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DEMS_BTRAN > UNIT1_Anatomy&Physiology > Flashcards

UNIT1_Anatomy&Physiology Flashcards

1
Q

Mucous neck cells: ?

A

Mucous neck cells: Mucus-secreting eosinophilic cells

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2
Q

Parietal (oxyntic) cells: ?

A

Parietal (oxyntic) cells: Larger eosinophilic cells that secrete hydrochloric acid (HCl) and intrinsic factor (IF)

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3
Q

Larger eosinophilic cells that secrete hydrochloric acid (HCl) and intrinsic factor (IF) –> ?

A

Parietal (oxyntic) cells:

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4
Q

Endocrine cells:?

A

Endocrine cells: Modulate gastric secretions

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5
Q

__________ cells: Modulate gastric secretions

A

Endocrine cells:

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6
Q

Enterochromaffin-like (ECL) cells: ?

A

Enterochromaffin-like (ECL) cells: Release histamine in response to gastrin produced by G cells. Histamine increases gastric acid secretion.

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7
Q

________________ cells: Release histamine in response to gastrin produced by G cells. Histamine increases gastric acid secretion.

A

Enterochromaffin-like (ECL) cells:

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8
Q

Chief (zymogen) cells: ?

A

Chief (zymogen) cells: Smaller basophilic cells that secrete pepsinogen

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9
Q

_______________ cells: Smaller basophilic cells that secrete pepsinogen

A

Chief (zymogen) cells:

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10
Q

The principal pathological abnormalities of the GI tract consist of what?

A

smooth muscle atrophy and gut wall fibrosis

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11
Q

What is Scleroderma/PSS? and what is the predominate process?

A

Scleroderm/PSS = smooth muscle atroophy & gut wall fibrosis.

Myopathic process

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12
Q

What do the following maniiifestiaton of scleroderm/PPS lead to?

Smooth Muscle Atrophy –> ?

Smooth Muscle Atrophy –> ?

Unrepentant GERD –> ?

A

Smooth Muscle Atrophy –> Weak Peristalsis –> Dyspahgia.

Smooth Muscle Atrophy –> Weak LES –> GERD.

Unrepentant GERD –> Esophagitis –> Stricture

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13
Q

How do you dX Esophageal disease?

A

Esophageal manometry

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14
Q

Is Peristalsis preserved in spastic disoders of the esophagus?

A

Yes!

Sx are usually chest pain and dysphagia

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15
Q

What class of GI diz has a Pathophysiology related to overactivity of excitatory nerves, an impairment of inhibitory innervation or overreactivity of the smooth muscle response.

A

Spastic Disorders of the Esophagus

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16
Q

Physiology of gastric emptying:

Receptive relaxation is mediated by: ?

Liquid emptying is mediated by: ?

Solid emptying is mediated by: ?

Residual solids is mediated by: ?

A

_ Receptive relaxation = swallowing-induced vagal response (vagally mediated inhibition of body tone)

  • Liquid emptying by tonic pressure gradient
  • Solid emptying by vagally-mediated contractions
  • Residual solids emptied during non-fed state by MMC every 90-120 minutes
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17
Q

Describe the gastric reservoir function of accommodation:

A
  • Smooth muscle relaxation elicited by mechanical distention of the stomach (Gastric mechanoreceptors).
  • Vagovagal response
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18
Q

__________ = stomach paralysis. impaired transit of food from the stomach to the duodenum. NOT a mechanical obstruction.

A

Gastroparesis:

Cx ppt:

Nausea
Vomiting
Early satiety
Postprandial abdominal distention
Postprandial abdominal pain
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19
Q

Etiology of Gastroparesis?

A
  • Idiopathic (? Post-infectious)
  • Post-surgical (vagal nerve injury)
    Gastric
    Esophageal
    Thoracic surgical procedures: Lung Transplant
  • Diabetic
  • Medication-related (opiates)
- Others
Paraneoplastic
Rheumatologic
Neurologic
Myopathic (Scleroderma!)
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20
Q

How do you Dx Gastroparesis?

A
  • Gastric emptying study
    Gastric scintigraphy
    Low fat EggBeaters radiolabelled with 1 mCi Technetium 99.
    Microwaved and served with toast, jam and water.

Abnormal: retention >60% at 2 hr or >10% at 4 hr.

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21
Q

How do you Tx Gastroparesis?

A
  • Lifestyle and dietary measures
    Small & frequent meals
    Low-fat & low-residue diet
    Glucose control in diabetics
  • Medications
    Prokinetic agents
    Antiemetics
  • Gastric electric stimulation
  • Surgery (~2%)
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22
Q

Describe the difference between Neuropathic and Myopathic small bowel motility disorders.

A
  • Neuropathic:
    Normal amp but sustain burst of uncoordinated phasic contractions.
    Early return of MMC.
    Increased frew. of MMC
  • Myopathic
    Decreased amp of contractions of complete lack of any motor activity.

Some bowel diz. have both!

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23
Q

What diz is a Major Manifestation of Small Intestinal Dysmotility?

A

Chronic Intestinal Psuedo-Obstruction (CIPO):

  • Signs and symptoms of mechanical obstruction of the small bowel without a lesion obstructing flow of intestinal contents.
  • Characterized by the presence of dilation of the bowel on imaging
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24
Q

What is a complication of CIPO?

A

Small Intestinal Bacterial Overgrowth a complication of CIPO: Stasis –> bacterial overgrowth –> fermentation and malabsorption.

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25
Q

What are the Etiologies of Small Intestinal Motility Disorders (and CIPO)?

A
  • Neuropathic
    Degenerative Neuropathies (eg Parkinon’s).
    Paraneoplastic Autoimmune (anti-Hu Ab).
    Chagas Disease: parasite Trypanosoma cruzi.
    Diabetes associated (neuropathy).
  • Mixed Myopathic and Neuopathic
    Infiltrative Conditions.
    Scleroderma, Amyloidosis, Eosinophilic Gastroenteritis.
    Idiopathic.
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26
Q

How does peds form of CIPO differ from the adult form?

A

In children:

Mostly congenital
Mostly primary condition (visceral neuropathy/myopathy)
Absent MMC predicts need for IV nutrition.

1/3 infants dies in 1st year

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27
Q

Causes of constipation:

A

Drugs
Mechanical
Metabolic: DM, hypoK, hyperCa, hypoMg, hypothyroid
Myopathy: Amyloid, Scleroderma
Neurogenic: Parkinson’s, spinal cord injury, MS, autonomic neuropathy, Hirschsprung’s
Other: pregnancy, immobility
IBS-C
Normal transit, slow transit, dyssynergic defecation

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28
Q

what test can be used to eval incontinence and constipation?

A

Anal Manometry

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29
Q

Inability to coordinate the abdominal, rectoanal and pelvic floor muscles during defecation is known as?

A

Pelvic Floor Dysfunction

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30
Q

What does an abnormal anorectal manometry reveal in Dyssynergia?

A

Reveals: Paradoxical contraction of the pelvic floor and external anal sphincters.

Tx: biofeedback therapy

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31
Q

Important normal GI motility patterns altered in disease are:

Small Bowel Peristalsis: ?

Colonic transit: ?

Sphincter dysfunction: ?

A

Small Bowel Peristalsis: CIPO (Scleroderma).

Colonic transit: Slow transit constipation (Scleroderma)

Sphincter dysfunction: Hirschsprung’s, Dysynergic defecation

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32
Q

important normal GI motility patterns altered in disease are:

Esophageal peristalsis: ?

LES relaxation: ?

LES tonic contraction: ?

Gastric emptying: ?

A

Esophageal peristalsis: Achalasia, Scleroderma.

LES relaxation: Achalasia.

LES tonic contraction: Scleroderma.

Gastric emptying: Gastroparesis, Functional dyspepsia.

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33
Q

What are the 3 stages of swallowing?

A

Stage 1: Voluntary (oral cavity then bolus pushed by tongue to oropharynx)

Stage 2: Involuntary (glottis covers trachea; UES relaxes)

Stage 3: Involuntary (esophageal peristalsis)

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34
Q

Inappropriate ____ relaxation can cause acid reflux and damage to the inner lining of the esophagus

A

LES: Lower Esophageal Sphincter

Failure to relax due to damage/loss of the enteric nerves of the LES wall is called achalasia and can make swallowing difficult

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35
Q

What are the steps involved in Emesis and how is it regulated?

A
  1. Salivation (HCO3-) & sensation of nausea.
  2. Reverse peristalsis from upper small intestine to stomach.
  3. Abdominal muscles contract & UES and LES relax.
  4. Gastric contents are ejected.

Centrally regulated by vomit center in the brain.

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36
Q

T/F?

The small intestine only has peristalsis movement.

A

FALSE!

Small intestine has BOTH peristaltic and segmentation motility

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37
Q

____________ - stomach activity stimulates movement of chyme through the ileocecal sphincter

____________ – food in stomach stimulates mass movement in colon

A

Gastroileal reflex - stomach activity stimulates movement of chyme through the ileocecal sphincter

Gastrocolic reflex – food in stomach stimulates mass movement in colon

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38
Q

Gastroileal reflex - ?

A

Gastroileal reflex - stomach activity stimulates movement of chyme through the ileocecal sphincter

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39
Q

Gastrocolic reflex – ?

A

Gastrocolic reflex – food in stomach stimulates mass movement in colon

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40
Q

What are intestinal reflexed mediated by?

A

Mediated by both ENS & external innervation.

enteric nerves = Localized peristaltic waves and segmentation mixing

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41
Q

What is the MMC?

A

Occurs in the absence of feeding (during fasting) – Housekeeping!

Occurs every 90-100 minutes with 3 phases starting from the stomach & propagating aborally to ileocecal valve. The hormone Motilin appears to initiate but appears to have a neural component as well.

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42
Q

What are the steps in the MMC?

A

Phase I
Quiescence occurs for 40-60% of the 90 min duration

Phase II
Motility increases but contractions are irregular
Fails to propel luminal content
Lasts 20-30% of MMC duration

Phase IIII
5-10 minutes of intense contractions
From body of stomach to pylorus to duodenum to ileocecal valve
Pylorus fully opens

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43
Q

What are the two types of motility in the Colon?

A

haustration & mass movement

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44
Q

Are there MMC in the colon?

A

NO!!!

Only haustration & mass movement

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45
Q

What are mass movements in the colon?

A

strong peristaltic waves 1-3 X/day.

Mass movement is a wave of contraction that usually follows a meal and that moves content over larger distance than with regular peristalsis; colon remains contracted for a while

Overall movement is slow (max 5-10 cm/hr)

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46
Q

In the mucosal defenses of the stomach, ___________ between cells prevent acid from infiltrating the layers of the wall

A

Tight junctions

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47
Q

Mucus layer and _____1_____ layer at the cell surface (surface mucus cells) protects the stomach lining – _____2_____ can increase mucus production

A
  1. alkaline (HCO3-)
  2. prostaglandins
    * Rapid cell turnover maintains surface integrity.
48
Q

Describe Intrinsic Factor & Vit B12 Absorption:

A
  • Dietary proteins contain Vitamin B12 (cobalamin) – important for RBC production.
  • B12 binds salivary R protein in stomach.
  • Pancreatic proteases remove R protein in duodenum.
  • IF from stomach then binds B12 in duodenum.
  • IF/B12 complex binds to receptor in terminal ileum for absorption (the receptor is for IF)
49
Q

What are the phases of of HCl Secretion during acid secretion in the stomach? (4)

A
  1. Interdigestive phase
  2. Cephalic phase
  3. Gastric phase
  4. Intestine phase
50
Q

Describe the following phases of HCl Secretion during acid secretion in the stomach.

Interdigestive (basal) phase.

A

Interdigestive (basal) phase – between meals following circadian rhythm (highest in the evening and lowest in the morning prior to waking

51
Q

Which phases of HCl secretion follows the circadian rhythm?

A

Interdigestive (basal) phase

52
Q

Describe the following phases of HCl Secretion during acid secretion in the stomach.

Cephalic phase

A

mostly neural regulation

53
Q

Describe the following phases of HCl Secretion during acid secretion in the stomach.

Gastric phase

A

initially neural reg. followed by endocrine (gastrin) and then neural reg.

Neuro –> endo –> neuro

54
Q

Describe the following phases of HCl Secretion during acid secretion in the stomach.

intestinal phase

A

mostly endocrine reg.

55
Q

Chloride Secretion in the Small Intestine are down via what?

A

Cells in the Crypts (villi)

56
Q

What is DIGESTION vs. ABSORPTION?

A

Digestion is the process of breaking down food into an absorbable form.

Absorption is the process by which molecules of food are transported across the enterocyte membrane (transcellular/cellular) or between cells (paracellular) and into the blood or lymph.

57
Q

dietary sugars like sucrose & lactose can be digested where?

A

at the surface of the enterocyte

58
Q

T/F?

Only simple monomeric sugars can be absorbed!

A

TRUE!

Only simple monomeric sugars can be absorbed!

59
Q

The final step in carbohydrate digestion occurs at the ____________ for all dietary carbohydrates:

A

enterocyte surface

60
Q

Enterocyte Surface Enzymes that Covert Small Polysaccharides to Sugar Monomers:

  • Isomaltase (alpha-dextrinase) – ?
  • Maltase – ?
  • Lactase – ?
  • Sucrase – ?
  • Trehalase – ?
A
  • Isomaltase (alpha-dextrinase) – converts alpha-limit dextrins to glucose
  • Maltase – converts maltose and maltotriose to glucose
  • Lactase – converts lactose to glucose and galactose
  • Sucrase – converts sucrose to glucose and fructose
  • Trehalase – converts trehalose to glucose
61
Q

What is the cause of lactose intolerance and what are the Sx?

A
  • Missing the brush border enzyme, lactase
  • Causes gas and diarrhea due to colonic bacterial digestion of lactose
  • Areas where dairy is not part of the staple (Asia) have a higher prevalence
62
Q

There are the enzymes contained in the Entrocytes?

A

Glycocalyx

63
Q

What is the ion needed for SGLT-1 co-transport?

A

Na+

64
Q

Transports _______ & _______ across the apical membrane of the enterocyte

A

glucose & galactose

65
Q

Transports glucose & galactose across the ________ membrane of the enterocyte

A

apical

66
Q

Fructose transport across the apical surface via _______ is sodium-independent

A

GLUT 5

67
Q

__________ transport across the apical surface via GLUT 5 is sodium-independent

A

Fructose

68
Q

What transporter can operate in the setting of secretory diarrhea (increased cAMP/cholera) so is important in oral rehydration?

A

SGLT-1

69
Q

Where do protein digestion occur? (4)

A

Stomach: Pepsin breaks down about 15% of proteins to small peptides

Small Intestine (lumen): Pancreatic proteases like trypsin, chymotrypsin, carboxypeptidase & elastase break down proteins to oligopeptides, di/tri-peptides and amino acids

Brush Border: Peptidases break down oligopeptides into amino acids, dipeptides, tripeptides

Intracellular peptidases: Peptidases in the enterocyte can break down di/tri-peptides into amino acids

70
Q

What happens in the Brush border in terms of protein digestion?

A

Brush Border: Peptidases break down oligopeptides into amino acids, dipeptides, tripeptides

71
Q

What are the pathways of protein uptake? (4)

A
  1. Sodium dependent co-transporters that utilize the N+/K+ ATPase gradient are the major route for the different classes of amino acids. Water follows.
  2. Sodium independent transporters of amino acids
  3. Specific carriers for small peptides (di- and tri-) linked to H+ uptake (co-transporter; example is PEP T1)
  4. Pinocytosis of small peptides by enterocytes (infants)
72
Q

What are the most abundant fat in our diet?

A

Triglycerides

Fats, in total, provide 30-40% of our caloric intake

73
Q

The body can make most lipids EXCEPT: ?

A

linoleic (an omega 6 fatty acid) acid converted to arachidonic acid and alpha-linolenic (omega-3)acid “essential fatty acids”

74
Q

Primary bile acids are produced in the liver from what?

A

cholesterol – cholic acid & chenodeoxycholic acid

75
Q

Secondary bile acids are formed by ?

A

bacteria in the intestines & colon

76
Q

What are bile salts made of?

A

Bile acids are complexed with glycine or taurine to make bile salts

77
Q

Bile is recycled during a meal by uptake in the distal ileum – This is called what?

A

enterohepatic circulation

78
Q

After the stomach, the small intestinal contents become __1__-osmotic with respect to the blood.

Water and ions can move _____2_____ and/or _____3_____, depending on location

A
  1. iso-osmotic
  2. paracellularly
  3. transcellularly
79
Q

There is a net fluid ____1____ from cells in the intestinal crypts and a net fluid ____2 ____ from enterocytes on the villi.

A
  1. secretion
  2. absorption

Villi surface area > crypt surface area

80
Q

Which is larger? Villi surface area or crypt surface area?

A

Villi surface area is LARGER!

81
Q

Discribe Sodium absorption:

Where is it absorbed the most?

What is the Mechanism?

A
  • Absorbed all along the intestine, with most absorption in the jejunum (60-80%).
  • Dependent on a gradient established by the Na+/K+ ATPase.
  • Water absorption is critically linked to Na+ absorption.
  • Mechanism is via Na+/glucose & galactose or Na+/amino acid cotransport, NaCl cotransport, Na+/H+ exchange or passive diffusion
82
Q

How is chloride absorbed?

A
  • Passive in the proximal intestine. (loose Tight Junctions here); offsets Na+ charge of the intercellular space.
  • In distal ileum & colon, (TJ are not leaky here); Cl- exchanged for HCO3-. this offsets acdis produced by bacteria (via bacterial CA)
83
Q

How is Potassium Absorbed?

A
  • Passively!
  • Paracellular movement in Jejunum (due to low concentration of K+ in the intercellular space from the N+/K+ ATPase).
  • BUT TRANSCELLULAR in colon.
  • K+ normally high in cells due to Na+/K+ ATPase. A gradient is established as luminal water decrease on approach to the colon, with passive flux of K+ into the cells.
84
Q

Severe diarrhea can cause significant loss of what ion and can lead to what?

A

K+ and hypokalemia

85
Q

What is Ca2+ and Mg2+ absorbed?

A
  • Ca++ and Mg++ compete for uptake by the cells. (both use same mechanism of absorption).
  • Ca++ enters enterocyte passively down its electrochemical gradient in proximal intestines.
  • Uptake of Ca++ in intracellular calcium stores maintains the gradient.
  • Ca++ ATPase pumps calcium out to the blood.
86
Q

Role of Vitamin D in Calcium Absorption:

A

Vit D stimulates the uptake of calcium by increasing Ca++ binding proteins and Ca++ ATPase molecules.

87
Q

Where is Vitamin D synthesized?

A

Vit D is synthesized in the skin or absorbed by intestine

88
Q

What happens to Vit.D in the liver and in the kidney?

A

Liver: Vit.D is 25-hydroxylated (25-OH)

Kidney: 25-OH is then 1-hydroxylated in presence of PTH.

89
Q

Describe Iron absorption:

A
  • Regulated absorption in the proximal intestines
  • Transported across apical membrane as either heme or Fe++ (receptor mediated)
  • Two possible fates:
    1. binds to apoferritin to form ferritin that stays in the cell and is lost when the cell dies
    2. binds to transferrin (carrier protein), leaves the cell and goes into the blood
90
Q

Where in the GI has the lowest paracellular permeability to water?

A

The colon; because it’s trying to solidify waste and it needs to link water movement to transcellular ion movement

91
Q

Paracellular water permeability __________ from proximal to distal in the small intestines

A

decreases

92
Q

What is the cause of Osmotic diarrhea?

A

caused by impaired digestion or defects in absorption.

  • Lactase deficiency .
  • Ileal resection – bile salts not absorbed.
  • Celiac disease (Sprue) with gluten sensitivity (gliaden-induced destruction of villi).
93
Q

What type of diarrhea may be caused by Vibrio cholerae. Increases cAMP levels in cells and this in turn activates the CF chloride channel, (and thus water) on the luminal surface

A

Secretory diarrhea

94
Q

What is Oral rehydration therapy?

A

ABX + KHCO3!

Works to prevent hypokalemia and metabolic acidosis, glucose (or amino acids) with NaCl to facilitate the absorption of electrolytes and water

95
Q

How many layers does the stomach’s muscularis externa have?

A

3 layers!:

  1. inner oblique
  2. middle circular
  3. outer longitudinal
96
Q

What are plicae circulares and what do they function in and where are they located?

A

plicae circulares are loc. in the small intestine.

plicae circulares slow movement of food in the s. intestine and also provide increased absorptive surface area.

97
Q

The duodenal submucosa contains specialized _____ glands that produce alkaline secretions to neutralize chyme/gastric acid from stomach

A

Brunner’s

98
Q

The duodenal submucosa contains specialized Brunner’s glands that produce what?

A

Brunner’s Glands produce alkaline secretions to neutralize chyme/gastric acid from stomach

99
Q

The __________________ controls secretions from the Ampulla of Vater into duodenum

A

Sphincter of Oddi

The sphincter controls the rate at which bile and pancreatic secretions are excreted into the duodenum.

100
Q

In the s. intestine, what do villi consist of? (3)

A
  1. Enterocytes, which are covered by microvilli that create a brush border to absorb nutrients.
  2. Goblet cells, which secrete mucus.
  3. Enteroendocrine cells, which regulate digestion.
101
Q

In the base of villi are crypts that contain Paneth cells. What are Paneth cells?

A

Secrete lysozyme, antimicrobial products (notably defensins), and immunomodulatory factors. Together, these secretions make up the mucosal defense.

102
Q

What two cells can you find in the crypts of the s. intestine?

A

Paneth Cells & Undifferentiated cells: Stem cells which differentiate to renew intestinal mucosa by migrating towards the tip of the villus.

103
Q

Does the ileum have short villi and smaller and plicae circularis?

A

No!

The ileum has short villi and smaller or absent plicae circularis.

104
Q

he ileum is the location of _______________, which are not found in the duodenum or the jejunum

A

Peyer’s patches (aggregated lymphoid nodules),

105
Q

The ileum is supplied by what artery?

Venous blood from the ileum first drains into ileal veins which are tributary to the superior mesenteric vein and then drains into the portal vein.

A

ileal arteries which are branches of the superior mesenteric artery.

106
Q

What is a secondary retroperitoneal structure?

A

econdarily retroperitoneal refers to structures that were originally suspended in a mesentery and later migrated posterior to the peritoneum during embryogenesis.

107
Q

The abdominal aorta and inferior vena cava are retroperitoneal or intraperitoneal?

A

The abdominal aorta and inferior vena cava are retroperitoneal

108
Q

The portal veins and hepatic arteries drain to the central veins through hepatic sinusoids. Hepatic sinusoids are made up of? (3)

A
  • Endothelial cells
  • Kupffer Cells
  • Stellate Cells
109
Q

_________ cells store lipid soluble vitamins (most notably Vitamin A) and fat. They secrete extracellular matrix components and contract, causing hepatic fibrosis in cirrhosis.

A

Stellate (Ito) cells

110
Q

Which zone of hepatic acinus is poorly oxygenated and is most sensitive to ischemia and metabolic toxins?

A

Zone 3 is poorly oxygenated and is the:

  • First site affected by ischemia
  • Most sensitive to metabolic toxins
  • Site of alcoholic hepatitis
  • Site of detoxification (location of the highest concentration of cytochrome P450 enzymes)
  • Glycolysis
  • Lipogenesis
111
Q

What is the purpose of the discontinuous sinusoidal capillaries in the liver?

A

The purpose of the discontinuous sinusoidal capillaries in the liver is to allow for maximal diffusion of nutrients, toxins, and metabolic products from plasma into hepatocytes and vice versa. These endothelial cells lack a basement membrane.

112
Q

What is the route that bile takes to be transported out of the liver?

A

Bile manufactured in hepatocytes flows along bile canaliculi, opposite to the flow of blood, into bile ducts. Bile ducts combine to form the right and left hepatic ducts of the right and left lobes of the liver, which feed into the biliary tree.

113
Q

Hepatotoxicity induced by viral hepatitis and cocaine first affects which zone of the liver

A

zone 1 (periportal zone)

114
Q

What are the func. of the liver? (7)

A
  • Detoxification and drug metabolism.
  • Production and secretion of bile
  • Glycogen storage
  • Triglyceride production and storage
  • Synthesis of certain plasma proteins (i.e. albumin and globulin), coagulants (i.e. fibrinogen and prothrombin), anticoagulations (i.e. heparin), and bile pigments (bilirubin and biliverdin)
  • Vitamin and other nutrient storage (i.e. iron and copper)
  • Fetal hematopoiesis
115
Q

Zone 1, of a hepatic acinus, is closest to the portal triad, highly oxygenated, and carries out processes most dependent upon oxygen such as: ? (3)

A
  • Gluconeogenesis
  • Beta-oxidation of fatty acids
  • Cholesterol synthesis

DEMS_BTRAN (8 decks)

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