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Anatomy Exam 2 > Pancreas, Appendix, Spleen and Stomach > Flashcards

Pancreas, Appendix, Spleen and Stomach Flashcards

1
Q

What is painless jaundice secondary to?

A

A tumor in the head of the pancreas

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2
Q

What vessels provide blood to the superior portion of the head of the pancreas?

A

Celiac trunk -> common hepatic -> gastroduodenal -> A/P superior pancreaticoduodenal arteries

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3
Q

What vessels provide blood to the inferior portion of the head of the pancreas?

A

A/P inferior pancreaticoduodenal arteries from the superior mesentric artery

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4
Q

What vessels provide blood to the body and tail of the pancreas?

A

Splenic artery

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5
Q

Where does the celiac trunk come off?

A

Abdominal aorta (at T12) and bifurcates into LT-gastric artery, splenic artery and common hepatic artery

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6
Q

What is the ampulla of Vater?

A

“Hepaticopancreatic ampulla”; union of the pancreatic duct and CBD
-any problems can cause back-up into pancreas, liver, gallbladder

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7
Q

What is an EGD?

A

Esophagogastroduodenoscopy- can remove a lodged stone or biopsy an ampullary tumor

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8
Q

What are some pancreatic enzymes?

A 
Amylase
Lipase
DNAase
RNAase
Trypsinogen
Chymotrypsinogen
Procarboxypeptidase A and B
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9
Q

What happens if there is a blockage due to pancreatic cancer?

A

Pancreatic enzymes will build-up in pancreas and begin to break itself down
-aka “pancreatic autodigestion” -> leads to acute pancreatitis

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10
Q

What are the congenital disorders of the pancreas?

A

1) Agenesis: non-forming pancreas, very rare
2) Pancreatic divisum: failure of 2 ducts to fuse, common, normally asymptomatic and seen on autopsy (30% occurrence)
3) Annular pancreas: pancreas encircles duodenum, rare
4) Ectopic pancreas: pancreas found anywhere else in the abdominal cavity, very common

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11
Q

What is acute pancreatitis?

A

Sudden inflammation of the pancreas, very serious

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12
Q

What are some causes of acute pancreatitis?

A
  • Multiple organ system failure (MOSF)
  • Acute respiratory distress syndrome (ARDS)
  • Acute renal failure
  • Disseminated intravascular coagulation (DIC)
  • Pancreatic abscess
  • Pancreatic pseudocyst
  • Duodenal obstruction
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13
Q

What is chronic pancreatitis?

A

Chronic inflammation of the pancreas that causes calcifications or a pseudocyst

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14
Q

What are some consequences of chronic pancreatitis?

A
  • Pseudocyst
  • Duct obstruction/stenosis
  • Malabsorption
  • Steatorrhea
  • Secondary diabetes
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15
Q

What is the incidence and complications of appendicitis?

A
  • 69% = ages 10 - 30
  • 30% are misdiagnosed
  • Mortality: 0.1-0.2% unruptured; 3-5% ruptured
  • 20-30% rupture during surgery, significant morbidity is associated with rupture (infection, peritonitis)
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16
Q

Where can the appendix be located?

A

Retrocecal - 65%
Pelvic - 31%
RUQ, LUQ, LLQ

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17
Q

What is the classic presentation of appendicitis?

A

Seen in 60%: anorexia, periumbilical pain, N/V, RLQ pain after 24 hours (visceral pain), rebound tenderness as a later finding (parietal pain)

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18
Q

What is McBurney’s point?

A

Area in RLQ where you’ll have maximum tenderness with appendicitis
-midway between umbilicus and iliac crest

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19
Q

What is a positive Rosving’s sign?

A

Palpation of the LLQ increases pain felt in RLQ

-indicative of appendicitis

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20
Q

What is a positive Psoas sign?

A

Abdominal pain results from passively extending the thigh of a patient laying on their side with knees flexed, or asking the patient to actively flex the thigh at the hip
-indicative of appendicitis

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21
Q

What is a positive obturator sign?

A

Pain felt in the RLQ when the knee is flexed, the ankle is held and the knee is internally rotated

  • indicative of appendicitis
  • pain comes in contact with the obturator internus muscle
22
Q

What is Mantrel’s score?

A

Established in 1986 because appendicitis misdiagnosed as gastritis, IBS, stomach flu

  • (M)igration of pain = 1
  • (A)norexia = 1
  • (N)ausea/vomiting = 1
  • (T)enderness RLQ = 2
  • (R)ebound = 1
  • (E)levated temp = 1
  • (L)eukocytosis = 2
  • (S)hift to left = 1
  • scoring: >5 high suspicion, 5-6 possible, 7-8 probably, 9-10 very probable
23
Q

What is the spleen the largest of in the body?

A

Largest lymphoid tissue of body

24
Q

What are 2 main functions of the spleen?

A

1) Filter blood to remove old/damaged RBC - “red pulp”

2) Secondary lymphoid tissue/removes infectious agents and uses them to activate lymphocytes - “white pulp”

25
Q

What is the spleen a significant reservoir for?

A

T lymphocytes

26
Q

What does the spleen play a significant role in the production of?

A

1) Production of IgM antibodies and complement needed to fight infection
2) Functional maturation of antibodies

27
Q

What is the white pulp?

A

Circular, composed of mostly lymphocytes, and functions similarly to the nodules of lymph nodes, removes infectious agents

28
Q

What is the red pulp?

A

Surrounds the white pulp, contains mainly RBCs and macrophages, phagocytizes old RBCs

29
Q

What does the spleen do during fetal development?

A

Produces RBC and WBC

-by the 5th month of gestation, the spleen loses hematopoietic function but can produce RBCS throughout life

30
Q

What happens to RBCs that pass through the spleen?

A

Spleen is a “sophisticated filter” (monitors/manages RBCs) –> RBCs undergo a cleaning or repair
-RBCs coated with IgG and IgM are removed/destroyed

31
Q

What happens in diseases such as hemolytic anemia and ITP?

A

Idiopathic thromocytopenic purpura and hemolytic anemia are autoimmune diseases that destroy the spleen, can be cured with a splenectomy and steroids

32
Q

What kind of immune responses is the spleen involved in?

A

Specific and nonspecific: promotes phagocytosis and destruction of bacteria

33
Q

What kind of injuries could cause splenic trauma?

A

Blunt upper abdominal injuries (bicycle, MVC), often associated with fracture ribs of the left chest

34
Q

What can splenic injuries cause?

A

Extensive and continued hemorrhage, or subcapsular hematomas that are subject to rupture at any time

35
Q

How are ruptured spleens treated?

A

Splenic preservation operations, partial splenectomies, capsular repairs, non-operative treatment

36
Q

What is the incidence of delayed rupture of the spleen?

A

15-30% of patients rupture within 2 weeks of injury

37
Q

What condition would result from a dysfunctional LES?

A

Esophagitis from the backup of stomach acid

38
Q

Where does the stomach get most of its blood supply from?

A

1) Anastomoses formed by the RT and LT gastric arteries (along lesser curvature)
2) RT and LT gastroepiploic arteries (along greater curvature)

39
Q

Where does the fundus and upper body of the stomach receive its blood from?

A

Short and posterior gastric arteries

40
Q

Where do the veins of the stomach lie?

A

Parallel to the arteries

41
Q

Where does the stomach receive its parasympathetic innervation from?

A

From the medulla via the vagus nerve

42
Q

Where does the stomach receive its sympathetic innerviation from?

A

Celiac ganglia arising from T5-T9

43
Q

Where do the lymph nodes of the stomach drain to?

A
  • Gastric lymph nodes
  • Pancreaticosplenic lymph nodes
  • Pyloric lymph nodes
  • Pancreaticoduodenal lymph nodes
  • -They all drain into the celiac lymph nodes
44
Q

What do mucous neck cells do?

A

Secrete mucous and bicarbonate, which provide a barrier between the gastric acid and epithelium of the stomach wall

45
Q

What do parietal cells do?

A
  • Stimulated by AcH, gastrin, histamine -> secrete gastric acid - activates pepsin and kills bacteria
  • Stimulated by AcH, gastrin, histamine -> secretes intrinsic factor - complex with B12 to permit absorption
46
Q

What do enterochromaffin-like cells do?

A

Stimulated by AcH and gastrin -> secrete histamine, stimulates gastric acid secretion

47
Q

What do chief cells do?

A

Stimulated by AcH, acid and secretin –> secrete pepsinogen and gastric lipase, which digest protein and fats

48
Q

What do D cells do?

A

Stimulated by acid in stomach -> secrete somatostatin which inhibits gastric acid secretion

49
Q

What do G cells do?

A

Stimulated by AcH, peptides and amino acids -> secrete gastrin which stimulates gastric acid secretion

50
Q

Why is taking too much NSAIDs bad for your stomach?

A

They inhibit prostaglandinds, which make mucous and bicarb, which buffer stomach acid

51
Q

What is an adenocarcinoma?

A

Most common malignancy of stomach

  • chronic inflammation promotes neoplastic progression
  • BRCA2 mutations are at increased risk of developing diffuse gastric cancer
  • TGFBRII, BAX, IGFRII and p16/INK4a: genes in sporadic intestinal-type gastric cancer
52
Q

What is the function of the stomach?

A

Mixing of food with acid/pepsin
-Unique acid environment requires functional gastric surface, mucus barrier, bicarbonate buffering and epithelial integrity

Anatomy Exam 2 (5 decks)

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