Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Digestive System Module > Lecture 26 > Flashcards

Lecture 26 Flashcards

1
Q

Cholestasis Cells

A

Cholestatic hepatocytes are enlarged wth dilated canalicular spaces
Apoptotic ells may be seen
Kupffer cells frequently contain regurgitated bile pigments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cholestatis

A

Obstructive liver disease

  1. -Intra hepatic (bile ducts or canaliculi within liver)
  2. -Extrahepatic (common bile duct of head of pancreas)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Autoimmune Cholangiopathies

A
  • autoimmune damage to bile ducts or bile canaliculi(rare or uncommon. react against own body)
    1. Primary Biliary Cirrhosis
  • autoimmune disorder leading to destruction of bile canaliculi
  • expansion of portal tract by infiltrate of lymphocytes and plasma cells (seen in normal immunological response) (granulomatous reaction to bile duct undergoing destruction)
  • fine nodularity and intense bile staining (of end stage biliary cirrhosis)
    2. Primary Sclerosing Cholangitis
  • autoimmune disorder leading to scarring of the bile ducts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Cholestasis of Sepsis

A

patients with blood cancers/infections with effected immune system
-abnormal liver enzymes and obstructive patterns (of sepsis)

Sepsis can affect the liver through:

  • Direct effets of intrahepatic infection (liver abcess, bacterial cholangitis (of bile ducts))
  • Ischaemia related to hypotension(shock)
  • Circulating microbial products (particularly in context of gram-negative (bacteria e.g E. coli, crebseala, pseudotomas) infection (this is most likely to lead to cholestatic picture))
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Circulatory Disorders: Impaired Blood Inflow

A

Impaired blood inflow:
Portal vein obstruction (primary liver disease/cirhossis)
Intra or Extrahepatic thrombosis (increase pressure and reverse flow)
—>
1. Esophageal varices (opening up of other capillary plexuses)
2. Splenomegaly (increased pressure of splenic vein)
3. Intestinal congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Circulatory Disorders: Impaired Intrahepatic Blood Inflow

A 
Impaired Intrahepatic Blood flow:
Cirrhosis
Sinusoid occlusion
-->
1. Ascites (cirrhosis)
2. Esophageal Varices (cirrhosis)
3. Hepatomegaly
4. Elevated amniotransferases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Circulatory Disorders: Hepatic Vein Outflow Obstructon

A 
(obstruction in venous sinuses)
Hepatic Vein Outflow Obstruction
Hepatic vein thrombosis (Budd-chiari syndrome)
Sinusoidal Obstructive syndrome
--->
1. Ascites
2. Hepatomegaly
3. Abdominal pain
4. Elevated aminotransferases
5. Jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Typical blood flow obstruction in liver

A

Normally venous

  • can occur at multiple places
  • will causes similar presentation (ascites, pot splenomegally)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Liver tumours

A
  1. Benign Neoplasms
    - Cavernous haemangiomas
    - Hepatocellular adenomas
  2. Malignant Neoplasms
    - Hepatocellular Carcinoma (/hepatoma. Complication of cirrhosis (Hep B, C, haemoachromatosis, alcohol). Primary tumour of hepatocytes.)
    - Heptoblastoma
    - Cholangiocarcinoma
    - Hepatic Metastases (most common type of cancer. Secondary cancer. Metastatic spread from Primary Bowel or Colorectal cancer)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hepatocellular Carcinoma

A

tumour cells on background of chirrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hepatic Metastases from adenocarcinoma colon

A

Multiple hepatic metastases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pancreatic and Gall Bladder Pathology

A

Pancreatic pathology:
1. Acute and chronic pancreatitis (inflammation)
2. Pancreatic adenocarcinoma (cancers)
Gall Bladder Pathology:
1. Acute and chronic cholecystitis (usually gall stone consequence)
2. Gall bladder adencarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

You are on your surgical placement when a 40 year old NZ European woman presents to the emergency department with sudden onset abdominal pain. She finds the pain severe and she has been vomiting. She has no relevant medical history. You go to see her with the surgical registrar.

A

Acute pancreatitis?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Normal Pancreas

A

Endocrine and Exocrine function
“Hidden” organ
-sits deep, tucked into 2nd part of duodenum. Therefore clinical signs of pancreas are often late and non-specific (may relate to gallbaldder/gastic/duodenal mucosa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pancreas Exocrine function

A

Composed of acinar cells and ducts
Acini cells –> ductles –> Pancreatic duct –> common bile duct at ampulla joining
Acinar cells contain zymogen granules (when cleaved for potential proteases, lipases and elastases) (proenzymes that can be activated)
“perfect storm around acute and potent inflammatory response”
Zymogens= inactive enzyme precursors for trypsin, chromotrypsin, amylase, lipase, nuclease, elastase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pancreas Endocrine function

A

Islets of Langerhans
-Alpha and Beta cells, encoding for number of homrones for metabolic pathway:
Secrete insulin, glucagon and other hormones
-Main pathology: Type 1 and 2 Diabetes Mellitus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pathology of the Pancreas

A

Congenital/Genetic: Cystic Fibrosis
Inflammatory/Infective: Acute and chronic Pancreatitis
Malignant: Carcinoma of the pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Acute Pancreatitis

A

Inflammation of the pancreas- associated with acinar cell injury
Swollen, Red, Vasodilation, Edmeatis
-Spectrum of severity duration and severity
-Mild 60-70% of cases- low mortality (majority of pancreatitis attacks)
-Severe 30-40% cases, 20-30% mortality (life threatening, usually linked to multi-organ failure as complication of pancreatitis)

19
Q

Key features of inflammation

A

Swollen
Red
Vasodilation
Edmeatis

20
Q

Etiology of Pancreatitis

A
  1. Metabolic: Alcohol (most common)
  2. Mechanical: Gallstone (obstruction, increased pressure, ischaemia and damage to pancreatic cells. Most common), trauma (damage to pancreatic acini cells)
    80-90% of pancreatitis patients = attributed to gallstone/cholilothiasis, or direct alcohol infection
  3. Vascular: Shock (trauma-hypotension, or sepsis-hypotension or reduced blood supply. Primarily with shock see toxicity (renal and neurological) can see pancreatic toxicity as consequence) Vasculitis(inflammation of arterial vessels, can effect blood supply to pancreas, can damage acinar cell damage)
  4. Infection: Mumps (also traditionally effect salivary gland- viral illness of parotid glands or enlargement of submandibular gland)
21
Q

Pathology of Pancreas

A

Autodigestion of pancreatic enzymes
-damage to acinar cells, releases pancreatic enzymes, which damages pancreatic tissue —continues same cycle
Cell injury response mediated by inflammatory cytokines (secondary inflammatory response) (TNFa, interlukin 6 and 2)-inducing inflammatory reaction

22
Q

Consequences of Pancreatic Protease enzyme release

A

destruction of acini, ducts, islets

-release and activate further enzymes

23
Q

Consequences of Pancreatic Lipases enzyme release

A

Fat necrosis- pancreas and other sites

24
Q

Consequences of Pancreatic Elastases enzyme release

A

Blood vessel destruction leading to interstitial haemorrhage (into inflamed tissue)

25
Q

Pancreatic Cell injury response caused as a consequence of enzyme release

A

Inflammation, Oedema, Imapired blood flow, Ischaemia

-significant inflammatory response and potential life threatening illness

26
Q

Acute pancreatitis post mortom

A

Oedemitis
Pink and Erythrotheamtis- due to vasodilation of BV
Dark areas of necrosis
Hemorrhage into pancreatic tissue (due to inflammatory response and enzyme release)

27
Q

What triggers the acute event?

A

Obstruction of the pancreatic duct (in common bile duct and ampulla of vata and pancreatic duct. Normal pancreatic secretions wont be secreted into duodenum, increased presure, oedema, reduced blood supply, eventually damage acinar cells, enzyme release)
Direct injury to acinar cells

28
Q

Duct obstruction

A
  1. Cholelithiasis (gallstones)
  2. ampullary Obstruction (tumour)
  3. Chronic Alcoholism (thickened pancreatic secretions which obstruct pancreatic duct)
  4. Ductal concretions
    - -> Interstitial Edema
    - -> Impaired Blood Flow
    - -> Ischaemia
    - -> eventually Damage to acinar cells
29
Q

Acinar Cell Injury

A
  1. Alcohol
  2. Drugs
  3. Trauma (car crash)
  4. Viruses (e.g. mumps virus)
  5. Ischemia (reduced blood supply from shock or vasculitis)
    - -> directly damage acinar cells
30
Q

Pancreatic Ischaemia onflow steps

A

Intracellular acitvation of trypsinogen
–> Intracellular activation and retention of other proenzymes
–> acinar cell injury
–> Proteolysis(Proteases) + Fat necrosis (lipase, phospholipase) + Hemorrhage (elastase/damages BV)
or
–> Acinar cel injury response –> interstitial Inflammation (release of inflammatory cytokines)
—> Acute Pancreatitis

31
Q

Hereditary

A

Mutations of cationic trypsinogen

–> Intracellular activation fo trypsinogen

32
Q

Clinical features of Acute pancreatitis

A

Acute abdominal pain - epigastric (upper abdominal pain)
Nausea and vomiting (as closely associated to duodenum)
Fever/Febrile, Tachycardia (part of inflammatory response and cytokine release) - may have unstable BP
Marked abdominal tenderness

33
Q

Acute pancreatitis Diagnosis

A
  1. Clinical symptoms and signs (not particularily specific)
  2. High WBC cell count (neutrophil leukocytose - increase in acute inflammatory response cells). Still not specific for acute pancreatitis. (could also be seen in acute cholecistisis)
  3. Elevated serum amylase and lipase
    - useful
    - enzymes released from pancreatic acinar cells
    - not specific for acute pancreatitis. Cholecystitis and gastritis may have mild elevation - often not to same extent as acute pancreatitis
  4. CT scan abdomen - oedema, necrosis, pseudocysts of the pancreas
  5. Rarely may need laparotomy to confirm diagnosis
    - abdominal surgery, perforated viscous or acute surgical problem. Less common due to imaging and lab investigations
34
Q

Acute Pancreatitis Management

A

“Rest the pancreas”

  • inflammatory process settle down, so reduce stimulation of pancreas (reduce pancreatic enzyme release)
  • not eating food by mouth- so not stimulating pancreatic enzymes
    1. IV fluids
    2. NG suction (remove gastric and duodenal secretions)
    3. Analgesia(often quite significant) (fluid replacement)
    4. Close monitoring (for complications)
35
Q

Chronic Pancreatitis

A

Defined as:
“Repeated bouts of pancreatic inflammation with loss of pancreatic parenchyma and replacement of fibrosis tissue”
Microscopic difference to acute P: -see more chronic inflammatory cells(macrophages) + repair mechanism of fibrosis and scarring
-Majority have heavy alcohol intake 60-70%

36
Q

Pathology of Chronic Pancreatitis

A

Fibrotic organ: can be rock hard
Atrophy of the exocrine component but relative sparing of the islets
-if ongoing can affect function of pancreas, tends to effect for exocrine components- lead to malabsorption problems (rather than endocrine). Therefore unusual to see Diabetes as a complication of chronic pancreatitis.
Mild chronic inflammatory infiltrate
Calcification (seen in CT scan)

37
Q

Clinical features of Chronic Pancreatitis

A

Repeated attacks of abdominal pain
-often bought on by alcohol
(sometimes clinically difficult to sort out. as person with heavy alcohol intake may also have alcoholic hepatitis- cause liver disfunction and upper abdominal pain)
-can also have gastritis and gastric ulceration
Can be more persistent pain
If ongoing:
1. Loss of exocrine function (malabsorption)
2. Pseudocysts (scarring and cavity formation/pseudocyts -seen on imaging)
3. Rarely diabetes mellitus
-if have repeated episodes Serum Amylase levels may not be as useful (less dramatic rises)

38
Q

Pancreatic Carcinoma

A

4th most common cause of cancer death
Males slightly more > Female
Most aged > over 50 (peak 60-80)
Prognosis remains poor (

39
Q

Pancreatic Carcinoma: Risk factors/associations

A
  • Tobacco smoking
  • Heavy alcohol intake
  • High BMI
  • coffee drinking as well
  • carcinogenic or lifestyle associations
40
Q

Pancreatic Carcinoma: Pathology

A

Pathology: Adenocarcinoma
-tumours: epithelial and form glandular structures
60-70% head (majority)
-invade Ampulla, biliary obstruction (common bile duct) (jaundice, pale stool, dark urine)
5-10% body
10-15% tail
-Body and Tail: remain silent, often large and disseminated at presentation, spread to nodes, adjacent organs, liver, bones, lungs (silent, late in presentation as consequence to anatomical site)
20% diffuse -throughout pancreas

41
Q

Pancreatic Carcinoma Clinical Features

A 
Obstructive Jaundice
Pain (invading adjacent structures/head of pancreas around duodenum)
Weight loss (malignancy possibility)
Pancreatitis (obstructing pancreatic duct/(commonly from gall stone or alcohol)
Thrombophlebitis/Venous thrombosis
-spontaneous clot formation, often in deep veins of legs. Long distance flying, immobile, come off plane and have swollen, painful leg. Scanned and have clot in leg. 
-Risk: can break off and embolyse the lung (pulmonary embolisms)
-anyone with cancer have higher risk of veinous thrombosis (pancreatic cancer has very high incidence of venous thrombosis, and variation of thrombophlebitis -superficial veins (of lower limbs esp.) clotted/thrombosed and associated inflammation around veins (assoc. with hypercoaguability of patients with malignancy/pancreatic cancer)
42
Q

Patient with Jaundice

A

Hepatobiliary pathology

  • age of malignancy
  • pot. tumour in pancreas head causing obstruction
  • pot. gallbladder pathology, with cholilothiasis shedding stones into common bile duct
43
Q

Clinical features of Pancreatic Carcinoma

A

Diagnosis usually suspected on imaging

Confirmed by CT (usually) or US guided FNA and core biopsy or open biopsy at laparotomy

44
Q

Pancreatic Endocrine Tumours

A

Islet cell tumours

  • rare
  • may secrete pancreatic hormones (insulin)
  • e.g. insulinoma
    1. Hypoglycaemia
    2. Most benign, 10% malignant
    3. Treat with resection (stop hypoglycaemia)

Digestive System Module (38 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions