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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
cholestasis
more serious stoppage of bile from liver into duodenum
26
cholangitis
inflammation of the bile ducts outside the liver due to bacterial infection
27
biliary cirrhosis
inflammation and obstruction of the bile duct inside the liver....dead cells replaced with fibrous scar tissue
28
gall stone disease treatment
cholecystectomy
29
lactase deficiency (lactose intolerance)
lactose passes into colon since not digested in the small intestine metabolized by colonic bacteria --> releases gas
30
sucrase-isomaltase deficiency
low digestion in the SI brush border --> lowers absorption, since cannot digest down to monosaccharides well
31
glucose-galactose malabsorption syndrome
rare genetic disorder cannot absorb Glu or Gal mutations in SGLT1 diarrhea milder mutations are associated with irritable bowel syndrome
32
trypsinogen deficiency
pancreatic insufficiency leads to low levels of plasma proteins
33
Hartnup disease
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
Cystinuria
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
atrophic gastritis
decreases secretion of intrinsic factor from parietal cells --> B12 deficiency
36
pancreatic exocrine insufficiency --> vitamin B12 deficiency
can interfere with the digestion of the binding proteins in the SI so that IF can bind to it
37
ileal disease or resection --> B12 deficiencyt
can decrease the binding and absorption of B12
38
hemochromatosis
hereditary disorder in which the body absorbs excessive iron from the diet treatment = phlebotomy
39
celiac sprue
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
causes of steatorrhea
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
Rickets
hypocalcemia, bone deformation (bow legs) lack of vitamin D causes it --> no Ca2+ absorption sunlight
42
bacterial exotoxin
peptide produces by bacteria
43
bacterial endotoxin
an exotoxin that induces changes in intestinal fluid and electrolyte movement
44
E. coli
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
3 mechanisms that secretagogues act by
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
salilvary gland fluidnature
alkaline
47
stomach fluid nature
highly acidic
48
biliary tree fluid nature
alkaline
49
pancreatic fluid nature
highly alkaline
50
jejunum and ileum fluid nature
alkaline
51
colon fluid nature
acidic
52
fecal excreta =
100mL water and 25-50 gram of solids
53
5 potential causes of diarrhea
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
secretory diarrhea
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
excessive vomitting
metabolic alkalosis loss of fluid, H, and Cl
56
congentical chloridorrhea
metabolic alkalosis loss of Cl- and Na+ and retention of HCO3-
57
normal stool lab values
Na = 20-30 K = 55-75 Cl = 15-25 HCO3 = 0
58
secretory diarrhea lab values
Na = 40-140 (high) K = 15-40 (low) Cl = 25-105 (normal-high) HCO3 = 20-75 (high)
59
congentical chloridiarrhea
Na = 30-80 (high) K = 15-60 (low - normal) Cl = 120-150 (very high) HCO3 <5 (barely high)
60
patient with Crohns disease....has the following, and what are the causes of each 1. cachexia 2. volume depletion 3. steatorrhea
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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