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Pathophys Semester 2 > GIT-Part 2 witwer > Flashcards

GIT-Part 2 witwer Flashcards

1
Q

Liver fx: storage

  • Glucose is stored as _______
  • Storage of which vitamins & minerals:
A
  • glycogen (glycogenesis)–> then back to glucose (glycogenolysis)
  • Vitamin A, D, B12, vitamin K, iron and copper
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2
Q

Liver fx: synthesis

A
  • Bile acids from cholesterol made by liver –for emulsification of fats
  • Protein metabolism – amino acids, clotting factors (fibrinogen, prothrombin, etc), vitamins, albumin, transport proteins, binding proteins
  • Carbohydrate metabolism including gluconeogenesis – synthesis of glucose
  • Lipid metabolism– including cholesterol synthesis (50% from liver, 50% from food), lipogenesis and triglyceride production
  • Conjugation of bilirubin
  • Ammonia formation

Angiotensin – part of RAAS

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3
Q

Liver fx: immunological

-describe Kupffer cells

A

Kupffer cells in sinusoids (part of the reticuloendothelial system) act as antigen presenting cells

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4
Q

Liver: detox fx

A

Detoxification/breakdown:
Toxins
Hormones
Drugs

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5
Q

Jaundice is caused by HIGH levels of ______

A

**bilirubin

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6
Q

Describe the process of RBC destruction

A
  • Red Blood cells are destroyed by the reticuloendothelial system
  • The iron is recycled
  • The heme portion of Hgb is broken down into fat soluble Bilirubin (Indirect Bilirubin)
  • The Liver converts the fat soluble Bilirubin into water soluble Bilirubin (Direct Bilirubin)
  • The water soluble Bilirubin is secreted into the Biliary System as part of bile and passes into the bowel
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7
Q

Pre-Hepatic Jaundice – usually occurs when:

A

when there is an excessive breakdown of RBCs as in hemolytic anemias and internal hemorrhage

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8
Q

Hepatic Jaundice occurs when:

A

liver cannot conjugate the fat soluble Bilirubin (indirect) into water soluble Bilirubin (direct)

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9
Q

Post-Hepatic Jaundice occurs when:

A

there is obstruction to the flow of bile usually from gallstones in the CBD or Carcinoma in the head of the Pancreas

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10
Q

normal levels of bilirubin=

A

<1 mg/dL

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11
Q

sceral icterus occurs when bilirubin is > than ____

A

3

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12
Q

conjugated bili is found in ____

A

urine

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13
Q

In newborns if the unconjugated bilirubin is >4 mg/dL there is the possibility of ________

A

Kernicterus.

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14
Q

Bilirubin is neurotoxic and can accumulate in the grey matter of the brain causing _______

A

Kernicterus, encephalopathy – cerebral palsy like disorder

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15
Q

tx of bili accumulation (toxic levels)?

A

phototherapy or exchange transfusion.

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16
Q

Describe breakdown of hgb (starting w/ heme) KNOW

A

Heme > biliverdin (greenish color of bruises) > unconjugated bilirubin > conjugated bilirubin (excreted as bile) > acted on by microbes > urobilinogen > 1) stercobilin giving feces their brown color and 2) converted into urobilin giving urine its yellow color.

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17
Q

Bruise Healing process=

A

Hgb–> biliverdin–> bilirubin

bruise—> healing

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18
Q

Bile is produced by ____ and stored in _______

A

liver

-gallbladder

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19
Q

Contents of bile=

A
  • Water 97%, bile salts 0.7%, bilirubin 0.2%, fats (cholesterol, fatty acids, lecithin 0.5%), inorganic salts
  • Bile acids/salts are steroid acids produced in liver and conjugated into bile salts.
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20
Q

Bile is discharged into duodenum for _____

A

Aids in digestion of lipids, emulsifies lipids

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21
Q

Bile salts are recycled via:

A

reabsorption in the enterohepatic circulation

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22
Q

Steroid based acids/salts synthesized in the ____

A

liver

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23
Q

There is an _________ circulation of bile salts.

A

enterohepatic

**Bile salts and Vitamin B12
absorbed in the Terminal Ileum and recycled

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24
Q

Describe Bile

A

Bile salts act as a surfactant,
emulsifying lipids

Aggregate around lipids
(triglycerides and phospholipids)
forming micelles

Greater surface area for pancreatic lipases to digest fats

Triglycerides > two fatty acids and a monoglyceride absorbed by villi, reform into triglycerides and are absorbed by the lymphatic system

Vitamins go along with fats

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25
Q

Bilirubin is excreted in bile as well as the _____

A

urine
-Bilirubin accounts for the yellow color of bruises, a breakdown product stercobilin the brown color of stools, and a breakdown product urobilin the yellow color of urine.

-Bilirubin acts as a cellular antioxidant

26
Q

Fatty liver changes can be secondary to:

A

alcoholism, metabolic syndrome, toxins, and hepatitis and **are reversible

27
Q

T/F: Cirrhotic Liver with scarring and regenerative nodules is irreversible

A

true

28
Q

Hepatic Cirrhosis:

-imaging findings

A

-U/S demonstrating enlargement and
increased echogenicity of liver parenchyma
-enlarged left and caudate lobes, fibrosis
and shrunken right lobe, and ascites

29
Q

Loss of liver function causes:

A

Hepatic Insufficiency
-Jaundice from bilirubin buildup
-Hyperestrinism from inability to metabolize estrogen
-Bleeding from decrease in clotting factors
-Ammonia build up – hepatic
encephalopathy .> asterixis

2) Portal Hypertension
- Esophageal varices
- Hemorrhoids
- Ascites
- Splenomegaly

30
Q

Viral hepatitis:

-Hepatitis C notorious for:

A

A mild acute infection with
chronic hepatitis in 85% if
not treated

20% develop post necrotic
cirrhosis

Complications:
Cirrhosis
Hepatocellular carcinoma

31
Q

What is the MC liver tumor?

A

**Cavernous Hemangioma Liver tumor

32
Q

What is the 2nd Mc liver tumor?

A

Focal Nodular HyperplasiaSecond Most Common Liver Tumor-Benign= Hyperplasic process with possible association with oral contraceptives

33
Q

Metastatic Disease to Liver: provide 1 ex

A

Diffuse metastatic breast carcinoma to
the liver with resulting portal hypertension
and umbilical vein enlargement

34
Q

Hemochromatosis:

  • describe this condition
  • can be 2/2 ?
A

=Iron deposition in liver, pancreas, and heart

-2/2: genetic disorder, Hereditary Hemochromatosis, or transfusion iron overload

35
Q

Gallstones:

-75% are _______

A

cholesterol stones–contain Ca 2+ carbonate,

36
Q

Black pigment stones=

-2/2 ?

A

chronic extravascular hemolytic anemia – calcium

bilirubinate stones

37
Q

Brown pigment stones=

2/2 ?

A

infection – Asians – unconjugated bilirubin

38
Q

Cholelithiasis:

  • pathogenesis?
  • risk factors?
A
  • Supersaturation of bile with cholesterol
  • Decrease bile salts/acids which solubilize cholesterol
  • Female >40
  • Use of oral contraceptives
  • Obesity
  • Rapid weight loss
  • Native Americans
39
Q

Cholelithiasis:

-complications?

A

Cholelithiasis with cholecystitis

-Common Bile Duct Obstruction

40
Q

Acute Cholecystitis:

-95% caused by _____

A

**Gallstones
Fair, fat, fecund and forty
From 40-60 yrs

41
Q

Acute Cholecystitis:

-pathogenesis?

A

Stone lodges in cystic duct or common bile duct
Food stimulus causes gallbladder contraction – biliary colic
Stone impacts in cystic duct
Mucus accumulates behind stone
-**Infection – most commonly E. coli, then Enterococcus, Bacteroides fragilis, and Clostridium

  • **RUQ pain, possible radiation to right shoulder
  • Localized peritonitis with rebound tenderness
  • **Positive Murphy sign

-**Neutrophilic leukocytosis
Stone may pass and attack subsides
If stone does not pass, perforation may occur

42
Q

Acute Cholecystitis:

-clinical presentation

A

Fever
Vomiting in 75%
Radiation of pain to right shoulder
-*Murphy sign
Palpable gallbladder 15%
Neutrophilic leukocytosis - >12K in 70%
-Jaundice 25% - CBD stone
-Increased AST/ALP with common duct stones
-**Increased serum bilirubin >4mg/dL indicates common duct stone
-Increased serum amylase indicates pancreatitis

43
Q

Acalculous Cholecystitisaka Necrotizing Cholecystis:

-is usually seen in ?

A

**critically ill patients with other coexistent disease processes.

Gallbladder stasis > ischemia > inflammation > necrosis and infection

Need to think about it. A “Don’t forget”

Usually a fulminant course with high rate of complications such as gangrene and perforation.

High morbidity and mortality.

44
Q

Cholelithiasis:

-gold standard dx test?

A

**Ultrasound is the gold standard >98% sensitivity to detect stones in gall bladder but not the cystic duct (only 30% sensitivity)

-Detects stones and sludge and pericystic inflammation

45
Q

Cholelithiasis:

-tx?

A

ERCP

46
Q

Cancer of the Gall Bladder:

  • demographic?
  • Precursor is _____
A

Unusual
Elderly females
Poor prognosis
Cholelithiasis in 95%

precursor= porcelain gallbladder**, must remove it

47
Q

Pancreatic secretions:

-Exocrine Gland Function

A

Controlled by hormones Gastrin,
Cholecytokinin, and Secretin from
Stomach and Duodenum

-Acinar Cells secrete bicarbonate ions,
and precursor proenzymes for proteases (trypsinogen, chymotrypsinogen),
pancreatic lipase, pancreatic amylase,
phospholipases, and cholesterol esterase.

48
Q

Pancreatic secretions:

Endocrine Gland Function:

A 
Pancreatic Islet Cells secrete:
	Glucagon – alpha cells
	Insulin – beta cells
	Somastatin – delta cells
	Pancreatic polypeptide – gamma cells
49
Q

Acute Pancreatitis:

-epidemiology?

A

Alcoholism and Gallstones major causes 80%
Gallstones most common acute cause (Dr Opie)

Activation of the proenzymes (zymogens) in the acinar cells of the pancreas, into enzymes that autodigest the panceas

  • Obstruction of main pancreatic duct or CBD
  • Gallstones
  • Alcohol thickens ductal secretions

Pathophys:
-**Trypsin important activator of proenzymes

Proteases damage acinar cell structure

-Lipases and phospholipases > enzymatic fat necrosis

Elastases damage vessel walls > hemorrhage

50
Q

Acute pancreatitis complications:

A

Peripancreatic Infection
Pseudocyst formation
Pancreatic Abscess
-Pancreatic Ascites from leaking pseudocyst

51
Q

Acute pancreatitis: clinical sx

A

Fever, nausea, vomiting
-Severe, boring, knife like pain in the midepigastrium with radiation to the back

Hypovolemic shock due to third spacing of fluids – peripancreatic fluids

Hypoxemia – loss of surfactant secondary to circulating pancreatic phospholipases > atelectasis (intrapulmonary shunting)

Grey-Turner Sign
Cullen Sign

DIC: Disseminated Intravascular Coagulopathy due to activation of prothrombin by trypsin

Tetany - hypocalcemia from enzymatic fat necrosis and saponification

52
Q

Acute Pancretitis: gold standard dx test?

A

CT is Gold Standard

53
Q

MCC of chronic pancreatitis?

A

alcoholism

-cystic fibrosis in children

Findings:
	Pancreatic pseudocysts
	Calcifications- saponification
	Scarred shrunken pancreas
	Residual Diabetes mellitus
	Residual malabsorption
54
Q

Chronic Pancreatitis:

-clinical findings

A

Severe pain radiating to the back
Malabsorption – indicates that 90% of exocrine function destroyed
Type 1 Diabetes Mellitus in 70%
Brittle Diabetics secondary to loss of glucagon and insulin
Pancreatic pseudocysts

55
Q

Cancer of the Pancreas:

  • demographic
  • which tumor is MC?
A

Occurs primarily from 60-80 yrs
-**Adenocarcinoma most common

Associations:

  • Smoking
  • Chronic Pancreatitis

Clinical:

  • Epigastric pain with weight loss >90%
  • Painless or painful jaundice
  • Light colored (clay colored) stools –
  • sister mary joseph sign= nodule at the umbilicas
  • Increased CA19-9 – Gold Standard
56
Q

DDX: RUQ pain

A
  • acute cholecystitis
  • Acute hepatitis
  • acute pancreatitis
57
Q

DDx: LUQ pain

A
  • acute pancreatitis

- splenic rupture

58
Q

DDX: RLQ pain

A
  • appendicits
  • PID
  • ruptured ectopic
59
Q

DDX: LLQ

A
  • endometriosis
  • strangulated inguinal hernia
  • PID
  • ruptured ectopic
60
Q

DDx: diffuse pain

A

acute pancreatitis
aortic dissection
bowel obstructoon
gastroenteritis

Pathophys Semester 2 (12 decks)

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