Case nº22

Explain the effect of alcohol in the pancreas ?

- Acute pancreatitis is a severe acute inflammation of the pancreas followed by the
release of enzymes resulting in tissue necrosis, particularly fats.
- Symptoms consist of intense and persistent epigastric pain or the left superior quadrant
that radiates to the ribs that aggravates in lying position.
- Sometimes there's only a slight pain in the umbilical region that’s not relieved with
vomiting.
- due to escape of inflammatory exudate and enzymes into the peritoneum; Edema and
distention of the pancreatic capsule; biliary obstruction

- The alcohol causes alterations in the enzymatic secretion with the precipitation of
proteins.
- Alcohol and it’s metabolites such , acetaldehyde, can have a direct toxic effect on
pancreatic acinar cells, leading to intracellular trypsin activation by the lysosomal
enzymes
- Alcohol also appears to increase the precipitation of pancreatic secretions to
form "protein plugs" in the small ductules.

Explain the physiopathology behind the symptoms ?

- The abdominal pain: Inflammation caused by alcohol, causing the pancreas the swell,
stretching from the pancreatic capsule, this will result in the sweeping of materials such
as inflammatory exudate, digested proteins and lipids into the retroperitoneum irritating
the retroperitoneal and peritoneal sensory nerve endings producing intense pain.

Explain the exam lab results

- Uremia - due to the shock kidney function is decreased and due to the digestion of the
pancreas we have proteins such as urea.
- Glucose - since the pancreas, or more specifically island cells are affected resulting in an
increase in glucose levels.
- Amylase - one of the biomarkers of pancreatitis. - enzymes that catalyze the hydrolysis
of amylopectin, amylose and glycogen into maltose and dextrins.

What indicates the fever ?

- Inflammation: fever, pathophysiological mechanism of destruction, inflammation and
tissue necrosis leads to the release of pyrogens endogenous (IL-1) by leukocytes

Why are urea levels high but not creatinine ?

- Our hypothesis is that the kidneys have just started to lose their function. However,
creatinine levels are within the superior margin of the reference value.
What are the complications of pathology ?
- Pancreatic Pseudocyst, peritonitis, adult respiratory distress syndrome, shock, chronic
pancreatitis (if the patient continues to drink alcohol excessively)

Case nª23
The effects of drugs and alcohol on the liver. Can the effects be reversed?
- Ethanol has both direct and indirect effects on the liver. Its direct effects may result from
increasing the fluidity of biologic membranes and thereby disrupting cellular functions. Its
indirect effects on the liver are in part a consequence of its metabolism. Ethanol is
sequentially oxidized to acetaldehyde and then to acetate, with the generation of
nicotinamide adenine dinucleotide hydride (NADH) and adenosine triphosphate (ATP).
As a result of the high ratio of reduced to oxidized NAD generated, the pathways of fatty
acid oxidation and gluconeogenesis are inhibited, whereas fatty acid synthesis is
promoted.
- If the patient stops drinking alcohol the liver could then recover on its own.

Explain the physiopathology behind the symptoms ?

- The increased or altered synthesis of collagen and other connective tissue or basement
membrane components of the extracellular matrix is implicated in the development of
hepatic fibrosis and thus in the pathogenesis of cirrhosis.
- Hepatic fibrosis occurs in three situations: (1) secondary to inflammation and the
subsequent activation of immune responses; (2) as part of the process of wound healing;
and (3) in response to agents that induce primary fibrogenesis.
- Agents such as carbon tetrachloride that attack and kill hepatocytes directly can produce
fibrosis as part of wound healing. In both immune responses and wound healing, the
fibrosis is triggered indirectly by the effects of cytokines released from invading
inflammatory cells. Finally, certain agents such as ethanol and iron may cause primary
fibrogenesis by directly increasing collagen gene transcription and thus also increasing
the amount of connective tissue secreted by cells.
- Chronic alcohol abuse is associated with impaired protein synthesis and secretion,
mitochondrial injury, lipid peroxidation, formation of acetaldehyde and its interaction with
cellular proteins and membrane lipids. cellular hypoxia, and both cell-mediated and
antibody-mediated cytotoxicity. The relative importance of each of these factors in
producing cell injury is unknown. Genetic, nutritional, and environmental factors
(including simultaneous exposure to other hepatotoxins) also influence the development
of liver disease in people with chronic alcoholism.
- Nausea and vomiting – is a clinical manifestation of progressive hepatocellular
dysfunction in cirrhosis;

Explain the mental confusion ?

- Known as hepatic encephalopathy: Impairment of the liver's ability to detoxify ammonia
to urea leads to hepatic encephalopathy that manifests as an altered mental status.
Ammonia comes from the deamination of glutamine.
- short chain fatty acids are neurotoxic
 - disturbance in protein and carbohydrate metabolism.

Explain the lab results ?

- Total bilirubin - caused by poor blood filtration in the liver resulting from portosystemic
shunt caused by portal hypertension.
- AST - caused by destruction of hepatocytes
- ALT - caused by destruction of hepatocytes
- Alkaline phosphatase (ALP) - is in normal values ​not indicating acute hepatitis
- Glucose - the liver's function of storing glucose in the form of glycogen (glycogenesis)
- Albumin - the liver's protein-making function is compromised in cirrhosis.
- G-GT - gamma-glutamyl transferase is high due to hepatocytes damage.
- Blood count - normocytic anemia, caused by splenomegaly and hypersplenism
- Reticulocytes - bone marrow's attempt to retrieve lost red blood cells from the spleen.
Compensation of normocytic anemia
- Platelets - there is a lowering of the levels of coagulation factors in the liver with
consequent dysregulation of the coagulation system. Bone marrow activity in producing
red blood cells rather than platelets can also cause thrombocytopenia.

Given the pathology, what are the main parameters that helped in the diagnosis.
- nausea, vomiting,, and tender hepatomegaly; and extrahepatic symptoms and signs:,
spider angiomas,
- encephalopathy.
- Edema in the lower body
- Gynecomastia
- Abdominal dilation.

Describe cirrhotic liver.

- Cirrhosis is an irreversible distortion of normal liver architecture characterized by hepatic
injury, fibrosis, and nodular regeneration. The clinical presentations of cirrhosis are a
consequence of both progressive hepatocellular dysfunction and portal hypertension

What is the cause of this pathology?

Cirrhosis is usually a result of liver damage from conditions such as hepatitis B or C, or chronic
alcohol use.

Case nº24
Explain the pathophysiology of the patient, relating it to the symptoms.

Cholecystitis consists of inflammation of the gallbladder, due to obstruction of the cystic or

common
hepatic ducts by gallstones. Infection by bacterial growth (E. coli) may occur.
The edema obstructs bile flow and chemically irritates the gallbladder, causing cell necrosis,
while the exudate covers the ulcerated areas with formation of adhesions to surrounding
structures.
The most common gallstones are cholesterol and pigmentary, the latter consisting of calcium
bilirubinate.

What does fever indicate in this pathology?

Inflammation –fever, pathophysiological mechanism of destruction, inflammation and tissue
necrosis leads to the release of pyrogens endogenous (IL-1) by leukocytes

Explain lab results.

Total bilirubin - high - caused by poor blood filtration in the liver resulting from portosystemic
shunt caused by portal hypertension.
Direct bilirubin - High
AST - High - caused by destruction of hepatocytes
ALT - High - caused by destruction of hepatocytes
Alkaline phosphatase - high
Leukocytes - high
What are the complications of pathology?
In 70% of the cases patients are asymptomatic.
- muscle hypertrophy and gallbladder wall thickening
- Greater predisposition to carcinoma in women over 70 years old – poor prognosis
- such inflammation and infection can lead to necrosis of the gallbladder and sepsis.
- If a gallstone becomes lodged in the common bile duct, it can cause obstructive
jaundice with an elevation in serum bilirubin levels.

What is the cause of the pathology ?