Pathophysiology Oral Topics Flashcards
Cellular Phase of Acute Inflammation
It involes the delivery of leukocytes, mainly neutrophil, to the site of injury so they can use their host defence function. This phase is devided into margination, adhesion, transmigration, chemotaxis and phagocytosis.
First the leukocyte will marginate to the vessel surface. Then it will adhere to the surface and transmigrate from the vascular space to the extravascular space which is facilitated by complementary adhesion molecules such as selectins and integrins. After the extravasation, the neutrophil will undergo chemotaxis which is a process of guiding the transmigrated leukocytes to the site of cell injury.
Pathophysiology of Cardiac Insufficiency
- Definition of Heart Failure
- Causes of Heart Failure
- Forms of Heart Failure
- Symptoms of Heart Failure
Pathophysiological compensatory mechanisms in heart failure
- Increases in left ventricular volume and pressure
- Ventricular remodeling
- Neurohormonal activation
What are the different type of hyperlipidemias in Fredrickson/WHO classification called?
Type I - Familial lipoprotein lipase deficiency
Type IIA - Familial hypercholesterolemia
Type IIB - Familial hyperbetalipoproteinemia
Type III - Familial dysbetalipoproteinemia
Type IV - Familial combined hyperlipidemia
Type V - Mixed hyperlipoproteinemia
Myocardial stunning
Refers to a prolonged period (hours, days) of reversible myocardial dysfunction after an ishemic event.
Hibernation
Occurs in the setting of chronic ischemia when oxygen delivery is adequate to maintain myocardial viability but inadequate to maintain normal function. The clinical importance of the hibernating states is that restoration of blood flow to the involved myocardium results in improved mechanical function
Regional myocardial hypoxia causes
Anaerobic glycolysis, lactate production, intracellular acidosis, and disordered calcium homeostasis. These intracellular changes induce abnormalities in myocardial relaxation, leading to reduced compliance and contraction, which cause regional wall abnormalities. Finally, ECG evidence of ischemia occurs, and angina pectoris ensues.
The size and pattern of an infarct depends on
- Location and extent of occlusion
- Amount of heart tisse supplied by the vessel
- Duration of the occlusion
- Metabolic needs of the affected tissue
- Extent of collateral circulation
- Heart rate, blood pressure, and cardiac rhythm
Arrhytmias are generally produced by one of three mechanisms
Enhanced automaticity
Triggered activity
Reentry
Delayed afterdepolarizations (DADs)
The presence of increased Calcium in the sarcoplasmic reticulum and cytosol leads to induction of DADs
Digitalis toxicity, catecholamines and reperfusion ventricular tachycardia (ischemia) can lead to increased calcium –> Thus, the formation of DADs
Early afterdepolarizations (EADs)
Arise from action potential prolongation and reactivation of depolarizing currents.
Hypokalemia, Hypomagnesemia, Bradycardia and drugs can predispose to generation of EADs.
Arrhythmias from abnormal automaticity
Sinus bradycardia
Sinus tachycardia
Atrial tachycardia
Ventricular fibrillation
Arrhythmias from triggered automaticity
Due to EADs:
Polymorphic ventricular tachycardia
Atrial tachycardia
Torsades de pointes
Arrhythmias from reentry
AVNRT AVRT Atrial fibrillation Atrial flutter Ventricular fibrillation
Most common complications of PUD
Hemorrhage
Perforation
Penetration
Gastric outlet obstruction
Four major causes of chronic diarrhea
Presence of hyperosmotic luminal contents
Increased intestinal secretory processes
Inflammatory conditions, and infectious processes
Factitious diarrhea
What is ulcerative proctitis, proctosigmoiditis, and pancolitis
It’s the length of lesion in ulcerative colitis. Ulcerative proctitis involve the rectum alone, proctosigmoiditis involves the rectum and sigmoid colon and pancolitis involves the entire colon.
Three factors that contribute to the formation of gallstones
Abnormalities in the composition of bile
Stasis of blie
Inflammation of the gallbladder
Causes of Ascites
Cirrhosis Portal hypertension Right-sided heart failure Nephrotic syndrome Hypoalbuminemia
GERD complications
Strictures of the esophagus
Barret’s esophagus
Hemorrhage
Erosive esophagitis
Release of Kallikrein and Chymotrypsin results in
increased capillary membrane permeability, leading to the leakage of fluid into the interstitum and development of edema and relative hypovolemia.
Release of Elastase results in
leads to dissolution of the elastic fibers of the blood vessels and cuts, leading to hemorrhage.
Release of Phospholipase A results in
in the presence of bile, destroys phospholipids of cell membranes causing severe pancreatic and adipose tissue necrosis.
Release of Lipase results in
flows into damaged tissue and is absorbed into systemic circulation, resulting in fat necrosis of the pancreas and surrounding tissue.
