glands
  2. Submucosa: dense connective tissue, adipocytes, nerves/blood vessels
  3. Muscular externa: smooth muscle
  4. Serosa: mesothelium
347
Q

Epithelial cells of the gastric pits

A

• foveolar cells
• located in gastric, surface of stomach
• columnar in shape, short microvilli on apical surface
• secrete soluble mucus (glycoproteins) and bicarbonate

348
Q

Epithelial cells of the gastric glands

A

• mucus neck cells, parietal cells, chief cells (zymogenic), enteroendocrine cells, undifferentiated adult stem cells

349
Q

What are mucus neck cells?

A

• located in the neck region of the gastric/fundic gland
• cuboidal to low columnar in shape
• secrete soluble mucus

350
Q

What are parietal cells (oxyntic)?

A

• eosinophilic, large, binucleate, spherical centrally placed nucleus, triangular, Apex toward lumen
• numerous in the neck and of proportion of the gland body, intracellular caniculi with microvilli
• intrinsic factor (b12 absorption), and secretion of HCL

351
Q

Secretion of parietal cells is activated by what?

A

• cholinergic nerve endings
• Gastrin
• histamine

352
Q

What are chief/zymogenic cells?

A

• most numerous at the base of the glands
• basophilic, protein secreting cells (rER)
• pepsinogen secretion which is converted to active protease (pepsin) in the presence of HCl

353
Q

What are enteroendocrine cells?

A

• part of the diffuse neuroendocrine system
• found out every level of the gastric glands, more prevalent at the base with the chief cells
• small size, clear faintly stained cytoplasm
• fxn: sample contents of lumen gland and then release hormones, control taste receptors

354
Q

What is the purpose of undifferentiated adult stem cells in the gastric glands?

A

• located in the isthmus of the gastric gland
• cells can replicate and differentiate to produce mucus cells (move up) or mucus neck, parietal, chief, enteroendocrine (all move down)

355
Q

Mucosa of the fundic region of the stomach

A
  • simple columnar epithelium, with mucus secreting cells
  • the gastric pits are 1/4 of the mucosal thickness
  • constant turnover (4-6 days) of epithelial cells
356
Q

Mucosa of the pyloric region of the stomach

A
  • simple columnar epithelium, mucus secreting cells
  • the gastric pits are 2/3 of the mucosal thickness
  • glandular region has simple branched coiled tubular glands
  • enteroendocrine and parietal cells present (no chief cell)
357
Q

Mucosa of the cardiac region of the stomach

A
  • simple columnar epithelium
  • gastric pits are 1/4 of of the thickness of the mucosa
  • coiled glands, cells are mucus neck type
  • absence of parietal/chief cells
358
Q

What is the pathogenesis of Gastroesophageal reflux disease?

A

• abnormal amount of Gastroesophageal reflux leading to heartburn, acid regurgitation, dysphasia, nausea, odynophasia, chest pain, cough
• caused by: transient lower esophageal sphincter relaxation, lower esophageal sphincter pressure, hiatal hernia/obesity

359
Q

When diagnosing GERD, what are you looking for with esophagogastroduodenoscopy?

A

EGD looks for erosive esophagitis (damage by gastric contents)

360
Q

What are the ways of pH testing for GERD?

A
  1. 24 hour pH NG catheter
  2. Bravo capsule placed in the esophagus during endoscopy (48 hours)
361
Q

What are the treatments/management of GERD?

A

#1:lifestyle modification: weight loss, sleep position, avoid eating for three hours prior to lying down
2. Antacid medication (proton pump inhibitors, H2 receptor blockers (famotidine), antacids
3. Surgery

362
Q

What cell is being targeted for medical management of Gerd?

A

The parietal cell:

Stimulants: histamine, acetylcholine, gastrin

Inhibitors: somatostatin, prostaglandins

363
Q

What causes dysphasia?

A

• mechanical obstruction: stricture, esophageal web, cricopharyngeal bar, zenkers diverticulum
• motility disorders: achalasia, scleroderma
• inflammation: eosinophilic esophagitis
• infections

364
Q

What are the clinical symptoms typically associated with esophageal cancers?

A
  • weight loss
  • does not want to eat eat/nothing tastes good
  • choking on liquids/solids
  • weakness/lightheadedness
  • cachectic and ill appearing
365
Q

What are the primary types of esophageal cancer?

A
  1. Squamous cell carcinoma
  2. Adenocarcinoma
366
Q

Describe squamous cell carcinoma of the esophagus

A

• typically the upper 2/3 of the esophagus, typically flat to the lumen, discolored
• high grade dysplasia with hyperchromatic and enlarged cells with loss of nuclear polarity
• most common cancer worldwide
• risk factors: smoking, alcohol, low SES
• five-year survival: 3% at stage four, 44% at stage one

367
Q

Describe adenocarcinoma of the esophagus

A

• typically found in the lower esophagus, large obstruction
• most common type of esophageal cancer in the US
• risk factors: male, central obesity, GERD, Barrett’s esophagus
• five year survival: 0% at stage four, 81% at stage one

368
Q

Describe eosinophilic esophagitis (EOE)

A

• typically seen in patients with asthma/seasonal allergies
• food feels “stuck” frequently, usually passes/able to vomit it up
• characterized by numerous eosinophils, dilated intracellular spaces, basal cell hyperplasia, and papillary elongation

369
Q

What are the treatments for eosinophilic esophagitis (EOE)?

A

• allergen controlled diet therapy
• proton pump inhibitors
• endoscopy with dilation
• glucocorticoids (fluticasone, budesonide orally)
• dupilumab (IL4R targeted monoclonal antibody to reduce inflammation)

370
Q

What is achalasia?

A

• esophageal motility disorder caused by failure of relaxation of the lower esophageal sphincter due to nerve damage
• common symptoms: regurgitation, heartburn, chest pain, dysphasia, weight loss, pneumonia
• Treatment: myotomy, or pneumatic dilation to disrupt esophageal sphincter

371
Q

What types of food commonly has vitamin A?

A

Red, yellow, orange fruits and vegetables

372
Q

What is dietary vitamin A converted to?

A

All-trans-retinol from dietary sources such as retinyl palmitate, beta carotene, and alpha carotene

373
Q

In the body, the alcohol of trans-retinol can be converted to?

A

• aldehyde (all-trans retinal)
• carboxylic acid (all-trans retinoic acid)
• Esther with fatty acid (retinyl palmitate; the vitamin A storage form)

374
Q

What form of vitamin A is soluble enough to be transported in the blood associated with albumin?

A

Retinoic acid. All others are transported in chylomicrons

375
Q

What serves as the reservoir for vitamin A storage?

A

Stellate cells in the liver

376
Q

Deficiency or toxicity of vitamin A can cause what?

A

Eye pathology (night blindness or blurred vision)

377
Q

What form of vitamin A is important for the eyes?

A

Cis-retinal (aldehyde)

378
Q

What vit A molecules act as ligand activated transcription factors?

A
  • RAR (retinoic acid receptors)
  • RXR (retinoic X receptors)
  • PPAR beta, and PPAR delta

~ these lead to recruitment of antibody secreting cells to the small intestine, differentiation of goblet cells, maturation of dendritic cells, apoptosis of cancer cells, and inhibition of keratinization

379
Q

What form of vitamin A can act as an antioxidant due to the double bonds?

A

Carotenes (alpha and Beta)

380
Q

What are the symptoms of a vitamin A deficiency?

A
  • anorexia
  • decreased growth
  • increased susceptibility to infection (GALT loses IgA)
  • alopecia
  • keratinization of epithelial cells (can lead to dryness, infertility
  • night blindness, xeropthalmia/dry eyes, and Bitot’s spots
381
Q

What is hypervitaminosis A?

A

• toxic level of vitamin A leading to nausea/vomiting, blurred vision, headache, desquamation of skin, alopecia, ataxia, liver damage

~ remember: vitamin A can be a terotogen

382
Q

What are the common forms of vitamin E?

A

• Tocopherols (saturated 16C acyl chains)
• tocotrienols (polyunsaturated 16C acyl chains)

383
Q

What foods are abundant in vitamin E?

A

Plant oils such as palm oil, sunflower oil, canola oil, wheat germ

384
Q

What is the function of vitamin E?

A

• works in the lipid by layers in intracellular and plasma membranes
• allows for stabilization of singlet oxygen and free radicals as a part of ROS defense

385
Q

Vitamin E neutralizing lipid peroxide radicals, leads to what new forms?

A

Alpha- tocopherol —> tocopheryl radical —> tocopheryl quinone

~ vitamin E is able to neutralize two lipid peroxides

386
Q

What are the symptoms of vitamin E deficiency (rare)?

A

• myopathy
• hemolytic anemia
• peripheral neuropathy: ataxia, loss of vibratory sense

387
Q

What is the main form of vitamin K in the diet?

A

Phylloquinone

~ another form produced by fermentation is menaquinone

388
Q

What is the purpose of vitamin K in the body?

A
  • Vit K acts as a co-factor for gamma glutamyl carboxylase ( this enzyme carboxylates glutamic acid side chains on blood clotting proteins)
389
Q

What factors are dependent on vitamin K due to vitamin K epoxide reductase?

A

2, 7, 9, 10

390
Q

What are the symptoms of a vitamin K deficiency?

A

• can occur in infants due to low breastmilk vitamin K
• symptoms: coagulation disorders such as increased PT time, and increased bleeding

391
Q

What is the dietary form of vitamin D?

A

Cholecalciferol

392
Q

What is the most important function of vitamin D?

A

Regulate calcium homeostasis

393
Q

What is the main form of vitamin D circulating throughout the blood?

A

25-hydroxycholecalciferol created in the liver

394
Q

Where does the hydroxylation to create active vitamin D occur?

A

In the kidney: producing 1, 25- dihydroxycholecalciferol (calcitriol)

~ this process occurs under the influence of parathyroid hormone which response to low calcium concentrations

395
Q

What gene transcription is increased when vitamin D receptor is activated in gut epithelial cells?

A
  1. Calbindin
  2. TRPV6
  3. PMCA1b

~ these are genes that are encoding calcium transport proteins

396
Q

What is the symptom of vitamin D deficiency?

A

Rickets: characterized by seizures, growth retardation, failure of bone mineralization (osteomalacia)

~ deficiency can be due to dietary, genetic, or secondary to an absorption problem such as Crohn’s disease

397
Q

What vitamin is most likely to have toxic effects of given too much?

A

Vitamin D—> this can lead to calcification of soft tissue (heart, lungs, blood vessels), hyperphosphatemia, hypertension

398
Q

Does vitamin D increase or decrease levels of colorectal cancer?

A

Decrease. This is due to vitamin D receptor physically interacting with beta-catenin, preventing its transact activation of genes that promote cellular proliferation, such as cyclin-D1

399
Q

What makes up a biofilm in the mouth?

A

Two or more species of bacteria that are enclosed in glycocalyx, and protein/DNA

400
Q

What do biofilms allow for?

A

• Adherence
• protection from the immune system
• protection from antibiotics
• symbiotic relationships in order to exist long-term
• survival and pH changes, and in a normally inhospitable environment

401
Q

What is the mechanism of dental caries?

A
  1. Toxin production
  2. Post immune response
  3. microbial proliferation and invasion, growth and spread of microbes
  4. Cancer- microbe promotes uncontrolled proliferation of cells and host organism

Fermentable sugar + acid producing bacteria —> low pH —> demineralization

402
Q

What is the common bacteria involved in dental caries?

A

• streptococcus viridans/mutans
• Gram positive cocci catalyst negative, anaerobe, alpha hemolytic, optochin resistant

403
Q

What are the virulence factors of streptococci leading to cavities?

A
  • adhesion like surface associated proteins (AGI/II family) capable of binding to pecille (teeth)
  • extracellular glycosyltransferases (Gtfs) that can synthesize glucans from sucrose creating an acidic environment
404
Q

What is periodontal disease?

A

• Infectious disease destroying supporting structures of teeth (gums)
• milder form: gingivitis
• irritation, redness, swelling of the gums
• severe form: periodontitis, infection of underlying tissue and bones

405
Q

How can you prevent dental caries and periodontal disease?

A

• less sugar in the diet
• brush frequently
• fluoride
• increased saliva flow (consider sugar-free gum)

406
Q

What are the treatments of periodontitis?

A
  • thoroughly clean surfaces to prevent bone damage or further bone damage
  • Root planing to discourage further bacteria growth
  • antibiotics— topical is common, empirical use of amoxicillin and metronidazole
407
Q

What bacteria is associated with severe juvenile periodontal disease?

A

Aggregatibacter actinomycetemcomitans (facultative anaerobe and gram- bacillus)

408
Q

What is a main keystone pathogen in periodontal disease?

A

porphyromonas gingivalis causing a dysbiotic state

409
Q

Microbes that cause caries are usually located in plaques on tooth surfaces, or in crevices between teeth. They are often what?

A

Gram-positive

410
Q

Microbes that cause periodontal disease are due to their destruction primarily below the gumline, in the subgingival space. They are primarily what?

A

Gram-negative

411
Q

Having periodontitis may be associated with:

A

• heart attack
• stroke
• lung disease
• premature birth or having a baby with low birth weight, in women
• diabetes

412
Q

What is the link between periodontal disease and diabetes?

A
  • diabetes can be worse with pro-inflammatory cytokines
  • periodontal disease creates pro-inflammatory cytokines that appear to increase insulin resistance
413
Q

How can periodontal disease lead to subacute bacterial endocarditis (SBE)?

A

break in mucosal barrier, dental manipulations may also be the cause —> Alpha hemolytic streptococci can implant on previously damaged heart valve surfaces and accumulate

414
Q

What is Ludwig’s angina?

A

• skin infection on the floor of the mouth, usually results from untreated dental infections. Swelling of infected area may block the airway or prevent swallowing of saliva
• symptoms: SOB, confusion, fever, neck pain, neck swelling, redness of the neck, weakness/fatigue/tiredness

415
Q

What is a unique physical exam finding in the mouth of someone with Ludwig’s angina?

A

Double tongue appearance

416
Q

Who are the most common individuals to get candidiasis in the mouth, throat, or esophagus?

A

• babies
• denture wearers
• diabetics
• cancer patient
• HIV/aids patient
• currently taking antibiotics or corticosteroids
• dry mouth (medication or otherwise)
• smokers

417
Q

When does Candidasis become dangerous?

A

When it invades the esophagus: life-threatening, highly prone to spreading

418
Q

What is the treatment of candidiasis?

A

• most commonly topical treatment: clotrimazole lozenge or nystatin suspension (swish and swallow)
• unresponsive cases: systemic antifungal such as fluconazole
• worst case: IV administration of amphotericin B

419
Q

What is general leukoplakia?

A

NOT caused by an organism, thought to be caused by smoking and chewing tobacco/other irritants

420
Q

What is the most common association with Hairy leukoplakia?

A

Epstein-Barr virus, almost always in HIV+ patients

421
Q

What does H.pylori look like?

A

Gram-negative, flagellated helix-shaped rod (spirilli), microaerophilic, catalase +, oxidase +, urease +, (triple positive)

422
Q

What can H. pylori lead to?

A

Asymptomatic gastritis —>
1. Symptomatic gastritis
2. Ulcers
3. Carcinoma
4. Lymphoma

423
Q

What are the symptoms of chronic gastritis caused by H. pylori?

A

• inflammation of the gastric mucosa
• burning ache in the upper abdomen. Worse/better with eating
• nausea, vomiting
• feeling a fullness in upper abdomen after eating

424
Q

What are the symptoms of a gastric ulcer?

A
  • open sores that develop on the inside stomach lining
  • burning abdominal pain from naval to breastbone
  • flares at night
  • temporarily relieved by eating foods
  • less common: vomiting/stools that are blood unexplained weight loss, appetite changes
425
Q

What are the major virulence and colonization factors of H.pylori?

A
  • immune evasion
  • urease - acid tolerance
  • motility and chemotaxis
  • VacA- forms poor that allows leakage of calcium from epithelial cell
  • adhesins (BabA and SabA)
  • TFSS + CagA - pokes hole, CagA travels into the wholesale and affects the proliferative actions, adhesion, cytoskeletal organization highly pro-inflammatory
426
Q

How does H. pylori cause a gastric ulcer?

A

Host damages itself by continual, ineffective immune response

427
Q

How can you diagnose H. pylori?

A

• endoscopy and culture
• breath test (second best option considering cost- tests for Urease)
• stool test (best option, Ag test)
• blood test (cannot show resolution of infection, Ab test)

428
Q

What is the triple therapy treatment for H. pylori infection?

A
  1. Clarithromycin
  2. Amoxicillin
  3. Proton pump inhibitor
429
Q

H. Pylori association with different cancers

A
  1. Causes mucosa associated lymphoid tissue lymphoma (MALT)
  2. Causes gastric carcinoma
  3. Reduces risk of esophageal adenocarcinoma
430
Q

What is gastric MALT?

A

• mucosa associated lymphoid tissue lymphoma in the stomach
• symptoms: indigestion, heartburn, inflammation
• tumors of B cells
• antibiotics are still a part of the treatment strategy

431
Q

What is gastric carcinoma?

A
  • cancer of the stomach lining (epithelial ), where 65 to 80% of gastric carcinoma is caused by H. pylori
  • symptoms: indigestion, heartburn, inflammation
432
Q

What is cholecystitis?

A
  • a complication of the obstruction of bile flow due to gallstones migrating into the ducts or bacteria (typhoid bacilli- typhoid fever)
  • most commonly seen in patients who are predisposed to gallstones, or have reduced arterial blood supply to the gallbladder wall
433
Q

What are the symptoms of cholecystitis?

A

Charcot’s Triad
1. right upper quadrant pain, biliary colic
2. Jaundice
3. Chills and a spiking fever

434
Q

What is it called when cholecystitis extends into the liver bile duct?

A

Cholangitis

435
Q

What is the treatment of cholecystitis?

A
  • antibiotic to treat the infection
  • removal of underlying obstruction (stone)
436
Q

What can cause a digoxin (weak base) overdose?

A

Pairing with proton pump inhibitor (omeprazole)

Symptoms: weakness, disequilibrium, nausea/vomiting, altered vision (yellow haze, xanthopsia), atrial fibrillation, bigeminy

437
Q

What are the gastric secretion/hormones of surface mucus cells?

A

• bicarbonate
• mucus
• prostaglandins

438
Q

What are the gastric secretion/hormones of parietal cells?

A

• HCl
• intrinsic factor
• Gastroferrin

439
Q

What are the gastric secretion/hormones of zymogenic/chief cells?

A

• pepsinogen
• lipase

440
Q

What are the gastric secretion/hormones of enteroendocrine cells?

A

• gastrin
• ghrelin
• histamine
• somatostatin

441
Q

How do we control acid secretion in the stomach?

A

• proton pump inhibitors (prazole)
• antacids
• H2 blockers
• Gastrin, acetylcholine, somatostatin

442
Q

What are the primary roles of HCl?

A
  1. Proteolysis, chemical digestion of proteins
  2. prevention of infection, kills pathogens
443
Q

What is Ménétrier disease?

A

• parietal cell atrophy leading to a gradual decrease in acid production (also includes hyperplasia of the goblet cells —> hypertrophied rugae)

444
Q

What is an alkaline tide?

A

The pumping of bicarbonate into the blood after eating a meal (normal unless following vomiting, can result in metabolic alkalosis)

445
Q

What is the difference between omeprazole and esomeprazole?

A

• omeprazole is a racemic mixture of the R-isomer and S-isomer
• esomeprazole is exclusively an S-isomer (this works better in poor metabolizers)

446
Q

What are the side effects of increasing the gastric pH?

A
  1. Increased respiratory/enteric infections including SIBO
  2. Increase/decrease absorption of weak acids and bases
  3. Rebound acid hypersecretion when stopped
447
Q

What is vonoprazan?

A
  • potassium competitive acid blocker(PCAB), reversible inhibitor of the hydrogen-potassium ATPase used to increase stomach pH
  • SE: hepatotoxicity, nasal pharyngitis, mild moderate constipation/diarrhea, diverticulitis
448
Q

What are the antacids?

A

• aluminum hydroxide
• calcium carbonate (Tums)
• magnesium hydroxide
• sodium bicarbonate

449
Q

What are the side effects of aluminum hydroxide?

A

Antacid: can cause constipation, rarely osteomalacia due to decreased phosphate absorption and calcium loss

450
Q

What are the side effects of magnesium hydroxide?

A

Antacid: can cause osmotic diarrhea, in patients with renal insufficiency it can cause hyperglycemia and cardio-toxicity

451
Q

What are the side effects of calcium carbonate and sodium bicarbonate?

A

• systemically absorbed
• metabolic alkalosis, hypercalcemia if taken with dairy products
• gastric distention, belching (can be treated with simethicone)
• alkalinizes urine, can cause fluid retention

452
Q

What are the phases of gastric acid secretion?

A
  1. Cephalic (increase when thinking about food)
  2. Gastric (most produced here)
  3. Intestinal
  4. Interdigestive
453
Q

What does gastrin do?

A

• Secreted by G cells in the atrum, duodenum, pancreas and acts on B receptors only
• increases: acid secretion, histamine (ECL cells), growth, pepsinogen, enzyme secretion in the pancreatic acini, can cause an increase in gastric/pancreatic/colon cancer
• decreases: somatostatin (D cell)

454
Q

What does cholecystokinin do?

A

• secreted by duodenal I cells on both A and B receptors
• increases: somatostatin (D cell), pepsinogen, enzyme secretion from the pancreatic acini, growth, contraction/motility, pancreatic cancer
• decreases: acid secretion

455
Q

What causes the release of histamine from ECL cells?

A

Gastrin or acetylcholine from enteric efferent neurons acting on M1 receptors

456
Q

Prostaglandins antagonize what?

A

The actions of histamine— a.k.a. they inhibit adenylate cyclase

457
Q

What are H2 blockers (cimetidine, famotidine, nizatidine, ranitidine)?

A

• highly selective, competitive H2 antagonist that decrease all forms of gastric acid secretion (especially nocturnal)
• SE: increased gastric pH, bradycardia, hypotension, decreased elimination of certain drugs

458
Q

What is unique about cimetidine?

A

• classic inhibitor of CYP450 (CYP1A1, 2D6, 3A4)
• significantly increases the effectiveness of drugs metabolized by these enzymes

• other potential SE: decreased binding of DHT to androgen receptors, decreased estrogen metabolism, increased prolactin leading to gynecomastia or galactorrhea

459
Q

What does acetylcholine do in the stomach?

A

Acts on the M1 and M3 receptors on ECL cells and M3 receptors on parietal cells —> increases histamine release and increases calcium in parietal cells

460
Q

What is a Cushing ulcer?

A

• and ulcer in the esophagus, stomach, duodenum associated with in increased intracranial pressure
• Cushing triad: hypertension, bradycardia, respiratory depression (Cheyenne Stokes respiration)

461
Q

What is somatostatin?

A

•Paracrine hormone released by D cells when the pH in the Antrum <3
• decreases the release of gastrin, histamine, and inhibits adenylate cyclase in parietal cells

462
Q

When food enters the stomach, pH increases and somatostatin secretion is (increased/decreased)

A

Decreased- inhibited

463
Q

What is the importance of intrinsic factor and Gastroferrin?

A

Intestinal absorption of B12 and iron

464
Q

What binds B12 in the stomach?

A

Haptocorrin (R protein)

465
Q

What is Gastroferrin?

A

Iron binding glycoprotein that allows Fe3+ to be transported to the small intestine for absorption without complexing with anions

466
Q

What cells secrete bicarbonate and mucus?

A

• neck cells and goblet cells
• catecholamines suppress bicarbonate secretion from these cells and can contribute to the formation of stress ulcers

467
Q

How do prostaglandins alter gastric pH?

A

1.) increased bicarbonate secretion
2.) decreased gastric acid production

~ this leads to a higher pH, long-term use of NSAIDs cause ulcers because you block these actions of prostaglandins

468
Q

What is misoprostol (methyl PGE1)?

A
  • a prostaglandin analog that reduces histamine stimulated acid secretion and stimulates mucus and bicarbonate secretion
  • reverses the action of NSAIDs locally in the stomach while allowing them to systemically act at their target sites
  • side effects: diarrhea, severe nausea and cramping, stimulates uterine contractions, teratogen - black box warning
469
Q

What is sucralfate?

A
  • sucrose sulfate- aluminum hydroxide complex that attaches to the basement membrane of an ulcer acting as a Band-Aid.
  • may stimulate mucosal prostaglandin and bicarbonate secretion, but no acid neutralizing properties
  • requires acidic environment to be given (empty stomach, cannot give with PPI)
470
Q

Using bismuth (for protection of ulcer surfaces and anti-microbial activity against H. pylori in the stomach) can lead to what side effects?

A

salicylate toxicity —> vomiting, tinnitus, confusion, hypothermia, respiratory alkalosis, metabolic acidosis

471
Q

What are the four types of gastric motility?

A
  1. Accommodation
  2. Mechanical digestion
  3. Peristalsis
  4. Migrating motor complex
472
Q

Explain accommodation as a gastric motility process

A

• the stomach remains at a relatively constant pressure despite dramatic increases and volume due to VIP/NO containing inhibitory neurons that allow relaxation of stomach muscles

473
Q

What is the Gastroileal reflex?

A

Relaxes ileocecal valve to transfer contents of small bowel into large bowel

474
Q

What is the gastrocolic reflex?

A

Induces the need to defecate after eating

475
Q

Mixing, grinding, receiving as my chemical digestion process (image)

A
476
Q

What is the basal electrical rhythm (BER) in the smooth muscle of the gut?

A
  • the smooth muscle is electrically coupled, leading to the rhythmic depolarization of smooth muscle cells in all regions distal to the esophagus
  • initiated at the interstitial cells of Cajal in the greater curvature of the stomach
477
Q

What conditions cause a decrease in the BER rate, slowing G.I. motility?

A

Hypothermia, hypothyroidism, hypoxia, mesenteric ischemia

478
Q

What is the migrating motor complex?

A

• growling of the stomach, hunger pangs
• cycles of motility during the fasted state lasting around 100 minutes that begin in the stomach and progressed to the large intestine in order to clear indigestible residues from the stomach

479
Q

What are the three phases of the migrating motor complex?

A
  1. Quiescence: 40-60% of cycle, no movement
  2. Irregular contraction similar to peristalsis: 20-30%
  3. Intense contraction: 5-10%, pylorus opens widely leading to the movement of undigested material into the small intestine
480
Q

What is the hormone that induces the motility motor complex?

A

motilin: inhibited with eating

481
Q

What is acute gastritis/acute hemorrhagic gastritis?

A

• acute transient mucosal damage with mucosal edema, erosion, hemorrhage
• caused by imbalance between mucosal defenses and acid (alcohol, NSAIDs, toxins, H. pylori, uremia, radiation, chemotherapy)

482
Q

What is acute gastritis/acute hemorrhagic gastritis?

A

• acute transient mucosal damage with mucosal edema, erosion, hemorrhage
• caused by imbalance between mucosal defenses and acid (alcohol, NSAIDs, toxins, H. pylori, uremia, radiation, chemotherapy)

483
Q

What are the protective mechanisms of the stomach?

A

• mucus surface protection (foveolar cells) and physical barrier to keep acid out of lamina propria
• bicarbonate secretion
• rapid cell turnover

484
Q

Which molecules help the protective mechanisms of the stomach?

A

COX and prostaglandins

485
Q

What is an acute stress related ulcer?

A

An ulcer resulting from acute physiologic (not psychologic) stress, leading to punched out ulcers in the stomach and duodenum

486
Q

What is the most common cause of chronic active gastritis?

A

H. pylori infection. You will see neutrophils in crypts and lamina propria, as well as high lymphocyte presence and reactive germinal centers

487
Q

Where are the most common sites for an H. pylori chronic gastritis?

A

antrum > cardia > fundus/body

~ typically superficial in the mucus surface and neck of the glands

488
Q

What are the long-term risks of an H. pylori infection?

A

• peptic ulcer disease (PUD)
• gastric adenocarcinoma via atrophy intestinal metaplasia-dysplasia
• gastric lymphoma (particularly MALT)

489
Q

What is another bacteria that can cause similar gastritis patterns as H. pylori?

A

Helicobacter heilmannii (vector is cats and dogs)

490
Q

What are the different types of gastritis?

A
  1. Acute (toxins, drugs, ischemia, H. pylori)
  2. Chronic (H. pylori or autoimmune)
  3. Chronic active (flares/inflammation with a background of H. pylori)
  4. Gastropathy (injury with little to no inflammation)
491
Q

In peptic ulcer disease, where are the most common sites of ulcers?

A

• 90% are duodenal ulcers from increased gastric acid secretion from the stomach
• 10% are gastric ulcers caused by H. pylori

492
Q

Pain is (better/worse) with food when you have a duodenal ulcer.

A

Pain is relieved with food due to the release of bicarbonate, and the pressure

493
Q

Pain is (better/worse) when eating with a gastric ulcer

A

Worse— influx of acids directly onto the wound make it painful

494
Q

Based on the area of the ulcer, what artery is a risk?

A

• posterior duodenal wall: gastroduodenal artery hemorrhage
• anterior duodenal wall: pneumoperitoneum
• curvature of the stomach: gastric artery hemorrhage

495
Q

What is the main finding on radiograph of a pneumoperitoneum?

A

Rupture of the anterior wall of the duodenum leads to air escaping into the peritoneum— visible as air under both diaphragms

496
Q

What is gastritis type A?

A

• autoimmune gastritis — typically an antibody of the parietal cells (against H-K ATPase or intrinsic factor)
• affects the fundus/body of the stomach
• leads to hypo/achlorhydria, vitamin B-12 loss, chief cell loss (decreased pepsinogen I levels)

497
Q

What cells are typically seen with autoimmune gastritis?

A

Deep/basal mucosal inflammation with lymphocytes, macrophages, plasma cells

498
Q

What happens to the endocrine cells in autoimmune gastritis?

A

Endocrine cell hyperplasia occurs due to feedback loop of increased gastric secretion in response to the decreasing acid (due to damaged parietal cells)

499
Q

In autoimmune gastritis with intestinal metaplasia, what does the fundus of the stomach typically resemble microscopically?

A

The antrum

500
Q

What is seen in atrophic gastritis?

A

• mucosal and submucosal capillaries/vessels are visible without excessive distention with air
• decrease in rugae folds
• Hyperplastic or adenomatous polyps

501
Q

Autoimmune gastritis can lead to what type of anemia?

A

Pernicious anemia/vitamin B12 deficiency —> megaloblastic anemia, atrophic glossitis, malabsorptive diarrhea, peripheral neuropathy, CNS alterations

502
Q

What is reactive gastropathy?

A

• typically due to chronic NSAID use or bile reflux, mucin loss of surface cells which can lead to gastric erosions and ulceration
• lacks inflammation
• characterized by foveolar hyperplasia and mucin depletion

503
Q

What is the cause of pyloric stenosis?

A

congenital: present 2-6 wks post birth, projectile vomiting of non-bilious fluid, firm “olive” on palpation of the epigastric region

adults acquired: results from gastritis/ulcers/masses impinging the area

504
Q

What is the most common extranodal site for lymphoma?

A

The stomach— MALT lymphoma, DLBCL

505
Q

What is seen on flow cytometry for MALT lymphoma?

A

• B cell +: CD19, CD 20, monoclonal light chain (Kappa OR lambda- not both)
• CD5 negative, positive for CD43 in 25%

506
Q

What are the two patterns of MALT lymphoma in the stomach, most related to H. pylori?

A

1. Negative for translocation, associated with H. pylori infection and chronic antigenic stimulation that activates transcription factors promoting B cell growth and survival

2. Positive for translocation t(11;18), involving the MALT1 gene on chromosome 18 and API2 gene on 11

507
Q

75% of gastric polyps are of what type?

A

Hyperplastic gastric polyps: non-neoplastic associated with chronic gastritis and H. pylori. Inflammatory and reactive/hyperplastic. foveolar hyperplasia

508
Q

What are fundic gland polyps?

A

• sporadic or caused by familial adenomatous polyposis (FAP), typically associated with overuse of PPIs—> increase gastrin secretion
• occurs in the body/fundus

509
Q

What do fundic gland polyps look like microscopically?

A

Dilated, irregular glands lined by flattened parietal and chief cells and foveolar cells due to too much NSAID use

510
Q

What are the risk factors for gastric adenoma?

A

• FAP
• chronic atrophic gastritis
• intestinal metaplasia

511
Q

What do gastric adenomas look like microscopically?

A

• cells with nuclear stratification, hyperchromatic pencil-shaped nuclei, and mucin depletion
• adenoarcinoma may be present in up to 30% of gastric adenomas

512
Q

What is Zollinger-Ellison syndrome?

A
  • gastrinoma: Gastrin secreting tumor, neuroendocrine
  • results in marked increase in parietal cells and mucus neck cells (hypertrophic mucosa)
  • causes intractable ulcers in the stomach, duodenum, esophagus
  • associated with MEN1 syndrome in 25% of cases
513
Q

What is Menetrier’s disease?

A
  • excessive secretion of TGF – alpha
  • diffuse foveolar hyperplasia of the body and fundus with excess mucus
  • protein losing enteropathy and hypoproteinemia with diarrhea, weight loss, peripheral edema
  • can be associated with CMV in children
514
Q

Adenocarcinoma of the stomach: intestinal type

A

• found in the antrum
• gland/solid nest forming bulky mass lesion/ulcer arising from precursor dysplasia

515
Q

Adenocarcinoma of the stomach: diffuse type

A

• signet ring/linitis plastica cells
• presents with thickened gastric wall and single signet ring cells, discohesive infiltration
• seen in young patients

516
Q

What is the pathophysiology of an intestinal type of gastric adenocarcinoma?

A
  • mutations increasing the signaling via WNT pathway
  • APC tumor suppressor gene
  • Beta-catenin overexpression
517
Q

What is the pathology of diffuse gastric adenocarcinoma?

A

• loss of function of tumor suppressor genes CDH1 encoding E-cadherin
• can be seen in familial CDH1 in very young patients

518
Q

What is a gastrointestinal stromal tumor (GIST)?

A

• spindle cell tumor that arises from the cells of Cajal (pacemaker or mesenchymal cells)
• most common mesenchymal tumor of the G.I. tract
• most commonly occur in the stomach, leading to mass effect (bleeding from ulcerative mucosa)

519
Q

What mutations are seen in GIST and what is the treatment?

A

• cKIT, CD117 (75%)
• PDGFRA (8%)

~ Tx: tyrosine kinase inhibitor: imantimib

520
Q

What are the causes of ascites?

A

• cirrhosis (most common)
• cancer
• heart failure
• tuberculosis
• renal failure that requires dialysis
• pancreatic diseases

521
Q

What are the diagnostic tests that are typically performed on ascitic fluid?

A

• CBC with diff
• culture, gram stain
• albumin, total protein (determine between exudate vs transudate
• fluid cytology

522
Q

Ascites fluid appearance and interpretation (graph/image)

A
523
Q

if ascites fluid is transudate, then the likely etiology is:

A

• liver cirrhosis
• congestive heart failure
• hypoalbuminemia
• massive liver metastasis

524
Q

If ascites fluid is exudative, then the likely etiology is:

A

• malignant
• tuberculosis peritonitis
• pancreatic

525
Q

What is peritonitis?

A

1. Infection from perforation (ulcer, diverticulum, tumor)
2. Spontaneous bacterial peritonitis (unknown, neutrophil common, culture and Gram stain required)

526
Q

What is the number one incidence of cysts/neoplasm in the peritoneal cavity?

A

Secondary metastatic tumors, typically from the ovaries

527
Q

What are the cysts of the peritoneal cavity?

A

• mesothelial inclusion cysts related to inflammation
• multicystic benign mesothelioma

528
Q

Primary malignant mesothelioma results in what?

A

• Similar to pleural tumors, associated with asbestos exposure
• papillary formations and desmoplastic stromal reaction (hypereosinophilic)
• immunoreactivity for calretinin

529
Q

What is a sister Mary Joseph nodule?

A

• palpable nodule bulging into the umbilicus as a result of intra-abdominal malignancy (stage 4 cancer staging)

530
Q

What is hematochezia?

A

Bright red blood coming from the rectum (bad prognostic sign, indicates blood is flowing very quickly)

531
Q

What is melena?

A

Black tarry stools coming from an upper G.I. bleed

532
Q

What is the appearance of hematemesis?

A

Vomit that is the appearance of coffee grounds due to blood coagulation with HCl in the stomach

533
Q

What are the obscure (indirect) signs of a G.I. bleed?

A

• iron deficiency anemia
• fatigue/paleness
• dyspnea
• angina

534
Q

What are the three most important things on initial assessment and resuscitation for an upper G.I. bleeding patient?

A
  1. ABCs: airway, breathing, circulation/CPR
  2. IV access: at least two large bore IVs
  3. Infusion of crystalloids (LR, NS) and blood products
535
Q

What are underlying patient conditions that can influence the treatment of an upper G.I. bleed?

A

• severe cardiac disease (cannot take large volume infusion)
• liver disease (varocele bleeds, hard to treat)
• coagulopathy (high INR, may need vitamin K or FFPs)

536
Q

What is the diagnostic test of choice for upper G.I. bleeds?

A

• EGD, a chip on a long flexible tube allowing for the insertion of epinephrine, cautery, and hemoclips in areas that are bleeding

537
Q

What are other diagnostic tests for upper G.I. bleeds if EGD is not available/does not work?

A

• barium study
• tagged RBC scan (radio labeled blood)
• capsule endoscopy

538
Q

What are the common causes of esophageal bleeding?

A

• esophageal varices
• esophagitis
• Malory Weiss tears
• tumors

539
Q

Explain esophageal varices as an upper G.I. bleed mechanism

A

• presents with dramatic bleeding, usually hematemesis
• typically caused by portal hypertension and associated with liver disease/cirrhosis
• Tx: octreotide/vasopresin to decrease liver pressure, PPI, beta blocker, variceal band ligation, or surgically shunting (TIPS)

540
Q

What is the Malory Weiss tear typically occur?

A

Located at the Gastro-esophageal junction, typically caused by aggressive vomiting

541
Q

What’s the difference between a peptic ulcer versus erosion?

A

Ulcer: break in mucosa with a appreciable depth or involvement with the submucosa

Erosion: break in mucosa without significant depth

542
Q

What two processes have a synergistic effect of causing peptic ulcer disease?

A

H. pylori and NSAID use

543
Q

What are the risk factors for peptic ulcer disease?

A

• NSAIDs
• H.pylori, family history of ulcers/infection
• cigarette smoking
• physiological stress

544
Q

Rifabutin

A
  • antibiotic used for H. pylori infections that inhibits DNA dependent RNA polymerase
  • actively secreted into stomach lumen, active over wide range of pH
  • side effects: myelosuppression, hepatotoxicity, CYP450 induction, orange/red stained body fluids
545
Q

H2 blockers are best at decreasing the spike of acidity during what time period?

A

Nocturnal— good for patients that experience GERD at night

546
Q

How is GERD treated in pregnancy?

A
  • lifestyle modification
  • drugs that are not normally systemically absorbed (aluminum hydroxide, magnesium hydroxide, calcium carbonate, sucralfate)
  • H2 blockers (risk)
  • PPI/PCAB (riskier)
547
Q

Drugs you need to know (graph/picture)

A

• eradication of H. pylori drugs
• promotion of mucosal defense drugs
• antacids
• H2 blockers
• proton pump inhibitors

548
Q

Name the cells seen in each layer of the stomach (lumen—>base of gastric unit) picture/image

A
549
Q

Name the cells seen in each layer of the stomach (lumen—>base of gastric unit)

A
550
Q

What is the difference between a foveolar cell and a neck/mucus cell?

A

Foveolar: secrete mucin and line the. Surfaces of the stomach and the gastric

Neck: located inside the gastric pits

GI (3 decks)

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