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PCM > GI Cases > Flashcards

GI Cases Flashcards

1
Q

Describe visceral pain

A

Stimuli resulting in tension, stretching and ischemia
Tissue congestion and inflammation lower threshold for stimuli
Bilateral pain fibers
Unmyelinated fibers
Enter spinal cord at multiple levels

Described as dull, poorly localized and usually felt midline

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2
Q

Describe parietal pain

A

Noxious stimuli to parietal peritoneum
Ischemia, inflammation, or stretching
Transmitted via myelinated afferent fibers to specific doral root ganglia
Occurs on same side and same dermatomal level as original pain

Described as:
Sharp, intense, localized
Coughing or moving can aggravate it

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3
Q

Describe referred pain

A

Characteristics similar to parietal pain but felt in remote area
b/c supplied by same dermatome as affected organ
Shared central pathway for afferent neurons from different sites

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4
Q

Describe mesenteric lymphadenitis

A 
Inflammation of mesenteric lymph nodes
Clinical presentation often difficult to differentiate from acute appendicitis
Generally benign 
Male equal to female
Occurs more in children <15 y/o
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5
Q

What are causative agents of mesenteric lymphadenitis?

A 
Beta hemolytic streptococcus
Staphlococcus species
E. coli
Streptococcal viridans
Yersinia species (most cases currently)
Mycobacterium tuberculosis
Viruses
Coxsackievirus A & B
Rubeola virus
EBV
Adenovirus serotypes 1,2,3,5 & 7
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6
Q

Treatment of mesenteric lymphadenitis?

A

General supportive care
Hydration
Pain medication

No antibiotics in mild uncomplicated cases

Surgery if signs of peritonitis, indication of abscess/suppuration or acute appendicitis unclear

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7
Q

Describe a cephalohematoma

A

neonatal subperiosteal hemorrhage that is confined by the suture lines

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8
Q

Describe the two types of hyperbilirubinemia

A

Direct (conjugated) hyperbilirubinemia
Relatively uncommon
Primarily biliary obstruction and metabolic disorders

Indirect (unconjugated) hyperbilirubinemia
More common

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9
Q

Describe increased bilirubin load as the cause of hyperbilirubinemia

A 
Increased Bilirubin load
Nonhemolytic causes
Extravascular sources
Polycythemia
Exaggerated enterohepatic circulation
Increased Bilirubin load
Hemolysis
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10
Q

What are some hemolytic causes of increased bilirubin load?

A 
Hemolysis due to:
Rh incompatibility
ABO incompatibility
Minor antigens (D type…)
RBC cell membrane defects
RBC enzyme defects
Medications 
Hemoglobinopathies
Sepsis
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11
Q

What are some non hemolytic causes of increased bilirubin?

A 
Extravascular sources:
Cephlohematoma
CNS hemorrhage
Swallowed blood
Bruising
Polycythemia
Fetal-maternal transfusion
Delayed cord clamping
Twin-twin transfusion
Exaggerated enterohepatic circulation
CF, ileal atresia, pyloric stenosis, breast milk jaundice, Hirschsprung’s
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12
Q

Describe decreased bilirubin conjugation causes

A 
Physiologic jaundice
Breast feeding
Breast milk
Gilbert’s
Criglar-Najar
Hypothyroidism
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13
Q

Describe impaired bilirubin excretion

A 
Biliary obstruction
Infection
Metabolic disorders
Chromosomal abnormalities
Drugs
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14
Q

How is newborn bilirubin production different from adult?

A

Newborns produce 2x the adult rate which declines to normal adult by 10-14 days

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15
Q

Why is hyperbilirubinemia more common in neonates?

A

Shortened life span of their red blood cells
Declining hematocrit
Immature liver uptake & conjugation of bilirubin
Increased enterohepatic circulation
Increased intestinal reabsorption of bilirubin
Intestinal bacteria can deconjugate bilirubin allowing for reabsorption of bilirubin into the circulation.

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16
Q

Describe heme degration pathway

A

An RBC dies, a macrophage engulfs it and the heme is released
Heme is reduced by hemeoxidase into the components iron and biliverdin
Biliverdin is reduced by biliverdin reductase into free bilirubin
Free (unconjugated) bilirubin is bound to albumin ( in plasma) and passes into he hepatocytes where it is released from the albumin and conjugated
Uridinediphosphateglucuronyltransferase (UDPGT) conjugates bilirubin into an excretable form.

17
Q

Where does jaundice usually appear and how does it progress?

A

Usually begins on the face and progresses caudally
Generally, the farther the jaundice progresses down the body, the higher the total serum bilirubin
The more intense the color (which can approach a yellow-orange) also suggests a higher total serum bilirubin
Jaundice may be clinically detected with a total serum bilirubin of 5 mg per dL.

18
Q

Clinical findings suggestive of physiologic hyperbili in neonate?

A

Bilirubin levels of 12 mg/dl by 3 days of life

19
Q

Describe physiologic jaundice

A

Physiological immaturity

Appears between 24-72 hours of age
Peaks by 4-5 days in term and 7th day in preterm neonates
Disappears by 10-14 days of life

It is predominantly unconjugated and levels usually do not exceed 12 mg/dl in those without multiple risk factors (in those may rise as high as 17 mg/dL)

20
Q

Describe difference btw breast feeding and breastmilk jaundice

A

Breastfeeding Jaundice
in breast-fed babies usually appears between 24-72 hours of age, peaks by 5-15 days of life and disappears by the third week of life.
Breast milk jaundice
Appears by day 3-4; Peaks by day 6-14
Approximately 2-4% of exclusively breast-fed term babies them have bilirubin in excess of 10 mg/dl in the third week of life (not seen clinically)
A diagnosis of breast milk jaundice should be considered if the serum bilirubin is predominantly unconjugated, other causes of prolonged jaundice have been excluded and the infant is in good health, vigorous and feeding well and gaining weight adequately.
Bilirubin levels usually subside over a period of time. Interruption of breast-feeding is not recommended unless levels exceed 20 mg/dl.

21
Q

Describe pathologic jaundice

A

Appearance of jaundice within 24 hours
Increase in serum bilirubin beyond 5 mg/dl/day
Peak levels above the expected normal range
Presence of clinical jaundice beyond 2 weeks
Elevated conjugated bilirubin

22
Q

Describe bili toxicity

A

Deposition of unconjugated bilirubin in brain tissue
Unconjugated form exceeds binding capacity of albumin
Unbound lipid soluble bilirubin crosses the blood-brain barrier
If blood-brain barrier damaged albumin-bound bilirubin may cross
Toxicity levels vary among ethnic groups, maturity level of neonate and presence of hemolytic disease
>25 mg/dL in healthy term neonate

23
Q

Describe kernicterus

A 
Effects are often irreversible
Early signs
Subtle
3-4 days after birth
Lethargy, poor feeding, hypotonia
Late signs
Occur after first week of life
Irritability, seizures, apnea, hypertonia, fever, etc.
Chronic signs
If neonate survives, chronic encephalopathy is seen
Evident by 3 years of age
Cerebral palsy, high frequency hearing loss, mild MR
24
Q

How do you treat unconjugated hyperbilirubinemia?

A

Continued monitoring
Increase feeding
Repeat levels frequently

Phototherapy
Usually 1-2 days

Exchange Transfusion
Rapidly reduce bilirubin in
blood

PCM (4 decks)

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