• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/22

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

22 Cards in this Set

  • Front
  • Back
Two Most Important Causes of Acute Pancreatitis
Alcoholism or Gallstones
(others include blunt trauma, surgery process, medications etc)
Clinical Manifestations that show the function of the pancreas has been compromised by Cystic Fibrosis
Fatty & foul smelling stool due to decrease of fat absorption be cause of an ABSENCE OF LIPASE
Lab diagnostic test in a patient suffering from acute pancreatitis
1: Blood tests (serum amylase elevated w/in 24 hours and serum lipase w/in 72-96)
2:Urinanalysis (urin amylase levels elevated)
3: Radiographic examination (shows enlarged inflamed pancreas)
Disorders associated with pancreas deemed to be genetic in origin
Diabetes and Cystic Fibrosis
What causative agent is common to both acute and chronic pancreatitis
Alcohol
Clinical Manifestations diagnostic of acute pancreatitis
Symptoms: Abdominal pain, Nauseas, vomiting, fever & sweating, tachycardia, malaise, weakness, mild jaundice (if caused by bile stones)
Complications of acute pancreatitis
Peripheral vascular collapse (shock) From fluid sequestration in the pancreas, electrolyte imbalance, release of vasoactive substances
Adult acute respiratory distress syndrome (ARDS)
Acute renal failure
Hypocalcemia
Pancreatic pseudocysts (luiquifed collection of necrotic debris and pancreatic enzymes surrounded by a rim of pancreatic tissue)
Abscess or chemical or septic peritonitis
List the chemical manifestation that indicates the beta cells of the endocrine pancreas have been affected
Decrease in insulin production?
What clinical manifestations or physiological changes will explain polyuria?
Arise from the osmotic effects of hyperglycemia
Why the complains of polyphagia?
catabolism of fats and protiens used as alternatives sources of energy. Common in type I less in type II
Complications arising from the conversion of glucose to sorbitol.
Sorbitol > ^ osmolarity > influx of water > osmotic cell injury

Sorbital impairs ion pumps > injury to schwann cells > damage to peripheral nerve cells (peripheral neuropathy) and injury to pericytes of retinal capillaries > retinopathy
What complication arises because of the irreversable glycosylation of protiens ( give rise to the advanced glycation end products (AEG's)) In what way does this happen?
Small blood vessel damage.

Due to basement membrane becoming leaky and trapping nonglycosylated plasma and interstitial proteins which in turn trap LDL which increases deposition of cholesterol in intima of blood vessel. This is how arthersclerosis develops.
List the changes that occur in a diabetic patient that will most likely result in the patient going into a coma
beta cell destruction> Insulin Deficiency > Decreased tissue glucose utelization > Increased lipolysis > Ketogenesis > Ketacidosis > Coma

Also Hyperglycemia > Glycoseurea > Polyurea > severe volume depletion > if untreated = coma
List clinical manifestation that show that patient has switched from carb to non-carb source for energy
Urinalysis - glycosuria and ketonuria
Features common in those suffering from type I and type II Diabetes
polydypsia, polyphagia, polyurea

Glucose intolerance for both types
Glycosurea
ketonuria
Long term diabetic complications that involve damaging changes to structure of other tissues
Microangiopathy
Gangrene
Retinopathy: hemmorages, exudates, blindness
Nephropathy: glomerular disease, chronic renal failure
Peripheral Neuropathy: pain, numbness
Accelerated atherosclerosis: Stroke, myocardial infarct
1. List the causes of liver diseases.
Infections, drug and toxin induced disease, inborn errors of metabolism, intrahepatic biliary tract problems, circulatory disorders of the liver circulatory system, hepatic complications of organ or bone marrow transplantation, tumors and tumorous conditions, biliary tract diseases, gall bladder disorders.
Which liver diseases cause direct damage and which indirect?
Alcoholism (60-70%)
Infection by viruses, viral hepatitis (~10%)

Indirect:
Biliary disorders (5-10%) Common bile duct obstructions
Inborn errors of metabolism
- Hemochromatosis
- Copper overload
- Alpha antitrypsin
- Unknown
Which ones involve inflammation and which ones do not? Which one has the highest
number of cases?
Direct -Viral hepatitis and alcohol related liver diseases involve inflammation. Alcohol has the greatest incidence (60-70%).

Indirect – See Table p. 185
List the clinical manifestation of liver disease indicative of the following structural or
functional deficit:
blank
List the changes in structure that is characteristic of cirrhosis of the liver.
3 Main characteristics from book: bridging fibrous septa, parenchymal nodules containing replicating hepatocytes, disruption of architecture of entire liver.
Patterned fibrosis (scarring – formation of bands or broad septa) this is irreversible and seen as end stage of chronic liver disease.
This fibrosis gives rise to changes in the architecture of the liver that results in functional losses and generates clinical manifestations. These changes include
- disruption of parenchymal architecture of entire liver
- presence of regenerative nodules
- Disruption of vascular flow
- Formation of abnormal interconnections between inflow and outflow
List in the correct sequence the process that gives rise to ascites in liver disease.
Definition- collection of fluid in the peritoneal cavity