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Physiology GI > Clinical > Flashcards

Clinical Flashcards

1
Q

Zollinger-Ellison Syndrome

A

gastrinomas = tumors producing excessive amounts of gastrin…stimulant for gastric parietal cells to secrete HCL

tumors outside the stomach –> do not have negative feedback loop so will stimulate overwhelming amounts of acid –> chronic ulcers that are too much for defense systems

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2
Q

Barrett’s esophagus

A

injured squamous epithelium is replaced with ‘specialized columnar’ epithelium

more acidic resistant…but risk of becoming an esophageal adenocarcinoma

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3
Q

gastroesophageal reflux

A

recurrent heart burn symptoms

indicates the esophageal epithelium is being exposed to and damaged by refluxed gastric acid

major mechanism = abnormal in neuromuscular function of the LES….particularly frequent transient LES relaxation

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4
Q

long term complications of gastroesophageal reflux –> dysphagia

A
  1. development of stricture
  2. damage to neuromuscular apparatus –> impaired esophageal peristalsis
  3. esophageal adenocarcinoma (BE)
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5
Q

Hirschsprung’s disease

A

constipation

defecation reflex is missing

reasons that this could happen
1. anti-Ach medication –> inhibits intestinal neurally mediated perstaltic movements

  1. narcotic meds –> inhibits contraction of intestinal SmM directly
  2. sedentary lifestyle –> inhibits extrinsic stimulation of intestinal muscle contraction
  3. low fiber diet –> limits formation of fecal residue buld which limits rectal distention
  4. conscious inhibition of relaxation of external anal sphincter
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6
Q

xerostomia

A

dry mouth

occurs largely by a reduction in salivary secretion in the mouth…or by drying out of these secretions faster than they can be produced

conditions that can cause dry mouth

  1. sjogren’s syndrome
  2. mouth breathing/dehumidified air
  3. medications - anti-Ach (bentyl) or tricyclic antidepressants (elavil)
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7
Q

consequences of xerostomia

A
  1. poor oral cleansing of food particles –> bacterial proliferation (halitosis, caries, gingivitis)
  2. poor lubrication - difficult mastication adn swalloing (dysphagia)
  3. poor acid buffering
    mout = caries, gingivitis
    esophagus = heartburn, esophagitis
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8
Q

Sjorgren’s syndrome

A

loos of salivary gland function and lacrimal gland function

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9
Q

achlorhydria –> pernicious anemia

A

vitamin B12 deficiency or malabsorption in terminal ileum

could be defective intrinsic factor

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10
Q

cimetidine and ranitidine

A

H2 receptor blockers

parietal cells = target

‘acid-suppressant drug’

side effects: diarrhea, headache, drowsiness, fatigue, constipation, hallucinations, gynecomastia (men), galactorrhea (women)

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11
Q

gastritis

A

inflammation of gastric mucosa

mild to moderate chronic gastritis is very common in the general population, especially in the middle to later years

can be superficial or deep and cause atrophy to mucosa

95% caused by chronic infection by Helicobacter pylori

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12
Q

Helicobacter Pylori (H. Pylori)

A

corkscrew in shape…so can easily penetrate the stomach’s protective lining , breaks down mucosal barrier and stimulates gastric secretion

can survive gastric acid due to urease enzyme

adheres to the epithelial cells stimulating adhesins, ammonia, proteases, and immune response

(+) gastrin by G cells via systemic circulation
(+) HCl by parietal

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13
Q

peptic ulcers

A

associated with chronic H. Pylori infections –> underlying epithelium exposed

and acid secretion brought by bacteria –> digest the gastroduodenal wall –> peptic ulcer

***during peptic ulcers due to H Pylori infection…although the acid secretion is increased - its augmentation occurs at a moderate rate

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14
Q

factors that predispose you to peptic ulcers besides bacteria

A
  1. smoking –> increased nervous stimulation of the stomach secretory glands
  2. alcohol –> tends to breakdown the mucosal barrier
  3. aspirin and NSAIDs –> breakdown mucosa
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15
Q

urease mechanism

A

urea + H20 –> NH3 + CO2

NH3 neutralizes the gastric acid

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16
Q

zollinger-ellison syndrome

A

abnormally high gastrin acid secretion rate = hallmark symptom
–> what separates it from gastric ulcers

= duodenal ulcers or tumors like gastrinomas…which secrete very high amounts of gastrin in an unregulated fashion

common gastrinoma location = pancreas

treatment = surgery to remove tumor if primary one can be found…otherwise proton pump inhibitors (PPIs) + H2 blockers

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17
Q

proton pump inhibitors (PPIs)

A

most popular agent to treat ulcer peptide disease

example = omeprazole –> binds the pump covalently on the extracytoplasmic surface

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18
Q

atropin, oxybutinin, diphenhrydamine

A

anticholinergic medications

decreases acid secretion

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19
Q

Cystic Fibrosis Transmembrane Regulator

A

the Cl- channel in the apical membrane of acinar cells in the exocrine pancreas

this is needed for HCO3- secretion…why see decrease in pancreatic function with cystic fibrosis

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20
Q

pancreatitis

A

most caused by gallstones that block the flow of pancreatic enzymes or by excessive amounts of alcohol

risk factors:

  1. alcohol abuse
  2. gallstones
  3. hyperlipidemia
  4. genetic (Cystic Fibrosis)
  5. hyperparathyroidism
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21
Q

2 main blood tests to diagnose pancreatitis

A
  1. serum amylase
    - an increase = pancreatitis
  2. serum lipase
    - acute will have raised levels

lower total cholesterol, HDL, LDL = severe acute pancreatitis

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22
Q

Cystic Fibrosis and chronic pancreatitis

A

most common lethal genetic disease in whites

AR, chromosome 7

clinical signs = recurrent pulmonary infection, chronic pancreatitis, abnormal sweat, malabsorption, and fat in shit

oral enzyme replacement therapy

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23
Q

gallstone disease

A

2 types = cholesterol or bilirubin (pigment stones)

most = cholesterol

balance between normal ratios of cholesterol to the other biliary lipids is disrupted

risk factors
- obesity, contraceptives, estrogen, old age, sudden weight loss, genetics

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24
Q

cholecystitis

A

inflammation of gallbladder when flow of bile is stopped

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25
Q

cholestasis

A

more serious stoppage of bile from liver into duodenum

26
Q

cholangitis

A

inflammation of the bile ducts outside the liver due to bacterial infection

27
Q

biliary cirrhosis

A

inflammation and obstruction of the bile duct inside the liver….dead cells replaced with fibrous scar tissue

28
Q

gall stone disease treatment

A

cholecystectomy

29
Q

lactase deficiency (lactose intolerance)

A

lactose passes into colon since not digested in the small intestine

metabolized by colonic bacteria –> releases gas

30
Q

sucrase-isomaltase deficiency

A

low digestion in the SI brush border –> lowers absorption, since cannot digest down to monosaccharides well

31
Q

glucose-galactose malabsorption syndrome

A

rare genetic disorder

cannot absorb Glu or Gal

mutations in SGLT1

diarrhea

milder mutations are associated with irritable bowel syndrome

32
Q

trypsinogen deficiency

A

pancreatic insufficiency leads to low levels of plasma proteins

33
Q

Hartnup disease

A

hereditary

defective renal and intestinal transport of netural amino acids (B transporters)

not protein deficient since normal absorption of oligopeptides

but lack niacin (B3) which is made from tryptophan (a neutral amino acid…which is lose in the urin)

34
Q

Cystinuria

A

defect in b0,+ transporters in renal and intestinal cells

accumulation of cysteine in urine and causes kidney stones

no protein deficiency because normal absorption of oligopeptides

35
Q

atrophic gastritis

A

decreases secretion of intrinsic factor from parietal cells

–> B12 deficiency

36
Q

pancreatic exocrine insufficiency –> vitamin B12 deficiency

A

can interfere with the digestion of the binding proteins in the SI so that IF can bind to it

37
Q

ileal disease or resection –> B12 deficiencyt

A

can decrease the binding and absorption of B12

38
Q

hemochromatosis

A

hereditary disorder in which the body absorbs excessive iron from the diet

treatment = phlebotomy

39
Q

celiac sprue

A

primary malabsorptive disorder which affects the SI mucosa

disease is due to toxic effect of gluten (protein in wheat flour)

causes villous atrophy

unabsorbed nutrients cause osmotic diarrhea

FAs are converting by bacteria to hyroxy-FAs which are powerful seretagogues in the colonic mucosa

symptoms: weight loss, fatty shit, anemia, vitamin deficient,

treatment = gluten free diet

40
Q

causes of steatorrhea

A

bile deficiency –> no absorption of cholesterol, cholE, and lipid soluble vitamins
*** still get TG digestion and absorption of FAs and 2MG is 50% normal

pancreatic insufficiency –> no pancreatic lipases and very little fat absorption occurs

41
Q

Rickets

A

hypocalcemia, bone deformation (bow legs)

lack of vitamin D causes it –> no Ca2+ absorption

sunlight

42
Q

bacterial exotoxin

A

peptide produces by bacteria

43
Q

bacterial endotoxin

A

an exotoxin that induces changes in intestinal fluid and electrolyte movement

44
Q

E. coli

A

produces two distinct enterotoxins (heat-labile and heat-stable, STa, toxins)

that induce fluid and electrolyte secretion via two distinct receptors and 2nd messengers systems

45
Q

3 mechanisms that secretagogues act by

A
  1. activate adenylyl cyclase on basolateral side –> cAMP –> PKA
    (VIP, heat labile toxin)
  2. guanylin receptor on apical side –> cGMP –> PKG
    (heat stable toxin, STa)
  3. stimulate phospholipase C –> IP3 –> DAG –> PKC –> [Ca2+]i –> PKC –> CaM kinase

***all promote net secretion by phosphorylating apical membrane transporters and other proteins

46
Q

salilvary gland fluidnature

A

alkaline

47
Q

stomach fluid nature

A

highly acidic

48
Q

biliary tree fluid nature

A

alkaline

49
Q

pancreatic fluid nature

A

highly alkaline

50
Q

jejunum and ileum fluid nature

A

alkaline

51
Q

colon fluid nature

A

acidic

52
Q

fecal excreta =

A

100mL water and 25-50 gram of solids

53
Q

5 potential causes of diarrhea

A
  1. deficiencies in normal transport systems
    - congential chloride diarrhea
    - glucose or galactose malabsorption
    - sucrase-isomaltase deficiency
  2. malabsorption of a nonelectrolyte (osmotic diarrhea)
  3. intestinal hypermotility (lower absorption)
  4. enhanced rate of net secretion due to luminal secretagogues
  5. reduction of mucosal surface area (celiac, IDB)
54
Q

secretory diarrhea

A

endogenous secretions of fluid and electrolytes from the intestine

leading causes (E. coli or traveler’s diarrhea) and vibrio

enterotoxins raises levels of cAMP, gGMP and Ca2+ –> increase secretions

***nutrient coupled Na+ absorption is not affected

oral rehydration solution containing Na, K, Cl, HCO3 and glucose is effective

metabolic acidosis….loss of Na, K, Cl, and HCO3

55
Q

excessive vomitting

A

metabolic alkalosis

loss of fluid, H, and Cl

56
Q

congentical chloridorrhea

A

metabolic alkalosis

loss of Cl- and Na+ and retention of HCO3-

57
Q

normal stool lab values

A

Na = 20-30

K = 55-75

Cl = 15-25

HCO3 = 0

58
Q

secretory diarrhea lab values

A

Na = 40-140 (high)

K = 15-40 (low)

Cl = 25-105 (normal-high)

HCO3 = 20-75 (high)

59
Q

congentical chloridiarrhea

A

Na = 30-80 (high)
K = 15-60 (low - normal)
Cl = 120-150 (very high)
HCO3 <5 (barely high)

60
Q

patient with Crohns disease….has the following, and what are the causes of each

  1. cachexia
  2. volume depletion
  3. steatorrhea
A
  1. inadequate uptake of calories and malabsorption of vitamins and minerals
  2. decreased intestinal transit time, increased osmolarity of the luminal content, decreased water and electrolyte absorption, decreased absorption of bile salts stimulates water secretion from the colon
  3. impaired micelle formation and decreased fat absorption

Physiology GI (11 decks)

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