Gastrointestinal, Neurologic, and Multi-System Disorders Flashcards

Fundamentals of Gastrointestinal Anatomy and Motility

• Gastrointestinal (GI) Structure: The GI tract consists of a continuous tube extending from the mouth to the anus, including the esophagus, stomach, small intestine (duodenum, jejunum, ileum), and large intestine (cecum, colon, rectum, anal canal). Accessory organs include the salivary glands, liver, gallbladder, and pancreas.
• Types of Movement:
  • Peristalsis: A propulsive movement characterized by a progressive wave of relaxation followed by a wave of contraction. This pushes the bolus or chyme forward through the tract.
  • Segmentation: Localized contractions of the circular muscle that mix chyme with digestive secretions, increasing the surface area for absorption without moving the content forward significantly.
• Nervous System Regulation:
  • Enteric Nervous System (ENS): Often called the "second brain," it is located within the walls of the GI tract (Auerbach’s/Myenteric plexus for motility and Meissner’s/Submucosal plexus for secretion). It functions independently but is modulated by the Autonomic Nervous System (ANS).
  • Parasympathetic Nervous System (PNS): Mediated primarily by the Vagus nerve, it increases GI motility and secretions (Rest and Digest).
  • Sympathetic Nervous System (SNS): Decreases GI motility and secretions while causing sphincter contraction (Fight or Flight).

GI Endocrinology and Immunity

• The Five Official GI Hormones:
  1. Gastrin: Produced by G cells in the antrum; stimulates gastric acid ($HCl$) secretion and mucosal growth.
  2. Secretin: Produced by S cells in the duodenum; stimulates pancreatic bicarbonate secretion to neutralize acidic chyme.
  3. Cholecystokinin (CCK): Produced by I cells; stimulates gallbladder contraction and pancreatic enzyme secretion; inhibits gastric emptying.
  4. Gastric Inhibitory Peptide (GIP): Produced by K cells; stimulates insulin release and inhibits gastric acid secretion.
  5. Motilin: Produced by M cells; initiates the Migrating Motor Complex (MMC) to clear the gut between meals.
• Peyer’s Patches and GALT: Peyer’s patches are organized lymphoid tissues in the ileum. They are a critical component of Gut-Associated Lymphoid Tissue (GALT), acting as an immune surveillance system that samples antigens from the intestinal lumen.
• Gut Microbiome: The normal flora consists of billions of bacteria that provide a barrier against pathogens, synthesize vitamins (Vitamin K and B12), and assist in the metabolism of bile acids and fiber.

Gastric Pathophysiology

• Gastroesophageal Reflux Disease (GERD): Occurs when the Lower Esophageal Sphincter (LES) becomes incompetent or relaxes inappropriately, allowing gastric contents to reflux into the esophagus, causing mucosal injury.
• Gastric Acid Secretion:
  • Parietal Cells: Responsible for secreting $HCl$ and Intrinsic Factor.
  • Pepsin: An enzyme derived from pepsinogen (secreted by Chief cells) that digests proteins; it is activated by low $pH$.
  • Gastrin: The primary hormone stimulating acid production.
• Phases of Gastric Acid Secretion:
  1. Cephalic Phase: Triggered by the thought, sight, or smell of food; mediated by the Vagus nerve.
  2. Gastric Phase: Triggered by stomach distension and the presence of amino acids; produces the highest volume of acid.
  3. Intestinal Phase: Triggered by chyme entering the duodenum; initially stimulatory but predominantly inhibitory to protect the small intestine.
• Protective Mechanisms: The stomach is protected by a mucus-bicarbonate barrier and tight epithelial junctions. Prostaglandins stimulate mucus production and blood flow.
• Peptic Ulcer Disease (PUD): The two primary causes are Helicobacter pylori infection and the chronic use of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs).

Hepatobiliary and Pancreatic Function

• Absorption in the Small Intestine: Maximized by a massive surface area created by circular folds (plicae circulares), villi, and microvilli (the brush border).
• Acute Pancreatitis: Physiologic causes include gallstones (obstructing the common bile duct) and alcohol consumption, leading to the premature activation of pancreatic enzymes (autodigestion).
• Celiac Disease: An autoimmune disorder where the ingestion of gluten leads to T-cell mediated destruction of the intestinal villi, resulting in malabsorption and diarrhea.
• Large Intestine: Major function is the absorption of water and electrolytes, as well as the storage and elimination of waste.
• IBD Differentiation:
  • Crohn's Disease: Can affect any part of the GI tract; involves transmural inflammation and "skip lesions."
  • Ulcerative Colitis: Limited to the colon and rectum; involves mucosal/submucosal inflammation and is continuous.
• Liver Blood Supply:
  • Hepatic Artery: Supplies oxygenated blood ($25\%$).
  • Portal Vein: Supplies nutrient-rich, deoxygenated blood from the GI tract ($75\%$).
• Bile Anatomy: Bile is produced by hepatocytes, stored and concentrated in the gallbladder, and released into the duodenum via the common bile duct to emulsify fats.
• Carbohydrate Metabolism:
  1. Glycogenesis: Creation of glycogen from glucose.
  2. Glycogenolysis: Breakdown of glycogen into glucose.
  3. Gluconeogenesis: Formation of glucose from non-carbohydrate sources (e.g., amino acids, lactate).
• Bilirubin Metabolism: RBC breakdown results in unconjugated (indirect) bilirubin, which is bound to albumin. In the liver, it is conjugated with glucuronic acid to become water-soluble (direct) bilirubin for excretion.
• Hepatitis Sources:
  • Hepatitis A: Fecal-oral route.
  • Hepatitis B & C: Blood-borne and sexual transmission.

Neurologic Foundations and Disorders

• White vs. Gray Matter: Gray matter contains cell bodies and dendrites (processing), while white matter contains myelinated axons (communication).
• Brain Lobes:
  • Frontal: Executive function, motor control, personality, and Broca’s area (speech production).
  • Parietal: Somatosensory processing and spatial orientation.
  • Temporal: Auditory processing, memory (Hippocampus), and Wernicke’s area (language comprehension).
  • Occipital: Visual processing.
• Meningeal Layers: Dura mater (outer), Arachnoid mater (middle), and Pia mater (inner).
• Limbic System: Includes the Hippocampus (memory) and Amygdala (emotion/fear).
• Neurophysiology:
  • Action Potential: Occurs when a neuron reaches a threshold ($\approx -55\,mV$), triggering an influx of $Na^+$ (depolarization) followed by an efflux of $K^+$ (repolarization).
  • Receptors: Ionotropic (fast, ligand-gated ion channels) and Metabotropic (slow, G-protein coupled).
  • Neurotransmitters:
    • Glutamate: Primary excitatory.
    • GABA: Primary inhibitory.
    • Serotonin: Mood and sleep regulation.
    • Acetylcholine (ACh): Vital for motor neurons at the neuromuscular junction.
    • Dopamine: Reward and motor coordination.
• Motor Neurons:
  • Upper Motor Neurons (UMN): Located in the brain/spinal cord. Injury leads to spasticity, hyperreflexia, and a positive Babinski sign.
  • Lower Motor Neurons (LMN): Travel from the spinal cord to the muscle. Injury leads to flaccidity, atrophy, and fasciculations.
• Neurologic Pathophysiology:
  • Parkinson’s: Loss of dopaminergic neurons in the substantia nigra; leads to tremors, bradykinesia, and rigidity.
  • Myasthenia Gravis: Autoimmune destruction of ACh receptors at the neuromuscular junction.
  • Multiple Sclerosis (MS): Demyelination of CNS axons.
  • ALS: Degeneration of both UMNs and LMNs.
  • Alzheimer’s 5 A’s: Amnesia, Aphasia, Agnosia, Apraxia, and Anomia.

Cell Biology, Genetics, and Muscle Contraction

• DNA Structure: A double helix composed of base pairs: Adenine-Thymine ($A-T$) and Cytosine-Guanine ($C-G$).
• Genetics:
  • Autosomes: 22 pairs of non-sex chromosomes.
  • Mitosis: Used by somatic cells for growth and repair. Phases: Prophase, Metaphase, Anaphase, Telophase.
  • Transcription: Occurs in the nucleus; DNA to mRNA.
  • Translation: Occurs in the cytoplasm (ribosomes); mRNA to protein using tRNA and rRNA.
• Muscle Contraction: The sarcolemma conducts action potentials; the sarcoplasmic reticulum stores calcium. Calcium binds to troponin, moving tropomyosin away from actin binding sites, allowing myosin heads to form cross-bridges.
• Cell Adaptation:
  • Atrophy: Decrease in size.
  • Hypertrophy: Increase in size.
  • Hyperplasia: Increase in cell number.
  • Metaplasia: Change in cell type.
  • Dysplasia: Deranged cell growth (pre-cancerous).

Hematology and Immunology

• RBC Indices: MCV (Mean Corpuscular Volume/size) and MCHC (Mean Corpuscular Hemoglobin Concentration/color).
• Hemoglobin: Composed of four subunits ($2\alpha, 2\beta$). Iron is central to the heme group for oxygen binding.
• Iron Metabolism: Iron is transported by transferrin and stored as ferritin. Iron deficiency anemia is characterized by microcytic, hypochromic RBCs.
• Hemostasis:
  • Primary: Platelet plug formation.
  • Secondary: Clotting cascade resulting in fibrin.
  • Intrinsic Pathway: Measured by aPTT.
  • Extrinsic Pathway: Measured by PT; Factor VII is activated first.
• Virchow’s Triad: Endothelial injury, Stasis of blood flow, and Hypercoagulability.
• Immune Cells:
  • Innate: Neutrophils (fast responders), Macrophages (phagocytosis), NK cells.
  • Adaptive: T-cells (cell-mediated) and B-cells (antibody-mediated).
  • MHC Classes: MHC I pairs with CD8 cells; MHC II pairs with CD4 cells.
• Antibodies: IgA (secretions), IgD (B-cell receptor), IgE (allergy/parasites), IgG (most abundant/crosses placenta), IgM (first produced).

Cardiovascular and Pulmonary Pathophysiology

• Atherosclerosis: Endothelial injury allows LDL to enter the vessel wall, where it is oxidized and engulfed by macrophages to become foam cells, eventually forming an atheroma.
• Heart Failure: Classified by Ejection Fraction (HFrEF vs. HFpEF). Left-sided failure leads to pulmonary edema; right-sided failure leads to peripheral edema.
• Lung Function:
  • Compliance: Ease of lung expansion ($\Delta V / \Delta P$).
  • Elastance: Ability of lung to recoil.
  • Surfactant: Produced by Type II alveolar cells to reduce surface tension and prevent collapse.
• Oxyhemoglobin Dissociation Curve:
  • Right Shift: Facilitates oxygen unloading ($\uparrow$ Temp, $\uparrow$ $CO_2$, $\downarrow$ $pH$).
  • Left Shift: Increases oxygen affinity ($\downarrow$ Temp, $\downarrow$ $CO_2$, $\uparrow$ $pH$).

Renal and Endocrine Disorders

• Glomerular Filtration Rate (GFR): Estimated using creatinine clearance. Controlled by hydrostatic pressure and the myogenic/tubuloglomerular feedback loops.
• Hormone Signaling:
  • Lipid Soluble: Can cross the cell membrane; act on intracellular receptors (e.g., steroids).
  • Water Soluble: Require secondary messengers (e.g., insulin).
• Pituitary Gland:
  • Anterior: GH, TSH, ACTH, FSH, LH, Prolactin.
  • Posterior: Oxytocin and ADH (produced in hypothalamus, stored in posterior pituitary).
• SIADH: Excessive ADH leads to water retention and hyponatremia.
• Hypothyroidism: High TSH, low T3/T4 (if primary). Symptoms: weight gain, cold intolerance, fatigue.