Patho Final Exam - Past Paper

Summary

This document is a past paper covering the gastrointestinal (GI) system and its accessory organs. It details four major functions of the GI system and various functions of the liver, pancreas, gallbladder, and stomach. It also explores small intestine section (duodenum and jejunum).

Full Transcript

Patho Final Exam ================ 19 GI 18 Neuro 13 Endocrine 5 Repro GI System --------- ### Four major functions - Digestion - Absorption nutrient - Secretion of hormones - Defense against pathogens (microbiome) Structural or neuro abnormality can obstruct or slow movement, loca...

Patho Final Exam ================ 19 GI 18 Neuro 13 Endocrine 5 Repro GI System --------- ### Four major functions - Digestion - Absorption nutrient - Secretion of hormones - Defense against pathogens (microbiome) Structural or neuro abnormality can obstruct or slow movement, local and systemic symptoms ### Accessory Organs - **Liver**- produce bile and metabolizes nutrients - Nutrients absorbed in the small intestine are transported to the liver via the portal vein where they are processed and transported into systemic circulation - Deamination/Transamination (metabolism) - Protein synthesis - Albumin - Complement - Hormones - Clotting Factors - Plasma Protein Carriers - Urea production and excretion - Bile Production - Bile produced in the liver is transported in the hepatic duct into the duodenum for lipid metabolism - Carbohydrate metabolism - Produce lipids, phospholipids, and cholesterol - Kupffer cells= specialized macrophages - **Pancreas**- major digestive enzymes synth within pancreatic acini, stored in secretory granules and stimulated by CCK. (problems with CCK will affect this enzymes) - Proteases **trypsin** and **chymotrypsin**: break down proteins to peptides and further to amino acids - **Amylase**---digests **starches**, synthesized and secreted from **salivary glands, pancreas and colon** - **Lipase**-- **digests TGs** into monoglycerides and free fatty acids for absorption into the bloodstream; release by pancreas - Insulin and glucagon - **Gallbladder**- stores and concentrates bile ### Stomach \* - Secrete Acid and Enzymes - Kill bacteria - Begin digestion - Storage - Above cardia, the fundus "accommodates" food bolus - Expands due to sight and smell of food - Adaptive relaxation due to the volume of food - Mixing - Digestion initiated in the body via pepsin and - Gastrin- secreted in response to distention stimulates acid secretion by patriatel cells, - Emptying - Pylorus- where **chyme** is propelled - Placing the G tube past the pyloric sphincter to reduce aspiration risk Small Intestine \*= Extends from **ligament of Treitz** = used to define upper and lower GI bleed - **[Duodenum]** -- begins by pyloric valve (25 centimeters) - Mixes chyme with bicarb, mucus and lipases - "sluggish" movement to allow for majority of DIGESTION - **Ampulla of vater** -- reservoir for pancreatic and hepatic bile ducts meet, entrance of the digestive enzymes from the liver, pancreas and gallbladder into the duodenum - **Sphincter of Oddi**- controls release of enzymes through ampulla of vater - prevents reflux of pancreatic enzymes, - Regulation of bile flow/ Prevention of reflux of pancreatic enzymes - Promotion of gallbladder filling - **Motilin** - **Secretion**- produced by the S cells of the duodenal mucosa, released when pH of duodenum is low, stimulates the secretion of bi-carb and water - Optimized pH for pancreatic enzyme action - **CCK**- released 30 min after meal to inhibit gastric emptying, relaxes sphincter of oddi to allow for digestion. - Duodenal ulcers occur here (in superior, posterior wall)- caused by H. Pylori - **[Jejunum]** - primarily responsible for ABSORBTION of carbs, lipids and proteins - **most functional** division of the small intestine, completes digestions**, primarily responsible for absorption** of simplified nutrients - Bile salts and pancreatic enzymes complete digestion - 2.5 meters long, with enterocytes with microvilli and goblet cells (protect mucosa and lubricate and aid removal of pathogens). - Ilium - **final absorption** stage, absorbs B12, bile salts and other nutrients; passes waste product of digestion and particles into the large intestine - **Absorbs B12**, **bile salts** and other nutrients - **Ileocecal valve** - Gastrin moves chyme along - Colon - stores and moves stool, **reabsorbs water**, expels stool out of the body Constipation = fewer than 3 poops per week - Caused by many factors, not entirely understood - Opioid induced (delays motility, and increased water absorb---hardened stool) - Primary/idiopathic= Diagnosis of exclusion - Reduced mobility - Neurological causes - Hirschsprung's disease - Withholding - Severe constipation can lead to bowel perforationperitonitis (shock, death etc) - Symptoms- n/v, cramping, colicky pain, overflow diarrhea (flows around impaction) - Management - Bulk forming lax - Stim lax - Osmotic lax - Fecal softeners Diarrhea: 3 or more loose stool in 24 hours - Acute- from infectious agent or medications - Chronic - **Osmotic** -- large vol of stool, draws excess of fluid into bowel (undigested substances draw water in the colon). - Will cease with fasting - **Secretory**- produces large vol due to mucosal secretions of excess chloride or bicarbonate (which also pulls moisture in the lumen) - Most common with enterotoxins - **Motility diarrhea**- cause by decreased transit time (fast moving flow) = moves through without being well digested. - **C.Diff** (g+): fecal oral, produces toxins A & B - Antibiotics will allow overgrowth - Oral vanco, Fidaxomicin (Dificid), IV metronidazole - Bezlotoxumab (Zinplava) or fecal transplant - IV fluids and electrolytes - Watch for dehydration and electolye imbalance and metabolic acidosis - hypoNa - Hypo K - Ulcerative Colitis - Irritable bowel Gi bleed: breakdown of mucosa, exposure of submucosa and vessels to HCL - Upper GI more common = also more lethal - Manifestation of Upper GI Bleed - **Melena (black tarry stools)- upper gi bleed** - **Hematemesis (bloody vomit)** - Hypovolemia - Shock - Elevated BUN (esp out of proportion to CR) - Aspiration pneumonitis - Diagnosis - Barium swallow- upper - When Upper GIB occurs blood is digested to protein, protein then is transported to the liver and metabolized. **Higher BUN levels can be associated with digestion of blood.** - BUN: measure of urea nitrogen in blood, represents terminal products of protein metabolism via ammonia. - Tx - Blood trans - Fluid resuscitation - Source control - Iron repletion - Causes - Oropharyngeal- usually a tumor or - Inflammatory esophagitis (MOST COMMONLY caused by GERD or RADIATION) - Chest pain and dysphagia - Barrett's esophagus= bleeding from discrete ulcerations (silent or non-silent reflux) - Varices= venous bleeds from **portal hypertension\*** - **High pressure in surrounding venous system (high hydrostatic pressure)** - Coughing can open up - Uncompensated cirrhosis - Mallory Weis tears= tear due to vomiting/retching - Superficial laceration - Erosive gastritis - Angiodysplasia= elastic dilation and thinning of vessel wals - Lower GI Bleeds - Manifestation of Upper GI Bleed - **Hematochezia (blood in stool)** - **Coffee ground emesis** - Causes - Polyps - Ulcerative colitis - Hemorrhoids - Aorto-enteric fistula - Malignancies - Diagnosis of bleeds - Occult blood - CT/MRI/x-ray- less helpful - Endoscopy/ Colonoscopy= USUAL method - Capsule endoscopy- for small bowel bleed - Barium enema- lower Bowel Obstruction- partial or complete fail of food to move (sm\>large): Obstruction causes dilation proximal and collapses distally=\> emesis (can be feculent (continuing stool) - Mechanical - **[Paralytic ileus]** (pseudo-obstruction) is a functional obstruction without structural abnormality, pseudo bowel obstruction caused without structural abnormalities in which there is partial or total loss of peristalsis of the intestine - Causes - Narcotics - Hypokalemia - Surgery/trauma - Peritonitis - Spinal cord injury - Pneumonia - Neuropathies/myopathies - **Ogilvie's syndrome**- colon distention of \>8cm - **TX** - Hydrate - Treat or exclude mechanical obstruction - Decompress with NG tube - **STOP OPIOIDS** - **[Herniation]** - may become strangulated though facial defects - Ischemia requires surgery to release strangulation - **[Adhesions]** - often occurs after surgery or trauma, creates traction or kinking of the bowel - Abdominal surgery =\> adhesions (scarring) of fibrous bands - **[Volvulus]**- twisting - **[Intussusception]** - inversion/telescoping, most commonly seen in children under 2 - Mgmt. - NG tube to decompress - Bowel rest (controversial) - Fluids/electrolytes - Chewing gum -- stimulates motility via cephalocaudal reflex - Neostigmine or Reglan to stimulate motility [(not recommended but still used)] **[Cholecystitis]** - Gallbladder becomes distended and inflamed, may cause ischemia, perforation, necrosis: most often associated with gallstones comprised of bilirubin, cholesterol or both. - **[Acute Cholecystitis]** typically involves obstruction of flow of bile from GB to duodenum because of a stone which has descended into the cystic or common bile duct distended, inflamed - Symptoms include: - Fever - Leukocytosis - Rebound Tenderness - Guarding - **RUQ pain radiating to the [right shoulder.]** - Colicky as GB contraction after eating intensifies pain of the inflamed GB **[Pancreatitis]** - **[Chronic]** - Bile Duct (more common) or pancreatic duct obstruction - Acinar cell injury: trauma, ischemia, drugs/alcohol - **[Acute]** - Most commonly caused by alcohol abuse, occurs after repeated acute episodes **[Cirrhosis]**- chronic liver disease - Acute Liver Injury - Causes - Drugs - Viral - Pregnancy - Manifestations - Hyperbilirubinemia - Reduced coagulopathy - encephalopathy secondary to ammonia build up - Fulminant Liver Failure: occurs when \>90% of hepatocytes are damaged/necrosis - Liver can regenerate if treated before 90% of cells are lost - Acetaminophen Toxicity - Caused by **[depletion of glutathione stores]** - Treated with **N-Acetylcysteine** which repletes glutathione stores - MAX daily APAP dose is 4 grams - Chronic Liver Disease - Compensated (asymptomatic) - Uncompensated (symptomatic) - Causes - Viral (Hep B/C) - Drugs/Alcohol - NASH/MASH - Wilson's disease - Manifestations - Encephalopathy from hyperammonemia (Confusion, decreased level of consciousness) - Jaundice (yellow to green) - Scleral icterus - Portal Hypertension: causes increased resistance to flow and increased dilation of GI arteries = major cause of mortality - Increased resistance to flow, increased flow dilation by nitic oxide - Increased pressure in peritoneal capillaries - Portosystemic shunting of bloodvarices and hemorrhoids - caput medusae - ascites - space of Disse - Compounded by hypoalbuminemia - Splenomegalyactive pancytopenia due to sequestering blood cells - Spontaneous bacterial peritonitis - Increased Estrogen (can no longer be metabolized by liver) - Spider angioma - Palmar erythema - Gynecomastia - Coagulation disorders - Higher MELD (3 mo. mortality) = higher chance of mortality - **[Cirrhosis]**= fibrosis and nodule formation secondary to chronic injury - Parenchymal nodules ### Abdominal Pain - Acute vs chronic - Sharp, dull, colicky - Rule out spontaneous peritonitis= localized and intense - Visceral= diffuse and vague - Radiating= visceral felt in localized distal structure The Brain and CNS ----------------- - **[Neurons:]** primary cells of nervous system - **[Neuroglial Cells]**: structural cells, provide support, nutrition, protection - **Astrocytes, microglia cells, oligodendrocytes** in CNS - **Schwann** and **satellite cells** in PNS - **[Nerve Fiber]**: any extension from cell body, either dendrite or axon - Cell Bodies - Dendrites - extensions of the cell body that carry *[impulses toward]* the cell body: **chemical messages are translated into electrical events for the cell body** - Axons - long conductive projections from cell bodies that carry *[impulses away]* from the cell body: Electrical messages are passed from dendrite to cell body to the **axon hillock which is where an action potential arises** - *\*\*Most nerves are mixed, containing both sensory and motor fibers, but can also be purely sensory or motor nerves.* **Impulse transmission is unidirectional** - Afferent nerve fibers - Efferent nerve fibers - **[Myelination]** allows for **saltatory conduction**, less axon membrane required for depolarization, impulse can skip node to node. Less ATP expended - Nerve impulses transmission along myelinated nerves of white matter are quicker and more energy efficient - **[Synapses:]** neuronal communication across a [chemical synapse] by way of secretion and diffusion of neurotransmitters - Acetylcholine (Both in CNS and PNS) is the most common neurotransmitter, which can attach to either stimulatory or inhibitory receptors in the post synaptic cell - PNS: activation of skeletal muscles via neuromuscular junction, stimulates muscle contractions - Norepinephrine is found primarily in the sympathetic nervous system; modulates the activity of neurons in SNS (fight/flight) and helps regulate - HR (contractility) - BP (vasoconstriction of smooth muscle cells of vessel walls) - Glutamine released from presynaptic neuron, taken up from and recycled by astrocytes then converted into: - Glutamate: excitatory neurotransmitter - GABA: inhibitory neurotransmitter - **[Action potentials/Impulses:]** momentary reversal to a more positive potential (when impulse occurs) - [Resting potential]- electrical potential that is not stimulated (-70 at rest) - [Depolarization]: reversal of resting state, cell is stimulated - Potential across the membrane becomes more positive (K and Na switch positions) - Action triggers the release of neurotransmitters - EXAMPLE: - Action potential travels to terminal end of presynaptic neuron, causes in influx of calcium which then releases acetylcholine - In a muscle cell, nicotinic post synaptic receptors receive the acetylcholine ion channel open depolarization \--\> action potential in muscle cell muscle contraction - [Repolarization]: makes it's way back to resting potential ### Brain and spinal cord anatomy [Divisions] - [CNS ] - [Peripheral] - [Autonomic] - Sympathetic - Parasympathetic - [Somatic] - Sensory (afferent) - Motor (efferent) [Regions/ Lobes] - Cerebrum/ Telencephalon - Prefrontal/frontal -- executive functioning/ reasoning/ problem solving (last part to mature -24y) - Precentral gyrus: primary motor area - **Broca's Area**: expressive language (expressive aphasia) - Parietal -- **processing sensory input/ language**/ analytics/ numbers - Postcentral gyrus: primary somatic area - Temporal -- **hippocampus (long term memory)**/ amygdala (emotional center) - **Wernicke's area:** understanding language/ receptive aphasia - Occipital -- visual processing - Cerebellum -- Higher learning, math, music, social skills, - Brainstem -- breathing, LOC - Pons - Meninges - protective covering - Pia - Arachnoid - Dura **CSF**- produced in ventricles by ependymal cells of choroid plexus, **clear, odorless fluid** - Buoyancy to cushion brain - 125-150cc - Flow is a result of a pressure gradient between arterial system (specifics of flow not needed), absorbed by arachnoid villi into venous system (one way valve system) - Flow stops below \ 40 infants, CPP\>60 in adults) - Monroe-Kellie Doctrine: fixed volume in brain, blood and CSF, if one increases the others will decrease - Brain 80% - Blood 10% - ICF 10% - Interventions - Gravity (sit up patient) - Craniectomy (remove bone flap, ipsilateral to infarction to allow outward herniation) - Ventricular drains - Increases above 15mmHg - **[Brain:]** Can be due to tumor, Encephalitis, hematoma, edema, abscess, infection - **[Blood:]** Systemic hypertension, increased arterial flow, decreased venous drainage, increased central venous pressure (in HF) - **[CSF:]** Hydrocephalus from increased production, obstruction of flow - Cerebral edema: Accumulation of fluid increases pressure - Types (don't need to know but could be helpful) - Vasogenic - Cytotoxic - Interstitial - Osmotic - Cerebral autoregulation - Stage 1: vasoconstriction to decrease blood flow when MAP increased/ vasodilate to increase when MAP too low - Stage 2: ICP too high to compensate with constriction/dilation - Stage 3: ICP equal to arterial pressure ischemia (autoregulation fails) - Stage 4: brain will herniateobstructive hydrocephalus, crush the brainstem - S/s - Headache, n/v - Dipolpia, pupillary dilation/sluggish response - Ipsilateral pupillary dilation - Exaggerated deep tendon reflexes - Seizures - Cushing's triad (bradycardia, wide pulse pressure (hypertension), irregular respirations - Change in LOC - Distended scalp veins, setting sun sign, high pitch cry bulging fontanel (infants) - Tx - External ventricular drain to reduce hydrocephalus (remove CFS) - Mannitol - 3% saline - Elevate head of bed - ABC (airway, breathing.. ) - If intubated, set to hyperventilation to allow move out CO2 to reduce dilation of cerebral arteries (short term intervention that reduces pressure but limits blood flow) - Non-contrast CT - Get repeat scans to review risk of expansion - Watch for swelling - May want to do a CTA - Check PTT/INR - Check blood pressure to reduce to \ 60 ### Spinal Cord - The spinal cord is about the diameter of a human finger - The cord is surrounded by clear CSF which cushions it from the bony vertebrae that surround it; The central canal is continuous with the ventricular system and receives CSF that then flows into the subarachnoid space. - **Pathways or tracts of nerves may ascend the cord to bring sensory information to the postcentral gyrus or descend the cord to carry motor action potentials from the precentral gyrus to peripheral nerves & ultimately effector glands & muscles.** - Afferent Nerve Fibers: carry information to CNS - Receive sensory information from PNS and ascent the tract to carry information to the post central gyrus for interpretation - Generally dorsal/posterior - **[Dorsal Column Tracts:]** highly myelinated localized sensation, ascends spinal cord on same side crosses at medulla oblongata - **[Spinothalamic Tracts:]** less myelinated, less localized, crosses over immediately to opposite side ascent of cord - - Efferent (Motor): carry information away from CNS - **Pyramidal or corticospinal tracts** that originate in the precentral gyrus, descend through thalamus, brainstem, and cord to synapse with lower motor neurons in anterior horn grey matter of cord - Lower motor neurons are the final common pathway for all motor impulses to travel in order to reach effector organs/muscles - **Damage to LMN innervating specific muscle will result in flaccid paralysis of that muscle** - Upper motor neurons descend the cord to allow the brain to control many spinal reflexes. They connect to lower motor neurons which are the motor arms of reflex arcs - **Damage to an upper motor neuron result in spastic paralysis as the reflex arc continues to function, but functions without higher brain control** ### Autonomic Nervous System - **[Enteric Nervous System]** -- A system of afferent neurons, interneurons, & motor neurons that form plexuses (networks of neurons), that surround the GI tract. - **[Sympathetic Nervous System]** -- Coordinates the visceral response in during stress - **[Parasympathetic Nervous System]** -- Coordinates the visceral response during rest. - The [afferent nerve fibers of the ANS] carry sensory impulses from the vessels, heart, & all of the organs in the chest, abdomen, & pelvis to the CNS (mainly to the pons, medulla, & hypothalamus for processing) - Controls involuntary responses such as heart rate, respiratory rate, & temperature so that an organism can respond to changes in its environment as well as to stressful situations. - Without the ANS, organs would function but would not have the ability to adapt responses to changes in environment. - Most afferent input does not reach consciousness, instead, reflex responses occur as a result of impulses reaching the brainstem and then exiting the CNS via efferent nerve fibers, to reach the effector organ - Alpha 1 - Vasoconstriction - increased peripheral resistance - increased blood pressure - Mydriasis - Increased closure of the bladder sphincter - Alpha 2 - Inhibition of NE release - Inhibition of ACH release - Inhibition of Insulin - Beta 1 - Tachycardia - Increased Lipolysis - Increased myocardial contractility - Increased release of renin (RAAS) - Beta 2 - Vasodilation - Slightly decreased peripheral resistance - Bronchodilation - Increased glycogenolysis (liver and muscle) - Increased release of glucagon - Relaxed uterine smooth muscle - **Norepinephrine** **alpha1 \> beta 1 \> beta 2** - **Epinephrine strongly stimulates all four types of receptors**. **Awareness:** refers to the subjective experience, such as perceiving a blue triangle vs a red square, the ability to follow commands **Arousal:** overall state of alertness (or wakefulness), indicated by opening the eyes - **Structural alterations** can be supratentorial, infratentorial, subdural, or extracerebral (encephalitis, tumors, closed head injury, herniation, cerebral infarction or hemorrhage, demyelinating diseases, abscesses). - **Metabolic alterations** involve an altered chemical environment within the brain (hypoxia, electrolyte imbalances, hypoglycemia, liver and renal failure). - **Psychogenic alterations** occur when one is physiologically awake yet appears unconscious (psychiatric disorders such as catatonia). - Evaluate level of consciousness, breathing patterns, pupils (CN III), oculocephalic reflex, oculovestibular reflex, purposeful motor responses/posturing. - **Pupillary changes could suggest increasing ICP due to cerebral edema (CT scan)** ### Cognitive Changes **Delerium**- sudden onset, infectious, metabolic, hemodynamic, respiratory, toxic, traumatic - EEG ALWAYS revels abnormally slow rhythm - Fidgety, agitated - Tx with antipsychotics **Dementia**- gradual - EEG appears normal - Sundowning - Tx with cholinesterase inhibitors (only offer transient slowing) - Beta amyloid plaques/tau protein/ ACTH loss - Shrinkage of cerebral cortex, hippocampus and enlarged ventricles - Neuron death and inflammation - Staged 1-7 1. normal 2. mild cognitive deficits 3. mild confusion (intentionally hidden often) noticed by family 4. inabilities to perform learned complex tasks (driving, balance checkbook) 5. requires assistance for daily living (meal planning, cooking, household management) 6. lacking awareness or memories of past/present, lose ADL 7. limited communication/feeding/thirst **Alzheimer\'s** - Extra-neuronal beta-amyloid protein plaques - Intraneuronal tau-protein neurofibrillary tangle - Acetylcholine deficit - All result in neuron death and inflammation, brain atrophy, particularly in cortex and hippocampus, evidence of enlargement of ventricles - Initially anticholinesterase agents were used to treat people, however they only over transient change - New treatments are looking to target critical steps in formation of plaques and tangles - Management currently involves environmental management, memory aids, and exercises to maintain current cognitive functions **Parkinsons** - Destruction of the dopamine producing neurons of the substantia nigra - Output of stimulation from the basal ganglia to the cortex is gradually lost - Loss of fine tuning of coordinated, smooth movement by the basal ganglia - Lewy bodies are esophonophilic intracytoplasmic occlusion bodies found in the soma of the substantia nigra, are a hallmark of the disease - Pyramidal motor tracts: originate in motor cortex -- control voluntary muscle movement **Multiple Sclerosis** - Autoimmune disease in which the CNS myelin is targeted for destruction in genetically susceptible individuals - Onset usually between ages 20-40 - Demyelination leads to scarring, stops or slow nerve conduction in affected nerves - Current treatments slow progress and decrease exacerbations for relapsing and remitting types **Guillain Bare** - An acute autoimmune demyelinating disease of the PNS - Triggered by a viral or bacterial infection - As long as the nerve cell body remains intact, the peripheral nerve will regenerate and function with be restored - Symptoms: - Numbness/pain may precede the hallmark ascending muscle paresis/paralysis - Process peaks and starts to recede after 4 weeks - Return of muscle function occurs gradually in a descending pattern over of days to months - Treatment: IVIG or plasmapheresis to shorten the course and decrease severity **Guillain Bare** - Autoimmune disease that affects normal neuromuscular junction impulse transmission - Autoantibodies bind to ACh receptors on post-synaptic muscle cell membrane - Receptors are blocked and reduced in number incomplete (weakness) or lost (no movement) depolarization of muscle fibers - Symptoms - Fatigue and weakness with activity that improves with rest and worsens with activity - Extraocular muscle are affects leading to diplopia and ptosis - Respiratory muscle weakness leads to decreased cough strength and ventilation - Facial muscles affected result in difficulty chewing and swallowing - Treatment: includes anticholinesterases, corticosteroids, immunosuppressant drugs, plasmapheresis **Schizophrenia** - Psychiatric illness that is related to specific brain findings: - Increased lateral and 3^rd^ ventricle size - Widened frontocortical fissures and sulci - Cortical gray matter loss in temporal lobes and portions of the cortex - **[Positive behaviors]**: result from increased dopamine release from ventral tegmental area and nucleus - Psychosis - Catatonia - **[Negative behaviors]**: result from increased dopamine release to the prefrontal cortex - Blunted affect Brain injury (CVA, TBI) ----------------------- - Contralateral injury/symptoms - Cerebral/Spinal cord- often secondary injury, due to increased ICP due to: - Ischemia - Edema - Hyperemia - Extent of cellular damage correlates to functional outcome - Time is tissue - TBI- acute loss of brain function due to force - leading cause of death/disability in children and young people - Closed head- impact of head striking surface, dura intact - Coup- focal injury (at point of impact) - Contrecoup- 2^nd^ focal injury (at opposite from coup injury) - Open head- penetrating trauma, dura interrupted - Epidural hematomas- bleeding between dura matter and skull - **LOC at time of injury followed by alertness followed by decompensation** - Arterial in nature - Mild Concussion: Transient confusion/amnesia - Classical Concussion: LOC up to 6 hours, amnesia, confusion hours to days - Attention/memory affected for weeks to months - May develop post-concussive syndrome - Symptoms of headache, anxiety, forgetfulness, fatigue - Subdural hematomas- venous bleed between dura and arachnoid - Headache, drowsy, slow cognition and confusion - Intracerebral hematoma- expanding mass of blood which increases ICP. - Prevent secondary injury by releasing pressure (external ventricular drain) - Diffuse axonal injury= widespread damage to axons due to accel/deceleration SHEARING injury - not detected on CT scan, but may be seen later on MRI. impacts white matter - Mild: come 6-24 hours - Mod: Coma \>24 hours, widespread deficits, w/ intake brainstem functions - **Severe: impaired brainstem function, 78% mortality, typically GCS \ - Understand the difference between focal and general progression - Provoked vs non provoked - Complications of any disease process - Alcohol - Recurrent unprovoked seizures define epilepsy - Status epilepticus = single or series of generalized convulsions \ 5 min ### Spinal Cord Injury - Injury that affect's the spinal cord's ability to send and receive messages from the brain to the body's systems that control sensory, motor, and autonomic function below the level of injury - Primary Injury: Mechanical trauma, damage to bones, ligaments, neural tissue or vertebral column, rotation, or hyperextension injuries - Secondary Injury: Ischemia, inflammation - **[Complete:]** total loss of function below level of injury - Paraplegia- full loss of lower limb - Tetraplegia -- full loss of all four limbs - C4 injury: Complete level of paralysis below the neck - C6 injury: Complete or partial paralysis of hands, arms, lower body - T6 injury: Paralysis below the chest - L1 injury: paralysis below the waist - **[Incomplete:]** some functioning below primary level of injury, functioning on one side of the body- see syndromes - Paraplegia- patchy loss of sensory and motor function (lower limb) - Tetraplegia- patchy loss of sensory and motor function (all four limbs) - [Anterior cord:] motor paralysis and loss of pain and temperature sensation with preserved proprioception. Touch, vibration sense - [Brown Sequard]: motor weakness on one side of the body and loss of sensation on the other - [Central Cord:] most common, impairment with upper body greater compared to lower body - [Posterior Cord:] preserved motor function with loss of sensory function **Intracerebral hypertension** ### Complications of Spinal Cord Injuries **Neurogenic shock** - Loss of sympathetic tone (parasympathetic is working un-opposed) - Bradycardia, hypotension, hypothermia **Spinal shock** - A complete loss of reflexes and flaccidity below the level of the injury - This may last for days to 3 months at which time the person develops hyperreflexia and spasms. - [Irritation (full bladder/bowels, pain) can prompt a **sympathetic storm** ] - The full bladder message attempts to travel up the afferent pathway. Can't get by the SCI at T6 or higher. Results in massive sympathetic (fight/flight) response that causes systemic vasoconstriction HTN the baroreceptors in the carotid arteries tell the brain there's a HTN crisis, the HR slows, but the descending inhibitory signals to other areas are blocked at the SCI again. - Heart rate slows - Blood pressure increases due to widespread vasoconstriction - [Treatment:] eliminate the stimuli, cautiously administer short acting anti-hypertensives other than beta blockers Endocrine --------- The major organs that comprise the endocrine system achieve their function by synthesizing, storing, secreting and responding to chemical substances known as **hormones** - Hormones - Autocrine - Paracrine - Exocrine - Peptide -- water soluble polypeptide chains - Amino Acid- water soluable substance from tyrosine and tryptophan - Ends with "in or ine" - Steroid- lipid soluble, bind to nuclear - Ends with "ol or one" - Secretion pattern - Diurnal - Pulsatile - Circadian - Melatonin/cortisol - With feedback mechanisms - Positive = oxytocin - Negative = LH - Hormonal - Humoral - Hormone receptors - Sensitivity of a cell is determined by the number of receptors, may be up or down regulated within hours (more receptors = more sensitive) - E.g. insulin resistance (fewer insulin receptors on cell surface) - Can be adjusted by body temp, pH, presents of other chemicals, mutations (e.g. thyroid receptor mutation) - Hormones act as **[First messengers]** in first and second messenger systems - Water Soluble Hormones: attach to plasma membrane receptors - G protein linked receptors - Ion channel receptors - Enzyme linked receptors - Lipid Soluble hormones attach to: - Plasma membrane receptors - Cytoplasmic receptors - Nuclear membrane receptors - **Hypothalamus** = (Located between two thalamus) [Links nervous and endocrine systems]: participate in almost every body function inc temp regulation, maintains homeostasis, food and water intake, sexual bx and reproduction, daily cycles/circadian rhythm, emotional and stress response, metabolism, growth - Nuclei produce hormones or hormone stimulating/inhibiting factors which will be transported or transmitted to the pituitary gland - To anterior pituitary - **Corticotropin releasing hormone**(Ant pit) ACTH (Adrenal cortex) Corticosteroids - **Thyrotropin releasing hormone**(Ant pit) TSH (thyroid) T4 - **Gonadotropin releasing hormone** (Ant pit) LH/FSH (gonads) Testost./Estrogen/Prog. - **Prolactin releasing peptide/Dopamine** (Ant pit) LH/FSH (mammary glands) milk - **Growth hormone releasing hormone/Somatostatin** (Ant pit) GH (bones/tissue) growth - **Pituitary** = known as master gland, Pea sized gland, attached to hypothalamus at the base of the brain - Anterior (hypothalamus sends releasing factors into local blood stream (portal vessels) to anterior pituitary endocrine cells. - ACTH (Adrenal cortex) Corticosteroids - TSH (thyroid) T4 - LH/FSH (gonads) Testosterone /Estrogen /Progesterone - GH (bones/tissue) growth - Posterior (unmyelinated secretory neurons)- (via axons or tracts and infundibular stalk): - **Oxytocin Mammary glands, uterine muscles** (positive feedback system), uterine contraction, attachment and milk let down - **ADH/Vasopressin kidney tubules** (negative feedback system), binding to V2 in renal distal tubule to increase number of aquaporin in collecting duct = increased water reabsorption/ reduce serum osmolality, also acts at V1 receptors in arteriole walls to increase vasoconstriction and increase blood pressure. - DI -- too little ADH (known as Arginine Vasopressin Deficiency) - Excessive water loss through urine and increase thirst (polyuria/polydipsia) - Neurogenic -- inadequate production (trauma, neurosurgery, cancer) - Nephrogenic- renal insensitivity - Dipsogenic- caused by water intoxication - Tx with vasopressin, matching fluid replacement to loss - SIADH -- too much circulating ADH = water retention (but not typically shown as EDEMA but as LOW SODIUM) seen as osmolarity decrease - 130-140 Na+ =thirst - 120-130 + vomiting, cramping - \>120 = risk of seizure - Hyperosmolarity of urine - Tx with fluid restriction and slow Na+ correction - Pancreas - Alpha cells = glucagon - Beta cells = Insulin - Insulin receptors allow the facilitated transport of glucose into cells by way of GLUT4 protein transporter. - Stimulates liver cells to convert and store glucose as glycogen. - Promotes the influx of potassium into cells by enhancing Na+ -K+ pump activity. - **Diabetes** - 1 = deficient production of insulin - 2 = insulin resistance and insulin deficiency - Gestational = temporary increase in blood sugar during pregnancy - Insulin resistance = proinflammatory cytokines and buildup of fatty acids which ultimately remove - DKA- **low pH (les than 7.3),** typically type 1, state of relative or absolute insulin deficiency (glucose between 250-600) \*n/v/abdominal pain\*, bicarb \< 15, **KEYTONES** - HHS- will not be acidotic, typically type 2, marked azotemia, **glucose 800-1200** = high dehydration do to serum osmolarity, require a ton of fluid), high morality, Seizures & Mental status changes common - **[Adrenal]** - Cortex - Mineralocorticoids = zona glomerulosa - Aldosterone - RAAS - Increase BP - Increase force of cardiac contraction - Glucocorticoids = zona fasciculata - Steroids/ cortisol (stim by ACTH) - Cushing's syndrome = chronic exposure to high cortisol, "buffalo hump", water retention, poor wound healing, sleep d/o, fatigue, central weight gain - ACTH dependent = lung cancer release of ACTH - ACTH independent = adrenal tumor, iatrogenic - **Cushing's Disease** = due to ACTH producing pituitary tumor - **Adrenal Insufficiency** = due to atrophy or trauma (often due to chronic use of exogenous steroids or hypothalamic or pituitary lesions) - Addisons Disease (congenital) - Adrenal crisis = Require high dose steroids - Absolute hypotension \ 140 - Fever over 104 - "Mortality is like around 20%" - Dying cells will leak T4 - **[Parathyroid]** = control serum calcium levels - Opposed by calcitonin from parafollicular cells in the thyroid - Bone - release Ca++ from the bone via osteoclasts - bone "resorbed" - Kidney - Reabsorption of Ca++ from urine - Activation of Vit D. - Small Intestine - Vit D. causes absorption of calcium from diet - **[Pineal]** = secretes melatonin derived from serotonin. - Release is stimulated by darkness - Controlled by hypothalamic input - Helps to regulate sleep/wake cycles Reproductive \* items in green noted as need to know ---------------------------------------------------- - **Identify and explain** the significant anatomical structures of the male and female reproductive organs, and their general functions. - Vulva - Labia majora and minora - Clitoris - Vestibule and vestibular glands (produce mucus) - Vaginal orifice -- opening into vagina - Ovaries -- female gonads - Fallopian tubes -- not connected to the ovary - Uterus -- pear shaped (sits on top of the bladder) - Cervix -- "neck region" - Vagina - Hymen - Hormones - Estrogen - Progesterone - Scrotum = house testes - Penis- contains urethra - Testes = male gonads (produce sperm and testosterone) - Epididymis -- mature sperm (just above testes) - Vas deferens -- tubes to move mature sperm - Urethra - Seminal vesicles -- produce fluid of semen, contains sugars and buffers - Bulbourethral gland - Prostate gland - - **Describe** the implications of the proximity of reproductive structures to adjacent abdominal and pelvic structures.  - Gametes - Ovum - Sperm - **Analyze** a woman's monthly cycle and alterations in menstruation.  - GnRHLH/FSHEstrogen/ Progestin (negative feedback) - Menstruation - Proliferative phase - Secretory phase - **Diagnostic Tests** - AFAB - Bimanual exam - Pap smear & biopsy (punch or cone biopsy- goes into uterus) - Hysterosalpingogram - D&C biopsy for endometrial d/o - Mammography - AMAB - Digital rectal exam - Cystoscopy- view into bladder via urethra - Prostate specific antigen (PSA) test - **Discuss** the pathophysiology, clinical presentation, clinical implications, and treatment of:  - Pelvic inflammatory disease  - Vaginitis - Endometriosis  - Ovarian cysts - Toxic shock syndrome  - Pelvic relaxation disorders  - Cervical, ovarian, uterine, and breast cancer  - Disorders associated with pregnancy - Ectopic pregnancy - Spontaneous abortion - Placenta abruption - Male & Female Infertility - Prostatitis  - Benign prostatic hyperplasia  - Prostate cancer  - Inflammation of male reproductive structures  - Testicular cancer  - Prostate diseases - Epididymitis - Orchitis - Urethral disorders - Sexually transmitted infections - Sexual dysfunction - Vaginal cancer - Puerperal sepsis - Hydatidiform mole - Effects of aging

Use Quizgecko on...
Browser
Browser