Pathophysiology Exam #5 Master Document PDF

**[Pathophysiology Exam \#5 Master Document]** This document should cover everything you need to know for the 5th Pathophysiology Exam! This document is subject to change when the exam blueprint gets released, as I remove content that is not important to know for the exam! That's it from me, the ac...

**[Pathophysiology Exam \#5 Master Document]** This document should cover everything you need to know for the 5th Pathophysiology Exam! This document is subject to change when the exam blueprint gets released, as I remove content that is not important to know for the exam! That's it from me, the actual content begins on the next page. Happy Studies! --- Seth Hacker **[Key:]** - **Green** = Big Topic (also similar to orange if it's under a subtopic!) - **Blue** = Subtopic - **Yellow** = Vocab and Important Concepts within Subtopics - **Orange** = Same as Yellow with Important Content Under It a. It helps me separate ideas out in a way that's easily readable b. **NOW BIGGER SUBTOPICS THAN BLUE BUT SMALLER THAN GREEN!** - **Red** = Specific examples/content that's probably not all that important a. **ALSO STATING WHAT IS IMPORTANT FOR THE EXAM!!** - **Gray** = Supplemental Info/ Info That was Stated Earlier! **[GI Disorders]** **inflammation:** - **Gastritis → Stomach Inflammation** - **Pancreatitis → Pancreas Inflammation** - **Inflammatory Bowel Disease (Crohn's and Ulcerative Colitis)** - **NOTE:** a. **Chronic Inflammation → INCREASES CANCER RISK** b. **Tissue Changes → INCREASES CANCER RISK** **Inflammation/Infection:** - **Hepatitis (Viral) → Liver Inflammation** **Stomach:** - **Functions of the stomach:** a. **Protection** - **Stomach acids → first line of defense (destroys harmful substances on contact)** - **Prostaglandins → Protection of the gastric mucosa** - **Gastric Mucosa → Highly vascular** a. **dependent on blood supply to support function.** b. **Alteration of blood flow → GASTRITIS** b. **Digestion** - **Food and liquids are mixed with gastric secretions in the lining of the stomach (epithelial tissue)** a. These secretions are composed of mucus, acid, enzymes, hormones and intrinsic factor (IF) c. **Absorption (mainly water and alcohol)** **ACUTE GASTRITIS: INFLAMMATION OF THE STOMACH LINING (Gastric Mucosa)** - **Acute Gastritis → Gastritis That Lasts A Short Period Of Time → Resolves When The Cause Is Removed** - **Causes:** a. **Aspirin** b. **Alcohol** c. Certain Microorganisms - **Symptoms:** a. **Abdominal Pain (Mild To Severe)** b. **Indigestion** c. **Loss Of Appetite (Anorexia)** d. **Nausea** e. **Vomiting** f. **Hiccups** - **Patho:** a. **Stomach → Lined By Tightly Connected Epithelial Cells (Protects Stomach From Gastric Acid)** - **Prostaglandins → Protects Gastric Mucosa (Via Stimulating A Mucus Barrier)** - **Gastric Mucosa Surface Barrier → Highly Vascular (Dependent On That Blood Supply To Support Function)** a. **NOTE: Alteration In Blood Flow → GASTRITIS!** b. **Stomach Exposed To Irritants → Gastric Mucosa Becomes More Vulnerable To The Acid → Inflammation (Ranges From Erythema To Erosions And Ulcerations (Perforations))** **CHRONIC GASTRITIS:** - **NOTE: Can lead to ulcers and gastric cancer** - **CAUSES:** a. **Unrelenting injury/insult** - **Chronic infection** - **autoimmunity** b. **Helicobacter pylori** - **Symptoms:** a. **Vague Epigastric discomfort (dyspepsia)** b. **nausea and heartburn** c. **NOTE: Most people are asymptomatic** - **PATHO:** a. **H. Pylori Neutralizes Gastric Acid And Produces Toxins → Destroys Gastric Mucosa!** **Pancreas: endocrine and exocrine gland** - **Endocrine Pancreas → PRODUCES INSULIN** - **Exocrine Pancreas → Produces Digestive Enzymes** a. **Produced By Acinar Cells → Packaged Into Zymogen Granules** - **Negative Feedback Loop → Production Of Enzymes Cease When Digestion Is Complete** b. **Responsible For Carbohydrate, Fat And Protein Metabolism** **Acute Pancreatitis: Acute Inflammation Of The Pancreas** - **Leads To Organ Dysfunction (And Systemic Multi-Organ Failure)** - **Causes:** a. **Duct Blockage By Gallstones** b. **Excessive Alcohol Use** - **Symptoms:** a. **Sudden Upper Abdomen Pain** - **Pain Can Radiate To The Back** b. **Nausea** c. **Vomiting** d. **Anorexia** e. **Diarrhea** - **Patho:** a. **Injury triggers blockage of enzymatic pathways → spills secretory enzymes → inflammation** b. **Response leads to:** - **increased vascular permeability** - **edema.** - **Hemorrhage** - **necrosis** - **granuloma** - **abscess formation** c. **NOTE: Recurrent acute pancreatitis can lead to necrosis and fibrosis** **Chronic Pancreatitis: Chronic Inflammation Of The Pancreas** - **Characterized By Irreversible Damage And Tissue Changes** - **Causes:** a. **Are Chronic Alcohol Use (60-70%) → MOST COMMON!!!** b. **Autoimmune** c. **Cystic fibrosis** d. Unknown Cause - **SYMPTOMS:** a. **Fibrotic Changes → HALLMARK SYMPTOM!!** b. **Abdominal Pain (Severe Intermittent Episodes)** c. **Diarrhea** d. **Steatorrhea (Fatty Stool)** e. **Weight Loss** - **PATHO:** a. **Alcohol Use → Obstruction Of Pancreatic Ducts (By Enzymes And Protein Accumulation) → Ischemia (This Is Compounded By Oxidative Stress From Alcohol Metabolism)** - **Autoimmune → Enlargement Of The Pancreas And Narrowing Of The Ducts** **Inflammatory Bowel Disease:** - **Chronic Inflammatory Processes** a. **Can Occur Anywhere Along The Gi Tract** - **Most Commonly Of Small And Large Intestine** - **MORE COMMON IN DEVELOPING COUNTRIES** - **INCREASED RISK FOR PEOPLE IN COLDER CLIMATES AND URBAN AREAS!** **Small Intestine → digestion and absorption** a. **PRIMARY ROLES:** - **Digestion:** a. **Villi → secreting enzymes** - **Absorption: In the intestinal mucosa** a. **Vitamins** b. **Minerals** c. **Fats** d. **Carbohydrates** e. **Proteins** f. **Water** g. **electrolytes (Na and K)** - **Lamina Propria → Houses Macrophages, Plasma Cells, And Lymphocytes** a. **Cells In These Areas → Specialized To Be Replaced Quickly If Damaged Or Injured** **Large Intestine → ABSORBS WATER AND ELECTROLYTES!!** - **No Villi!!!** - **Mucosa:** a. **Columnar Epithelial Cells** b. **Mucus-Secreting Cells** **Crohn\'s Disease → PATCHY INFLAMMATION (INFLAMMATION SKIPS SEGMENTS)** - **Chronic Inflammation In The Small Intestine** a. **Recurrent** b. **Characterized By A "Granulomatous Inflammatory Process"** - **Symptoms:** a. **Rapid Stool Transit Time → Food Comes In And Goes Out Quickly** b. **Intestinal Edema** c. **Fibrosis** d. **Fever** e. **Weight Loss** f. **Fatigue** g. **Non-Bloody Diarrhea (Not Always)** - **Patho:** a. **Chronic Inflammation Occurs In Patchy Segments (Called "Skip Lesions") → Penetrates All Layers Of The Intestine** b. **Inflammation Begins In Mucosa And Submucosa!** c. **Increased Permeability And Vascularity → Edema And Fibrosis.** d. **Macrophages, Plasma Cells, And Lymphocytes Are Released → Inflammation → Granulomas Develop To Wall Off Affected Areas** - **NOTE: SUBMUCOSAL LAYERS OF THE SMALL INTESTINE AND ASCENDING COLON → MOST COMMON LOCATION!** **Ulcerative Colitis → NON-PATCHY INFLAMMATION (DOES NOT SKIP SEGMENTS!)** - **Begins In The Distal Region Of The Rectum → Extends Up The Descending Colon** a. **Invades The Superficial Mucosa → Causes Friability → CAUSES BLEEDING** b. **NOTE: ULCERATIVE COLITIS DOES NOT SKIP ANY AREAS!!!** - **HIGHER RISK FOR COLORECTAL CANCER THAN PEOPLE WITH CROHN'S!!** - **Potential Complications:** a. **Obstruction** b. **Perforation** c. **Massive Hemorrhage** - **Symptoms:** a. **Diarrhea (often with rectal bleeding) → MOST COMMON SYMPTOM!!!** b. **Abdominal pain** c. **Fever** d. **Weakness** e. **Fatigue** f. **Anemia** **LIVER DISORDERS:** **Liver:** - **Roles:** a. **Bile secretion → HEPATOCYTES (FUNCTIONAL CELLS of the Liver)** - **Fat Emulsification and Absorption!** b. **DETOXIFICATION!! (REMOVES TOXINS FROM THE BODY!)** - **DAMAGE → NO TOXIN REMOVAL!** c. **Bilirubin metabolism** - **BILIRUBIN ACCUMULATION → JAUNDICE!** d. **Blood storage** - **BREAKS DOWN AND REMOVES ALL RED BLOOD CELLS → KUPFURR CELLS → SEPARATES HEMOGLOBIN INTO HEME AND GLOBIN → HEME BREAKS DOWN INTO AMINO ACIDS!** e. **Clotting factor synthesis** - **LIVER DISEASE → BLEEDING AND BRUISING** f. **Nutrient metabolism** g. **Mineral and vitamin storage** - **LIVER IS ENCAPSULATED BY THE GLISSON CAPSULE** - **Takes In All Of The Blood From Digestive Organs (So All Those Nutrients Pass Through The Liver)** - **LIVER DISEASE → PATIENT NEEDS SPECIFIC MEDICATION DOSE!** **Hepatitis (Viral) → Liver Inflammation Caused By Viral Infection** - **Types of Hepatitis:** a. **Hepatitis A:** - **Transmission: FECAL - ORAL ROUTE** - **Incubation Period: 1-2 MONTHS** - **Carrier State: NO** - **Chronic: YES** - **Vaccine: YES** b. **Hepatitis B:** - **Transmission: CONTACT WITH INFECTED BLOOD (AND BODY FLUIDS)** - **Incubation Period: 2-3 MONTHS** - **Carrier State: YES** - **Chronic: YES** - **Vaccine: YES** c. **Hepatitis C:** - **Transmission: CONTACT WITH INFECTED BLOOD** - **Incubation Period: 2-3 MONTHS** - **Carrier State: YES** - **Chronic: YES** - **Vaccine: NO** d. **Hepatitis D:** - **Transmission: CONTACT WITH INFECTED BLOOD (AND BODY FLUIDS)** - **Incubation Period: 2-3 MONTHS** - **Carrier State: YES** - **Chronic: YES** - **Vaccine: NO** e. **Hepatitis E:** - **Transmission: FECAL - ORAL ROUTE** - **Incubation Period: 1-2 MONTHS** - **Carrier State: NO** - **Chronic: NO** - **Vaccine: NO** - **Hepatitis Patho:** a. **Hepatitis Can Be Acute Or Chronic** b. **Level Of Damage Can Vary From Death Of A Few Hepatocytes To Massive Hepatic Necrosis** c. **Inflammatory Response Starts → Local Kupffer Cells Help Remove Necrotic Cells → Affected Hepatocytes Regenerate (Begins Within 48 Hours Of Hepatocyte Necrosis)** d. **Severe Infection → Fulminant Hepatitis (Hepatic Failure)** e. **Obstruction Can Occur In Liver Blood Vessels → Tissue Hypoxia!** - **Bile Flow Can Also Become Obstructed** - **HEPATITIS CLINICAL MANIFESTATIONS → 3 STAGES!!** 1. **Prodromal → Period Of Fatigue, Anorexia, Malaise, Headache, And Low-Grade Fever.** - **Usually Lasts About 2 Weeks.** 2. **Icterus: Onset Of Jaundice, Dark Urine, And Clay-Colored Stools (Liver Is Enlarged And Tender)** - **2 Weeks After Exposure To The Virus.** - **Lasts Approximately 2 To 6 Weeks.** 3. **Recovery → Resolution Of Jaundice** - **Around 8 Weeks After The Initial Exposure** - **Signs And Symptoms Improve** a. **Liver Remains Enlarged And Tender For An Additional 1 To 4 Weeks** - **NOTE: The only Treatment Mentioned By Dr. Ware was Low-fat diet!** **Altered Fluid-Balance** **Liver Cirrhosis → Local Blood Flow Interference And Hepatocyte Damage** - **Ascites (Fluid in Abdomen) → MOST COMMON COMPLICATION OF CIRRHOSIS!** a. Ascites→ Manifestation Of The Combination Of Hydrostatic Pressure, Colloid Osmotic Pressure, And Capillary Permeability - **SYMPTOMS:** a. **abdominal discomfort (Moderate to severe)** b. **Increased abdominal girth** c. **Increased weight** d. **Severe sodium retention** e. **Dilutional hyponatremia** f. **Renal failure (oliguria and increase in serum creatinine)** - **PATHO:** a. **Cirrhosis → Characterized By Local Blood Flow Interference And Hepatocyte Damage** **Alteration in Bowel Elimination:** **Production of Stool** - **Stool production:** a. **Large intestine → Final site for establishing water and electrolyte balance.** - **Small Intestine → Absorbs More Water** - **Large Intestine → Absorbs Higher Percentage of Water Than Small Intestine (But A Smaller Amount!)** b. **Stool includes approximately 100 to 200 mL of water.** c. **Movement of Fecal Matter:** - **Fecal matter moves from the cecum, via the ileocecal valve, toward the rectum for excretion.** d. **Water and Electrolyte Absorption:** - **large intestine → reabsorbs water and electrolytes from fecal matter** a. NOTE: Small intestine absorbs MORE water, but the Large Intestine absorbs a HIGHER PERCENTAGE of Water! - **Around 1 to 1.5 L of water entering daily** - **Stool → 100 to 200 mL of Water.** e. **Conversion of Chyme:** - Chyme → initially a semiliquid, becomes semi solid as it passes through the ascending and transverse large intestine segments. f. **Nutrient Absorption:** - **Small Intestine → Most Nutrient Absorption** - **Large Intestine → Absorbs Remaining Electrolytes (Sodium, Magnesium, And Chloride) And B Complex Vitamins And Vitamin K** a. **Note: B Complex Vitamins And Vitamin K → PRODUCED BY INTESTINAL BACTERIA!** g. **Dietary Fiber and Bacterial Byproducts:** - **intestinal bacteria → Breaks down Indigestible carbohydrates and dietary fiber → produces short-chain fatty acids → used by colon epithelial cells.** h. **Intestinal Flora → GUT BACTERIA!** - **Large Intestine → Has a LOT of anaerobic bacteria** - **anaerobic bacteria → essential for:** a. **breakdown of fiber** b. **production of vital byproducts** c. **maintain local homeostasis** d. **protect the intestine from harmful pathogens** i. **Tiny Note: Dr. Ware Noted This:** - **WHAT ABSORBS VITAMINS?** - **NOTE THE PASSAGE OF STOOL, KNOW WHERE THE MOST FLUID IS ABSORBED, AND WHERE THE OTHER COMPONENTS ARE BROKEN DOWN AND ABSORBED!!!**  **Stool Characteristics:** - **Color** - **Consistency** - **Amount** - **Frequency** - **NOTE: Multiple changes from infancy through adulthood** **Alteration in Motility:** - **Rate of motility → affects nutrition and electrolyte balance** - **The rate of motility → influenced by the intestinal flora (MICROORGANISMS)** - **Diarrhea and constipation → Most common clinical manifestations of altered motility** - **Foods affect transit time** **Alteration in Neuromuscular Function:** - **Coordination of neurologic and muscular functions is essential to optimal bowel function.** - **Impaired function from loss of propulsive activity → results from:** a. **Abdominal surgery** b. **Electrolyte imbalances → affects contractile function** c. **Peritonitis** d. **spinal trauma** - **Impaired motility → Side effect of narcotic analgesia.** - **Stress → alters stool elimination processes** - **Reduced activity → slows stool elimination** **Alteration in Perfusion:** - **No Oxygen → Hypoxia → Cell Death (Necrosis)** - **When GI Circulation is Impaired → Blood Flow is Prioritized in the Vital Organs** - **Alteration in Perfusion is Caused By:** a. **Infection** b. **Blockage** c. **Clot** d. **Obstructed Blood Flow** e. **Trauma** f. **Ulceration** g. **Etc.** - **Appendicitis → Infection!** a. **Caused By: Fecal Material Trapped In The Appendix.** b. **Obstruction Causes An Inflammatory Response → Infection!** c. **If Left Untreated, Appendix Rupture Is Likely To Occur** - **Upon Rupture → Bacteria Escapes Into The Peritoneal Cavity → Causes Peritonitis And Septic Shock!** - **Septic Shock → Reduced Perfusion To All Organ Systems (Especially The Gi Tract)** **Alteration in Patency:** - **Bowel Obstruction:** a. **Caused By:** - **space-occupying lesion** b. **Symptoms:** - **Changes in bowel sounds** - **Changes in stool color, consistency, etc.** - **Pain (visceral, somatic, referred)** - **Anorexia** - **Nausea/Vomiting** - **Fever** **[Genitourinary System]** **Kidneys:** - **Structure:** a. **Multi-lobular structure (composed of up to 18 lobes)** b. **Lobule → Composed of NEPHRONS (Functional Units Of The Kidney)** - **Location** a. **Outside the peritoneal cavity → back of the upper abdomen (retroperitoneal)** b. **Each Side of the 12th thoracic to 3rd lumbar vertebrae!** - **Glomerular Filtration Rate → Rate of How Fast the Glomerulus Filters Blood!** a. **NORMAL → 125 mL/Min!!** b. **\>90 mL/min → BAD!!!** **Renal (Kidney) System Functions: "A WET BED"** - **Acid-Base Balance** - **Water Balance** - **Electrolyte Balance** - **Toxin Removal** - **Blood Pressure Control:** a. **Renin (RAAS)** - **Erythropoietin (Hormone) → Tells Your Bone Marrow To Make Red Blood Cells!** - **Vitamin D Metabolism** a. **Kidneys Convert Vitamin D Into An Active Form Of Vitamin D** **Renin Angiotensin Aldosterone System (RAAS):** responds to kidney perfusion changes **(Raises BP WHEN IT DROPS!)** - **Blood Pressure DECREASES:** 1. Kidneys sense the DROP in BP 2. **Renin** is **released** 3. Renin **releases Angiotensin (IN THE LIVER)** 4. **Angiotensin turns into Angiotensin I** 5. **Angiotensin I turns into Angiotensin II** a. **Angiotensin II activates [Aldosterone]:** - Aldosterone Retains Water and Sodium - Aldosterone DROPS POTASSIUM (K)!!! - CAUSES SODIUM RETENTION - BLOOD PRESSURE RISES! b. **Angiotensin II causes Vasoconstriction:** - BLOOD PRESSURE RISES! **NOTE: ACE Inhibitors block RAAS** **Urine Production!** - **Nephron Function: reabsorb filtered nutrients, water and electrolytes and to secrete waste** a. **Filtration** (Water-Soluble Substances From the Blood): - OCCURS IN AFFERENT ARTERIOLE b. **Reabsorption** (Filtered Nutrients, Water, and Electrolytes) c. **Secretion** (Secretes Waste) **Bladder:** - **Detrusor Muscle → Contracts to Begin Urination!** a. **Made of Cuboidal Epithelium → Stretches When The Bladder Is Full!** - Bladder Walls are Mucosal!  **Altered Urinary Elimination:** - **Causes:** a. **Motility:** - **Stasis** - **Precipitation** b. **Neuromuscular:** - **Retention** - **Incontinence** c. **Perfusion:** - **Ischemia** d. **Patency:** - **Hydronephrosis: Swelling Of The Kidney Due To A Buildup Of Urine** a. When Urine Cannot Flow Out Of The Kidney Properly Because Of A Blockage - **Manifestations:** a. **Altered volume of urine** - **Oliguria → Almost No Urine** - **Anuria → No Urine** b. **Altered urine characteristics** - **Proteinuria → Increased Protein in Urine** - **Glycosuria → Increased Glucose in Urine** - **Pyuria → Pus In Urine** c. **Bleeding (hematuria)** d. **Pain (CVA → Costovertebral Angle)** e. **Distention** f. Anorexia g. Nausea h. Vomiting i. Fever **Urolithiasis (Kidney Stones):** - **Patho:** a. **Renal calculi → usually made of salts or inorganic/organic acids → precipitates out of urinary filtrate → Builds up to form a Kidney Stone!** - **Calcium (oxalate and phosphate) → most common component of Kidney Stones** - 3 Major Kinds of Stones: a. Struvite → Usually UTI Related b. Uric Acid → Increased Purines, Proteins, Gout c. Cystine → Leaks into the urine and forms crystals - **Symptoms:** a. **Pain!** - **Usually Flank Pain (Radiates From the Back to the Front)** b. **Hematuria** c. **Nausea/Vomiting** d. **Dysuria** e. **Urgency to Urinate** - **Causes:** a. **Dietary factors may predispose** b. **More Frequent in Males:** c. **history of urinary tract infection** d. **cystic kidney disease** e. **Diabetes** f. **Obesity** g. **Gout** h. **Hyperparathyroidism** i. **Gastric Bypass.** **Urinary Tract Infection (UTI)** - **Patho:** a. **UTI is an Acute Inflammatory Response:** - **Caused By Invading Bacteria (Attaching To Epithelium)** - **Makes Tissue Edematous (Swelled) And Hyperemic (Blood Filled)** b. **Urinary Tract is Usually Sterile → But Not When Patient has a UTI!** c. **Mechanical Obstructions And Catheters Can Also Lead To An Infection** - **Symptoms:** a. **Frequency, Urgency** b. **Burning With Urination** c. **Dysuria (Pain)** d. **Hematuria** e. **Some Purulent Discharge → Can Make Urine Look Cloudy** - **NOTE:** a. **Uti Can Occur Anywhere Along The Urinary Tract** b. **Ascending (Starts From The Bottom And Goes Up!)** c. **Most commonly caused by E. Coli!** **Acute Pyelonephritis → Sudden And Severe Infection Of The Kidneys** - **Patho:** a. **Results From Bacterial Infection Of The Renal Parenchyma (E. Coli)** - **Risk Factors:** a. **Urinary Obstruction** b. **Incomplete Bladder Emptying** c. **Frequent Intercourse** d. **STI's (Sexually Transmitted Infections)** e. **Pregnancy/Hormonal Changes** - **Symptoms:** a. **Usually Fever** b. **Costovertebral Angle Pain** c. **Nausea/Vomiting** d. **This Is In Addition To Uti Manifestations** e. **NOTE: May Range From Mild To Severe** **Renal (Kidney) Failure:** - **Causes:** a. **Diabetes Mellitus** b. **Hypertension** c. **Prerenal Insult → Before the Kidneys** - **Something Happens Before Your Kidneys To Cause Your Kidneys To Fail** d. **Intrarenal Insult → In the Kidneys** - **Medications That Cause Kidney Damage** - EX: CAT Scan Contrast Dye Can Damage Kidneys e. **Postrenal Insult → After the Kidneys** - **Backup Of Urine That Affects The Kidney's Ability To Function** a. **A** - **Symptoms → Related to Kidney Functions!** a. Edema b. Acidosis c. Hypertension d. Hyperthyroidism e. Coagulopathies → Problems With Blood Clotting (Too Much Or Not Enough Clotting!) f. Osteodystrophies → Bone Disorders g. Skin Disorders h. Heart Failure i. Pericarditis j. Sexual Dysfunction k. G.I. Manifestations l. Neurological Manifestations m. Anemia n. HyperKalemia o. Uremia p. Etc. - **NOTE: Occurs in STAGES! (That's all you need to know about that according to Dr. Ware)** A diagram of a chronic kidney failure Description automatically generated **Know about Perfusion and Inflammation!** **NOTE: YOU DON'T NEED TO KNOW DR. SOMMERALL'S SLIDES!!** **[Endocrine Disorders]** **Endocrine System → Glands that Makes and Release Hormones!** - **Hormones →** chemical messengers produced to target a specific cell a. **Types of Hormones: (WILL BE ON TEST)** - **Endo**crine **Hormone → Travels through the bloodstream to Affect distant cells.** - **Para**crine **Hormone → Affects nearby cells** - **Auto**crine **Hormone → Affects the same cells that produce them** **Positive Vs. Negative Feedback!** - **Positive Feedback → Pushes Response Further In The Same Direction** a. **Hormone Production Continues to INCREASE (amplifying response)** b. **Ex: Corticotropin Hormone → Causes Uterine Contraction!** - **Negative Feedback → Reduce or stabilize a response to maintain balance** a. **Hormone Production STOPS once Homeostasis Has Been Reached!** b. **Ex: Blood Glucose Levels → Causes Release of Insulin (If BG is TOO HIGH) or Glucagon (If BG is TOO LOW!)** **Classification of Endocrine Disorders:** - **Primary Disorder → Problem In The Target Gland (The Gland Producing The Hormone)** - **Secondary Disorder → Problem in the Pituitary** a. Note: Target gland is normal, but since the pituitary isn't releasing the proper amount of stimulating hormones or releasing factors, its function is altered - **Tertiary Disorder → Problem in the Hypothalamus** a. **Both The Pituitary And Target Organ Are Affected** **Naming of Endocrine Disorders** - **Hormone Excess → "Hyper\_\_\_ism"** - **Hormone Deficiency → "Hypo\_\_\_ism"** - **Hormone Resistance → "\_\_\_ Resistance"** **Categories of Disturbances of Endocrine Function:** - **Hypofunction →** Underproduction Of Hormone a. **Causes:** - Congenital defects - Disruption in blood flow - Autoimmune responses - Decline in function with aging - Atrophy as the result of drug therapy - **Hyperfunction** → Excessive Hormone Production a. **Causes:** - Excessive stimulation of the endocrine gland - Hormone-producing tumor of the gland **Pituitary Gland:** - **Anterior Pituitary:** a. **Follicle Stimulating Hormone (FSH)** - **Regulates Reproduction** b. **Luteinizing Hormone (LH)** - **Works with FSH in Reproduction** c. **Adrenocorticotropic Hormone (ACTH)** - **Stimulates Adrenal Glands To Release Hormones** d. **Thyroid Stimulating Hormone (TSH)** - **Stimulates Thyroid Gland To Release Hormones** - **Note: Hypothalamus Tells The Pituitary To Make TSH** e. **Prolactin** - **Milk Production** f. **Growth Hormone (GH →** Also Called Somatotropin) - **Important For Linear Bone Growth In Children** - **Stimulates Cells To Increase In Size And Divide More Rapidly** - **Increases The Metabolic Rate** - **Posterior Pituitary:** a. **Oxytocin** - **Uterine Contractions During Labor** b. **Antidiuretic Hormone (ADH) → Also Called Arginine Vasopressin (AVP)** - **INCREASES Vasoconstriction** - **DECREASES Peeing!** - **Note: Know These Hormones!!** **Pituitary Gland Disorders:** a. **Primary tumors → tumors in the gland** - Prolactinoma → Overproduction of Prolactin - Acromegaly → Overproduction of Growth Hormone - Cushing's disease → Overproduction of ACTH b. **Secondary tumors** - **Metastatic lesions** c. **Functional tumors** - **Secrete pituitary hormones** **Antidiuretic Hormone (ADH) Disorders:** - **ADH Deficiency Disease → Always peeing (No Off Switch)** a. **Called "Diabetes Insipidus"** - **ADH Excess Disease → Not Peeing AT ALL** a. **Called "Syndrome of Inappropriate Antidiuretic Hormone"** **Growth Hormone Disorders** - **Growth Hormone Deficiency:** a. **Patho:** - **Interferes With Linear Bone Growth** - **Results In Short Stature Or Dwarfism** - **NOTE: Fusion of the Epiphyseal Plates → We Can't Grow Taller Once This Happens!** b. **Diagnostics:** - **Serum IGF-1 (collected between 0000 -- 0200)** - **Insulin stimulation test:** a. **Decreased blood sugar stimulates release of GH** b. **If GH INCREASES → Test is normal (indicates GH reserve)** - **X-rays → Assesses Bone Age** - **MRI → Assesses For Hypothalamic-Pituitary Lesion** - **Growth Hormone Excess:** a. **Gigantism → BEFORE FUSION OF EPIPHYSEAL PLATES** - **Promotes increased linear bone growth → Rapid Growth** b. **Acromegaly → AFTER FUSION OF EPIPHYSEAL PLATES** - **Symptoms:** a. **Overgrowth of Skeletal Cartilage** b. **Heart (and other organ) Enlargement** c. **Altered fat metabolism** d. **Impaired glucose tolerance** e. **Prominent Chin and Jaw** f. **Large Hands** - **Causes:** g. **Adenoma (MOST COMMON CAUSE → 95%)** **Thyroid Gland Disorders:** a. **NOTE: T3 IS THE ACTIVE FORM OF THYROID HORMONE!** b. **Thyroid Hormone Functions:** - **INCREASES metabolism and protein synthesis** a. **Metabolic rate** b. **CardioVascular function** c. **Respiratory function** d. **GI function** - **Influences Growth And Development In Children** a. **Mental development** b. **Attainment of sexual maturity** c. **Diagnostics:** - **Thyroid auto-antibodies → Checks to ensure your body is making antibodies against thyroid hormones** - **Ultrasound → Looks at Thyroid** - **Assessing Hormone Levels → TSH, T3(Active Form), Free T4 Levels** d. **Primary Hypothyroidism:** - **Causes:** a. **Hashimoto Thyroiditis → MOST COMMON CAUSE** - **Autoimmune Disorder → Can Destroy the Thyroid** - **Note: Hashimoto Makes The Thyroid HOLD BACK** b. **Thyroidectomy** c. **Radiation Therapy → Destroys the Thyroid** d. **NOTE: PREDOMINANTLY WOMEN** - **Symptoms:** a. **Intolerant to Cold** b. **Constipation** c. **Lethargy** d. **Low Metabolism** e. **Anorexia** f. **INCREASED TSH** g. **DECREASED Serum T4** h. **Presence Of Antithyroid Antibodies** i. **NOTE: THAT'S ALL YOU NEED TO KNOW (ACCORDING TO Dr. Latimer!)** e. **Congenital Hypothyroidism (aka CRETONISM) → Congenital means You\'re Born With It** - **Note: Just Know It Exists!** f. **Hyperthyroidism → Over Activation Of The Thyroid Gland** - **Causes:** a. **Graves Disease** b. **Thyroid nodules** c. **Excessive Iodine intake** - **Symptoms:** a. **Intolerant to Heat** b. **Diarrhea** c. **GOITER** d. **High Metabolism (Patient will be THIN)** e. **BULGING EYES!! (COMMON IN GRAVES DISEASE!)** g. **Graves Disease → State of Hyperthyroidism** - **Patho:** a. **Autoimmune disorder that Stimulates the Thyroid!** b. **NOTE: Causes Goiter over Time!!** - **Diagnostics:** a. **Normal or decreased TSH with elevated T3 and T4** b. Familial Tendency is Evident - **Note: Graves Makes The Thyroid GO** **Adrenal Gland Disorders:** - **Steroid Hormones Produced by Adrenal Cortex:** a. **Mineralocorticoids (aldosterone)** - **Sodium Balance** - **Potassium Balance** - **Water Balance** b. **Glucocorticoids (Cortisol → stress hormone)** - **Regulates Metabolic Functions** - **Controls Inflammatory Response** c. **Adrenal sex hormones (androgens)** - **Mainly As Source Of Androgens For Women** - **Adrenal Cortical Insufficiency (HYPO):** a. **Addison Disease → HYPOCORTISOLISM (NOT ENOUGH CORTISOL!)** - **Patho:** a. **LOW CORTISOL (Stress Hormone)** b. **HIGH ACTH (Electrolyte Balance)** - **Causes:** a. **Autoimmune → Destroys Adrenal Cortex** b. Tuberculosis c. Metastatic Carcinoma d. Fungal Infections e. CMV infection - **Symptoms (KNOW THESE):** a. **Hypoglycemia** b. **Weight Loss** c. **GI Disturbances** d. **Muscle Weakness** e. **Hypotension** f. **Bronze Pigmentation of Skin** - **Note: This Disease is RARE!** b. **Cushing's Disease → HYPERCORTISOLISM (TOO MUCH CORTISOL!)** - **Causes:** a. **Benign Or Malignant Adrenal Tumor** - **Symptoms:** a. **Hyperglycemia** b. **Weight Gain (With Thin Arms and Legs)** c. **Abdominal and Neck Fat Depositions** - Called a Buffalo Hump **Pancreas (Cell Types and Functions):** - **Cell Types:** a. **Acini → Secretes Digestive Juices into the Duodenum** b. **Islets of Langerhans → Secretes Hormones into the Blood** - **Composed of: (MATCHING QUESTION!)** a. **Alpha Cells → Secretes Glucagon** b. **Beta Cells → Secretes Insulin** - **Insulin:** a. **Anabolic → BUILDS UP** b. **Lowers Blood Glucose Levels** c. **Promotes Glucose Uptake** - **Targets Cells → Provides For Glucose Storage As Glycogen!** c. **Delta Cells → Secretes Somatostatin** **Pancreas Gland Disorders:** - **Diabetes Mellitus:** a. **Types of Diabetes:** - **Type 1 Diabetes → insufficient PRODUCTION of insulin** a. **Most Common in Children!** b. **Most Commonly AUTOIMMUNE!** - STARTS TO DESTROY BETA CELLS - **Type 2 Diabetes → insufficient RESPONSE of insulin** a. **Most Common in Adults!** - **Mainly Obese or Overweight** b. **Insulin Resistant!** b. **Symptoms:** - **INCREASED BLOOD GLUCOSE!** a. **Polyuria → Excessive Urination** - Elevated Blood Glucose results in Glycosuria (Glucose in Pee) → accompanied by large losses of water in the urine! b. **Polydipsia → Excessive Thirst** - Polyuria causes intracellular dehydration (water is pulled out of the cells) → results in excess thirst (polydipsia) c. **Polyphagia → Excessive Hunger** - Results From Cellular Starvation - **NOTE: NOT SEEN IN TYPE 2 DIABETES!!** c. **Patho:** - **Blood Glucose Levels Are Elevated → Body Cells Are Starved** - **Breakdown Of Fat And Protein INCREASE → Generates Alternative Fuels** d. **Diagnostics:** - **Glycated Hemoglobin (A1C) Test → (\ - **ACCORDING TO DR. LATIMER: "I Will Give You Normal Ranges On The Exam, Cause I Will Ask You About Labs"** e. **Treatment:** - **Diet and Exercise** - **Exogenous Insulin** - **Oral Medications** a. Ex: Metformin - **Non-Insulin Injections** a. Ex: Ozempic f. **Diabetic Ketoacidosis (DKA) → LIFE THREATENING DM COMPLICATION** - **Patho:** a. **Body starts Breaking Down Fat Too Fast** b. **Fat is Processed into Energy → Produces Ketone Bodies as Waste** c. **Ketones are ACIDS → LOWERS BLOOD PH!** - **Note: Patients with DKA Will Begin To Hyperventilate → In an attempt to RAISE Blood PH**