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GI > Clinical Presentation of GI > Flashcards

Clinical Presentation of GI Flashcards

1
Q

what’s retching

A

forced inspiration against closed mouth and glottis (dry heaves). Muscular activity of abdomen and thorax, often voluntary.

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2
Q

what’s vomiting

A

involuntary contractions of abdominal, thoracic & GI (smooth) muscles leads to forceful expulsion of stomach contents

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3
Q

what’s the differences and similarities btwn vomiting and regurgitation

A

vomiting is forceful, and can be assoc w/ nausea
regurgitation is effortless return of esophageal or gastric contents into the mouth but isn’t assoc w/ nausea or involuntary muscle contractions.

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4
Q

where are the 3 main neurological pathways located for vomiting?

A
  1. medulla
  2. spinal cord
  3. GI tract
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5
Q

what population is psychogenic vomiting most commonly seen in? what might it also co-exist with?

A 
young females (but rarely occurs in public & minimum or no nausea)
may co-exist w/ eating disorders, laxatives or diuretic abuse; also psychological disturbances common
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6
Q

what’s surreptitous vomiting?

A

signs and symptoms of vomiting (like electrolyte disturbances, unexplained weight loss, etc) but no history of vomiting.

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7
Q

what’s the signs of nutritional complications of vomiting in adults vs kids?

A

adults: weight loss
kids: failure to thrive

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8
Q

what are mallory weiss tears and what are they associated with?
what could it eventually lead to?

A

painful and/or bleeding tears at the GE junction assoc with vomiting.
It could lead to perforation leading to Boorhaave’s syndrome where contents leaks out

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9
Q

what renal complications can occur with vomiting?

A

prerenal azotemia, ATN or hypokalemic nephropathy

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10
Q

what are electrolyte and acid-base disorders assoc w/ vomiting?

Explain why each occur

A

Metabolic alkalosis due to bicarb retention and volume contraction
Hypokalemia: loss of K (renally and GI) and decreased K intake
Hypochloremia: due to gastric chloride losses
Hyponatremia: due to free water retention from volume contraction

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11
Q

what’s the difference btwn dysphagia and odynophagia?

A

Dysphagia: difficulty swallowing, the sensation of food being hindered in its norm passage
Odynophagia: painful swallowing

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12
Q

what are the 3 different types of dysphagia pathology

A
  1. Extrinsic dysphagia
  2. Intrinsic dysphagia - due to the wall
  3. Intrinsic dysphagia - due to inside the lumen
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13
Q

what are the 2 major categories of dysphagia

A

esophageal and oro-pharygeal dysphagia

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14
Q

what type of fibers is most nocipetion from abdominal viscera being conveyed by?
describe this pain?
what are they mainly sensitive to?

A

C fibers
pain: dull, burning, poorly localized
they’re sensitive to stretch (cutting, tearing or crushing viscera doesn’t result in pain)

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15
Q

abdominal visceral nociceptors are responsive to stretch and also various chemical stimuli. Where do these chemical stimuli come from?

A

substances released in response to local mechanical injury, inflammation, tissue ischemia and necrosis and noxious thermal or radiation injury

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16
Q

what’s the major differences betwn somatoparietal pain and visceral pain?
What can aggravate it?

A

somatoparietal pain is more intense and more localized

Movement or coughing can aggravate this pain

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17
Q

In acute appendicitis, describe the visceral and somatoparietal pain.

A

Visceral pain: periumbilical pain

Somatoparietal pain: RLQ McBurney’s pt pain (inflammatory involvement of the parietal peritoneum)

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18
Q

what 3 factors do you want to ask your patient about in regards to their pain?

A
  1. Chronology (acute vs chronic)
  2. constancy (constant vs intermittent)
  3. Severity (increasing vs decreasing)
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19
Q

where can GB pain refer to?

A

back and shoulder/scapula

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20
Q

is WBC useful for appendicitis?

A

no

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21
Q

what’s the definition of unitentional weight loss

A

weight loss of 5 kg or more than 5% of usual weight over 6-12 months (assoc w/ increased mortality)

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22
Q

if a patient has involuntary weight loss but has an increased appetite, what 3 diseases might you consider?

A
  1. DM
  2. Malabsorption
  3. Hyperthyroidism
23
Q

if a patient has involuntary weight loss but has an decreased appetite, what 3 pathways might you consider?

A
  1. Organic issue (cancer or noncancer)
  2. Psychiatric (depression, dementia)
  3. Idiopathic
24
Q

what’s the weight to determine stool is diarrhea?

A

> 250 g/24 hrs

25
Q

what’s the Rome 3 criteria for diagnosing constipation?

A

pt must have at least 2 of the following:

  1. at least 25% bowel movements assoc w/ straining, hard stools, incomplete bowel evacuation, anorectal obstruction, manual manoeuvres or < 3 bowel movements/wk
  2. loose stools rare without use of laxatives
  3. insufficient criteria for IBS
26
Q

what separates upper vs lower GI bleeding sites?

A

upper bleeding: ligament of treitz (start of jejunum)

27
Q

In GI bleeding, what’s the difference between overt and occult bleeding?

A

Overt bleeding: visible bleeding

Occult bleeding: microscopic bleeding present but not obvious

28
Q

what does coffee-ground emesis mean?

A

it means the blood has been acted on by stomach acid

29
Q

what’s hematochezia?

A

passage of bright red blood per rectum

30
Q

what’s melena

A

shiny, jet-black, sticky stool with a specific odor (no Fe/Bi use). it’s been acted on by the stomach acid but passes through the system

31
Q

what happens to hematocrit with acute blood loss?

A

initially, proportionate loss of plasma volume & RBC, so hct may not change.
Later as extravascular fluid shifts into intravascular compartment, Hct acutely falls for 48-72 hours

32
Q

In acute blood loss how will IV fluids and packed RBCs effect the hct level?

A

IV fluids will exaggerate hct falling

PRBCs will minimize hct changes

33
Q

what happens to BM & plasma iron, ferritin, RDW, iron, TIBC, Hgb & MCV change with chronic blood loss?

how might the peripheral blood smear look?

A 
BM & plasma iron levels decrease
Ferritin: decrease
RDW: increases 
TIBC: increases 
Hgb: decreases 
MCV: decreases

PBS: hypochromatic microcytic anemia

34
Q

what lab tests show true liver synthetic function?

A

total protein, serum albumin, total bili, prothrombin time (PT/INR)

35
Q

what’s ALT?

what’s a normal range?

A 
Alanine Aminotransferase (SGPT): enzyme found primarily in hepatocytes, released w/ injury. 
Norm btwn 5-40 U/L
36
Q

what’s AST?

what’s a normal range?

A 
Aspartate Aminotransferase (SGOT): enzyme in liver, heart, muscle, intestine, pancreas. Not very specific for liver dx but often folllows ALT.
Norm: 8-20 U/L
37
Q

When AST:ALT is elevated 2 or 3:1 what might this suggest?

A

Alcoholic

38
Q

What’s alkaline phosphatase?
normal values?
when does it increase?

A

enzyme found in liver (esp biliary tract), bones, intestines & placenta
Norm: 20-70 U/L
increased w/ obstruction or infiltrative dx (stones or tumors)

39
Q

what’s direct/conjugated bilirubin?
normal range?
what might occur if it’s increased? at what level

A

breakdown product of old RBCs, liver adds glucuronic acid to make it water soluble for excretion. It’s excreted in bile
Norm: .3 - 1 mg/dL
bili > 2 can lead to jaundice

40
Q

what does elevations in ALT and AST only suggest?

A

liver cellular injury (gold standard would be to do a liver biopsy but try to avoid this)
extreme elevations could be from acute viral hepatitis or acetominophen toxicity

41
Q

what does elevations in alk phos and bili suggest?

A

cholestasis or obstruction

42
Q

describe the pathway of bilirubin excretion

A

formed from breakdown of hemoglobin in spleen, transported to the liver by albumin, in hepatocyte it’s conjugated with glucuronic acid to become water soluble, secreted into bile then in ileum and colon it’s converted to urobilinogen (10-20% reabsorbed into portal circulation into bile or urine)

43
Q

whats a differential diagnosis for unconjugated hyperbilirubinemia due to increased bilirubin production

A
  1. extravascular hemolysis (RBCs destroyed by MO in spleen, liver or BM)
  2. extravasation of blood into tissues
  3. intravascular hemolysis (rupture of RBCs)
  4. errors in production of RBCs
44
Q

whats a differential diagnosis for unconjugated hyperbilirubinemia due to impaired hepatic bili uptake (transport)

A
  1. CHF
  2. Portosystemic shunts
  3. Drug inhibition: rifampin, probenecid
45
Q

whats a differential diagnosis for unconjugated hyperbilirubinemia due to impaired bili conjugation?

A
  1. Gilbert’s dx
  2. Crigler- Najjar syndrome
  3. Neonatal jaundice (physiologic)
  4. Hyperthyroidism
  5. Estrogens
  6. Liver diseases (chronic hepatitis, cirrhosis, Wilson’s dx)
46
Q

whats a differential diagnosis for conjugated hyperbilirubinemia due to intrahepatic cholestasis/ impaired excretion?

A
  1. Hepatitis (viral, alcoholic & non-alcoholic)
  2. Primary biliary cirrhosis or end-stage liver dx
  3. Sepsis & hypo-perfusion states
  4. TPN
  5. Pregnancy
  6. Infiltrative dx: TB, amyloid, sarcoid, lymphoma
  7. Drugs/toxins: chlorpromazine, arsenic
    8: post op or post transplant
  8. Hepatic crisis in sickle cell dx
47
Q

whats a differential diagnosis for extrahepatic cholestasis causing obstructive jaundice?

A
  1. Choledocholthiaisis
  2. Cancer (prei-ampullary or cholangiocarcinomia)
  3. strictures after invasive procedures
  4. acute and chronic pancreatitis
  5. primary scerlosing cholangitis (PSC)
  6. parasitic infections (ascaris lumbricoides, liver flukes)
48
Q

At what fluid level does ascites become symptomatic? (what causes it?)
what’s assoc w/ it?

A

fluid > 400 ml (due to decompensated liver cirrhosis)

increased abd girth, pain, early satiety, pedal edema, weight gain, respiratory distress

49
Q

what physical exam findings are assoc w/ ascites?

A

umbilicus eversion, tympany at the top of the abd, fluid wave, peripheral edema, shifting dullness & bulging flanks

50
Q

when is ascities infected?

A

> 250 PMN = spontaneous bacterial peritonitis

51
Q

what test can determine if portal hypertension is present w/ ascites?

A

SAAG: serum to ascites albumin gradient

SAAG > 1.1 g/dL = portal hypertension

52
Q

what would the ascites glucose levels be if a pt had infection or malignancy and why?

A

low b/c they’d consume glucose

53
Q

what cancers commonly cause malignant ascites?

A

breast, bronchus, ovary, stomach, pancreas and colon

GI (8 decks)

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