THIS IS NOT AN ACTUAL PATIENT BASED CASE PRESENTATION. MADE BY ME... HEHEHEHE... FROM PPTS CDO...BATCH 2Full description
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When you are healthy, your body has over a trillion cells that divide at standard rate and pace. When you develop cancer your normal cells turn into cancer cells. Cancer cells have different…Full description
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This is a pathophysiology of acute gastroenteritis. It is not that specific but you can use this as a guide.Full description
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Excess Hypothalamic Secretion Hypersecreting Thyroid Tumor Hypothalamus Pituitary Gland Excess Pituitary Secretion Thyroid Gland Presence of TSI Excess THYROID HORMONE • T3 • T4 Hyperm…Full description
Pathophysiology of cholelithiasisFull description
Pathophysiology Increased blood glucose Absolute lack of insulin
level: more than 250 mg/dL
Transport of glucose to cells is impossible
Fat breakdown (lipolysis) Protein breakdown
as source of fuel for cells
for fuelling cells
Release of ketones as byDecreased glucose levels
Transport impossible;
inside the cell
glucose stays in the
product
bloodstream Increased ketones in the blood Cell hunger/ (-) ATP inside cells
Cell hunger/ (-) ATP inside cells DIABETIC KETOACIDOSIS
Stimulation of hypothalamus (hunger center)
Acetone breath
Lungs compensate through increasing exhalation of CO2
Kidney corrects metabolic acidosis
More breakdown of carbohydrates into glucose Kussmaul’s respiration –
deep, rapid breathing
Ketonuria - Increased excretion of ketones in
No insulin to transport glucose into cells; increase serum glucose level