Exam 3 Terms & Concepts PDF

dro Lecture Topic Ch. # Exam Blueprint 10/28 Neuro 13-16 11/4 Integumentary & Burns 51 & 52 11/4 Musculoskeletal 47-50 11/11 Endocrine & DM 40 & 4...

dro Lecture Topic Ch. # Exam Blueprint 10/28 Neuro 13-16 11/4 Integumentary & Burns 51 & 52 11/4 Musculoskeletal 47-50 11/11 Endocrine & DM 40 & 41 11/18 Renal & GU 32-35 11/21 EXAM 3 Notes by Objective: Neuro: Distinguish b/w functions of the neurons & neuroglial cells of the nervous system. Nervous tissue contains 2 types of cells: ○ neurons → fundamental unit of the neurological system exhibit excitability & conduct impulses afferent = sensory → send info to CNS efferent = motor → carry info away from CNS gray matter is mostly neuronal cell bodies ○ neuroglial cells → create the scaffolding protections & support, glycogen storage astrocytes form the BBB oligodendrocytes & Schwann cells produce myelin → increase velocity of nerve impulses white matter is mostly glial cells & myelinated axons (myelin has a high lipid content, hence the whitish color) Components of neurons: know what parts send signals and receive signals ○ Dendrites → have receptors for NT binding, RECEIVE signals ○ Cell body (soma) → RECEIVE signals ○ Axon → SEND signals ○ Axon terminals → release NTs Explain the metabolic requirements of nervous tissue. Brain receives 15%-20% of the total resting CO & consumes 20% of its oxygen → LARGE energy requirements No way of storing oxygen → vulnerable to hypoxia → results in a rapid onset of clinical signs: ○ AMS/confusion/restlessness ○ lethargic or combative ○ loss of consciousness → occurs almost simultaneously w/ cardiac arrest cell death begins within 4-6 mins ○ seizure activity Main energy source = glucose ○ small glycogen stores within supporting neuroglial cells ○ brain still vulnerable & sensitive to hypoglycemia → checking BS is protocol in an AMS pt Summarize the gate control theory of pain. experience of pain is modulated by a “gate” mechanism in the spinal cord; there are two proposed pathways: ○ descending (efferent) pathways interfere w/ ascending (afferent) pain signals → can either amplify or inhibit cognitive or emotional factors “mind over matter” i.e. benefit of meditation, monks ○ ascending (afferent) signals from peripheral nerves COMPETE large-diameter A-beta fibers (associated w/ non-nociceptive input, like touch) are faster & activate inhibitory interneurons in the dorsal horn that “close” the gate on pain transmission rubbing, massage, vibration, TENS ○ Transcutaneous electrical nerve stimulation (TENS) uses low-voltage electrical currents to relieve pain. A TENS unit is a small device that delivers the current at or near your nerves to block or change your perception of pain small-diameter A-delta (associated w/ nociceptive input, like pain) are excitatory & contribute to pain transmission Differentiate b/w neuropathic pain, neuralgias, and phantom limb pain. Types of pain:  ○ cutaneous → arises from superficial structures, sharp, burning qualities (scrape, burn, cellulitis) ○ deep somatic → originates in deep body structures (ischemia, sprained ankle) ○ visceral → originates from internal organs (contractions, distention, ischemia); diffuse @ 1st & can later become localized (appendicitis) ○ referred → pain perceived at a different site than its point of origin but innervated by the same spinal segment → be familiar with the concept of dermatomes neuropathic pain → BROAD category of nerve-related pain; refers to a stimulus stemming directly from neuronal cells, versus non-neuronal tissue, due to some kind of damage to the nerve ○ peripheral nerve damage in a single area: nerve entrapment nerve compression tumor mass neuralgias ○ peripheral nerve damage in a wide area: diabetes mellitus long-term alcohol-use hypothyroidism amputation → phantom limb pains ○ CNS lesion/dysfunction neuralgia → symptom of neuropathy; characterized by severe, brief, often repetitive attacks of lightening-like or throbbing pain ○ trigeminal neuralgia ○ postherpetic neuralgia (i.e. shingles) ○ phantom limb pain → results from a mismatch b/w the brain’s “map” of the body and sensory input; the brain continues to send signals to the area where the limb used to be, and without feedback from the missing limb, it can create pain sensations as part of the adaptive response Discuss alterations in structure or function, risk factors, clinical manifestations, and selected treatments for the following conditions: Skeletal Muscle Disorders: ○ Muscular dystrophy → genetic disorders that produce progressive deterioration of skeletal muscle bc of mixed muscle cell hypertrophy, atrophy, & necrosis most common type: Duchenne’s or DMD as muscle undergoes necrosis, fat & CT replace muscle fibers (pseudohypertrophy) → increases muscle size & results in muscle weakness insidious in onset but continually progressive clinical manifestations:  frequent falling → evident at 2-3 years of age pseudohypertrophy of calf muscles imbalances b/w agonist & antagonist muscles → abnormal posture, contractures & joint immobility; scoliosis is common respiratory muscle involvement → breathing problems cardiac muscle involvement → cardiomyopathy Disorders of the Neuromuscular Junction (NMJ) ○ Myasthenia gravis (“grave weakness”) → autoimmune disease; antibody-mediated attack on acetylcholine receptors in the NMJ → leads to fewer receptors on post-synaptic cleft & impaired signal transmission acetylcholine = NT that triggers muscle contraction; enables voluntary muscle movements & helps regulate involuntary functions (i.e. HR & digestion) clinical manifestations: ptosis d/t eyelid weakness diplopia d/t extraocular muscle weakness chewing & swallowing difficulty (dysphagia) slurred speech predisposition to rapid fatigue symptoms worse in the afternoon, evening Peripheral Nerve Disorders: ○ Guillain-Barre → acute autoimmune attack on myelin sheath; lower motor neuron disorder most people report having an acute, influenza-like illness before the onset of symptoms clinical manifestations: progressive ascending muscle weakness of the limbs → symmetric flaccid paralysis paresthesia & numbness respiratory muscle paralysis → ventilator required severity & duration can range from mild weakness w/ spontaneous recovery to developing tetraplegic & ventilator dependence w/ no signs of recovery for several months or longer ascending GBS a lot more common than descending GBS cervical 3,4,5 keep the patient alive Disorders of the Basal Ganglia: ○ Parkinson's disease → degenerative disorder caused by destruction of dopaminergic neuronal cells in the substantia nigra in the basal ganglia; results in an imbalance b/w dopamine & ACh dopamine = allows for controlled movement & suppression of involuntary or unnecessary motor activity acetylcholine = excitatory neurotransmitter  in Parkinson's → too little dopamine, unopposed acetylcholine risk factors: genetic linkage TBI antipsychotic drug use CO poisoning diagnostic: Lewy bodies clinical manifestations: tremors → rhythmic, alternating flexion & contraction movements, “rolling a pill” w/ thumb & forefinger ○ occurs at rest, disappears w/ movement & sleep ○ initially unilateral; progresses bilaterally rigidity → reduced ROM, flexion contractions bradykinesia → slowness in initiating & performing movements & difficulty w/ sudden, unexpected stopping of voluntary movements ○ akinesia → complete absence of movement loss of postural reflexes → shuffling gait, “crouched” stance, predisposition to falling treatment: replace dopamine → levodopa (precursor to dopamine) restore DA/ACh balance → anticholinergic drugs (i.e. benztropine) Upper Motor Neuron Disorders: ○ Amyotrophic lateral sclerosis (Lou Gehrig’s disease) → debilitating autoimmune disorder; both UMNs (in the brain) & LMNs (in spinal cord & brainstem) degenerate → breakdown of NMJs, preventing effective communication b/w nerves & muscles loss of motor neurons disrupts voluntary muscle control → leads to progressive muscle weakness, paralysis, & eventual death (usually within 3 years) sensory & cognitive functions are usually preserved clinical manifestations: muscle weakness & atrophy ○ most common = slowly progressive weakness & atrophy in distal muscles of one upper extremity spasticity & hyperreflexia difficulty speaking & swallowing respiratory compromise ○ Multiple sclerosis → chronic autoimmune disease that affects the CNS, leading to progressive damage of the myelin sheath → demyelination process leaves scar tissue, or “sclerosis/plaques,” at multiple sites → over time, attacks lead to axon loss & permanent/irreversible nerve damage  clinical manifestations: muscle weakness, spasticity, & gait difficulties; reduced mobility over time numbness, tingling, & neuropathic pain vision & hearing loss memory issues, attention deficits, executive function difficulties, emotional & mood dysregulation FATIGUE bowel & bladder dysfunction complications: paralysis of legs epilepsy depression treatment: slow damage → corticosteroids & interferons symptoms management → antidepressants, anticholinergics, laxatives Differentiate b/w epidural, subdural, and intracerebral bleeds. epidural → b/w skull & outermost membrane layer (dura) ○ head trauma → briefly knocked unconscious → full return to lucidity → hematoma grows & is followed by rapid loss of consciousness for the 2nd time ○ associated with arterial bleeding d/t skull fractures ○ manifestations: focal symptoms ipsilateral pupil dilation contralateral hemiparesis ○ prognosis: excellent if hematoma removed before 2nd loss of consciousness subdural → b/w dura mater & arachnoid ○ vein tear or rupture → develops more slowly, depending on the extent of tear acute → progresses rapidly subacute → s/s within days or weeks after injury chronic → s/s take weeks & months to appear ○ higher mortality rate d/t severe secondary injuries related to edema & increased ICP intracerebral → occurring in lobes, brainstem, cerebellum ○ etiology: hemorrhagic stroke, head injury, aneurysm, tumor, HTN  ○ think stroke symptoms: confusion headache slurred speech loss of movement (paralysis) on opposite side of the body from the head injury Major areas of the brain = LOBES ○ frontal → voluntary motor, personality, executive function prefrontal cortex primary motor cortex ○ parietal → processes sensory information related to touch, temperature, pain, & spatial awareness, hand-eye coordination somatosensory cortex ○ occipital → visual processing, object recognition primary visual cortex ○ temporal → hearing, smell, memory primary auditory cortex hippocampus Compare and contrast ischemic & hemorrhagic stroke. ischemic → obstruction of oxygen delivery d/t a clot ○ ischemic band of cells (the ones dying d/t a lack of O2 & glucose) = penumbra ○ thrombotic → atherosclerotic blood vessels ○ cardiogenic embolic → vegetation (endocarditis), plaque breakage, clot formation (afib); essentially moving clot ○ transient ischemic attack (TIA) → have multiples, precursor to actual stroke, no permanent damage ○ Treatment: supplemental, high-flow O2 diagnose → CT to rule out hemorrhagic clot buster → TPA hemorrhagic → disruption of oxygen delivery d/t ruptured artery, usually fatal ○ hard to recognize early enough to remedy ○ pt experiences headache (“worst headache of my life”) & n/v → contralateral hemiplegia w/ initial flaccidity → progresses to spasticity ○ Risk factors: anticoagulant-use HTN  structural abnormality (i.e. previous aneurysm → weakening of arterial wall) General stroke risk factors: ○ diabetes ○ smoking ○ a-fib ○ hyperlipidemia ○ CAD ○ coagulation disorders ○ heavy alcohol use Describe alterations in structure, risk factors, and clinical manifestations of subarachnoid hemorrhage & cerebral aneurysm. subarachnoid hemorrhage → most commonly caused by rupture of cerebral aneurysm (also caused by trauma & arteriovenous malformations (AV malformation)) ○ AV malformations: tangle of blood vessels → arteries & veins are directly connected w/o capillaries → high-pressure, fast-flow system thin walls of veins are vulnerable to arterial pressure → they stretch, weaken, & become prone to rupture ○ complications: increase in ICP disruption of CSF flow ○ clinical manifestations: before rupture → atypical headache after rupture → “worst headache of my life” → photophobia → vomiting → nuchal rigidity → collapse/loss of consciousness cerebral aneurysm → bulge/ballooning at site of localized weakness of arterial wall Describe the etiology, diagnosis, and treatment of seizures. abnormal, excessive nerve-firing prodromal → aura → ictus → post-ictus Generalized: entire brain is affected ○ tonic-clonic: may begin with an aura initial stiffening (tonic) stage → pt falls and muscle tenses up (10-30 seconds) clonic stage → uncontrolled convulsions (30-60 seconds) post-seizure phase → confusion & muscle aches ○ myoclonic: sudden jerking or stiffening of the extremities ○ absence: blank stare, “spacing out,” more common in children, looks like daydreaming, no recovery period ○ atonic: “drop attacks” Partial/focal: one area of the brain is affected ○ simple partial: consciousness & awareness are preserved ○ complex partial consciousness & awareness is impaired Integumentary & Burns Correlate the pathophysiology of burn injury to the major complications. Types of burns: ○ thermal → scald & flame; fire, hot liquid, or steam ○ chemical → industrial agents; strong acids, alkalis, or corrosive substances ○ electrical → usually more extensive d/t internal tissue injury & presence of entrance & exit wounds ○ radiation → typically from exposure to UV light or radiation therapy effects of UVA & UVB (sunburn rays) → short-lived & reversible erythema pigmentation injury to Langerhans cells & keratinocytes (in epidermis) → weakens skin’s protective functions ○ Langerhans cells: APCs, activation of innate immune response ○ Keratinocytes: produces protective protein that strengthens skin, release cytokines that help regulate immune response Depths of burns: Class 1st-Degree burns 2nd-Degree burns 3rd/4th-Degree Burns Depth Superficial Partial-thickness Full thickness Layers affected only epidermis epidermis & part of extends through all skin dermis layers clinical red, dry, painful w/o redness, blistering (shiny, dry, waxy white, leathery, manifestations blisters wet), swelling, severe hard skin, no pain pain nursing requires hospitalization requires immediate considerations if > 25% of BSA hospitalization examples sunburn tar burn, flame exposure to flames, electricity or chemicals Local response: ○ inflammatory → release of histamines, bradykinin, & cytokines → vasodilation & ↑ capillary permeability ○ fluid shift → proteins & fluids leak into surrounding tissues → edema ○ nerve damage & pain Systemic response: (first 24 hours)  ○ Cardiovascular → hypovolemia from massive fluid shift → ↓ CO → reflex tachycardia to compensate → high risk of shock epinephrine secreted to induce vasoconstriction → shunts blood to vital organs ○ Renal → baroreceptors trigger compensatory mechanisms UO decreases → causes by convervation effort or lack of renal perfusion RAAS system → ADH & aldosterone secretion → effort to retain Na+ & H2O ○ Respiratory → inhalation injuries can result in airway edema **maintaining airway patency is priority nursing intervention here ○ Immune → loss of protective skin barrier exposes body to pathogens → high risk for infection & sepsis ○ Metabolic → increased energy needs to support wound healing & recovery → can lead to catabolism pts put on high-calorie, high-protein diets Major Complications: ○ Hypovolemic shock Priority nursing intervention: FLUID REPLACEMENT albumin given to maintain vascular tone Fluid volume assessment: urine output Kidney perfusion assessment: GFR (90-120 mL/min) Calculate the total body surface area affected by a burn using the rule of 9s. A patient has sustained partial-thickness burns on their entire right arm and the anterior portion of their right leg. ○ entire right arm: 9% ○ anterior RT leg: 9% A patient presents with burns on the anterior trunk and both anterior thighs. ○ anterior trunk: 18% ○ both anterior thighs: 9% A patient has sustained third-degree burns to the entire anterior and posterior right arm, the entire anterior chest and abdomen, and perineal area. ○ entire RT arm: 9% ○ entire anterior chest: 9% ○ anterior abdomen: 9% ○ perineal area: 1% Musculoskeletal State the function of parathyroid hormone, calcitonin, and vitamin D in terms of bone formation and metabolism. Parathyroid hormone (PTH): released by parathyroid glands in response to low blood Ca2+ levels ○ stimulates osteoCLAST activity → break down of bone to increase Ca2+ levels in blood Calcitonin: produced by thyroid gland when blood Ca2+ levels are high ○ inhibits osteoclast & stimulates osteoBLAST activity → bones absorb Ca2+ from blood stream to decreases levels in the blood Vitamin D (Calcitriol): increases calcium absorption in the intestines Differentiate between contusion, hematoma, and laceration. Contusion: injury to soft tissue that results from direct trauma Hematoma: large area of local hemorrhage Laceration: skin is torn or its continuity disrupted Compare and contrast the traumatic musculoskeletal injuries. Fractures: a break in continuity of a bone ○ could be caused by direct blow/impact, crushing forces, extreme muscle contractions ○ could also be secondary to an underlying condition: osteoporosis, osteomyelitis, tumor, infection, metabolic bone disorders → “pathological fx” ○ s/s: pain, swelling, deformity, impaired function, impaired sensation, muscle spasm ○ TYPES complete v. incomplete open v. closed → dependent on soft tissue involvement greenstick: seen among children directions: linear, oblique, spiral, transverse, comminuted pathologic/spontaneous a fall of a pt with osteoporosis can lead to snapping the head of the femur bone other secondary causes: tumor, osteomyelitis Dislocations: joint moved out of its normal position Strains: tear or injury to TENDON Sprains: tear or injury to LIGAMENT–Type III is a complete severing of a ligament Examine complications of musculoskeletal injuries to include compartment syndrome, venous thromboembolism, and fat embolism. Compartment syndrome: increased pressure within limited space that compromises circulation and function of tissues within the space ○ can cause permanent nerve damage and possibly loss of limb ○ treatment: cut into the space to relieve pressure & restore circulation — fasciotomy ○ etiology: trauma, swelling, vascular injury, venous obstruction ○ s/s: pain, pulselessness, paresthesia, polar, paralysis, pallor Venous thromboembolism: ○ Virchow’s Triad: venous stasis, immobilization vessel wall injury hyper-coagulability Fat embolism: fat cells within bone can be released when fracture and effectively become a traveling clot Trace the mechanism of Osteomalacia. bones that are being made are very weak — inadequate mineralized bone matrix kidneys are responsible for metabolizing Vitamin D & converting it to active form, calcitriol Causes: ○ dietary deficiency in vitamin D, calcium, or phosphorus ○ deficient vitamin D metabolism — lowers absorption of calcium from intestines ○ renal tubular phosphate loss (hereditary) → decreased resorption of phosphate Treatment: oral supplements vitamin D- deficiency is a greater risk for kids who were breast fed Foods high in Ca2+: ○ dairy products ○ green leafy vegetables ○ fortified foods → OJ, plant-based milks, cereals ○ nuts & seeds ○ tofu Foods high in phosphorus: ○ meat, fish, eggs ○ dairy products ○ whole grains ○ potatoes ○ nuts & seeds Summarize alterations in structure or function, risk factors, clinical manifestations, and treatments for the following musculoskeletal disorders: Osteomyelitis: damage to the bone + opportunistic pathogen Osteoporosis: reduced bone mineral density, imbalance in bone formation (clast>blast) ○ risk factors: sex, advancing age, body size, race, family hx, changes to hormones, diet, long-term use of certain meds (glucocorticoids…), drinking, smoking, inactivity low estrogen levels in women after menopause low levels of testosterone men Paget disease: chronic condition of bone turnover characterized by disorder of normal bone remodeling process ○ excessive breakdown of bone tissue (overly active clast activity), followed by abnormal bone formation (dysfunctional blast activity) ○ normal bone marrow is replaced by vascular, fibrous, connective tissue that leads to formation of larger, disorganized, & weaker bone tissue Rheumatoid arthritis: autoimmune disease ○ the more they move around, the better it is for long-term mobility Osteoarthritis: age-related, degenerative joint disease Gout: build up of uric acid levels in the body, high serum level > 8.5 mg/dL ○ foods high in purines → red meat/organ meats, seafood, alcohol, sugary drinks, high fructose corn syrup Endocrine: Identify the source and major action of the following hormones: Hypothalamus: ‘R’ = releasing CRH TRH GHRH Somatostatin: inhibits GH & TSH Pituitary gland: GH: stimulates growth of the bone & muscle, promotes protein synthesis & fat metabolism, decreases carbohydrate metabolism ACTH: stimulates synthesis & secretion of adrenal cortical hormones TSH: stimulates synthesis & secretion of thyroid hormone ADH: ↑ H2O reabsorption by kidneys Adrenal Cortex: Aldosterone: ↑ Na+ reabsorption & K+ loss by kidneys (indirectly promoting water retention) Cortisol: affects metabolism of all nutrients; regulates blood glucose levels, affects growth, has anti-inflammatory action, & decreases effects of stress (in the short-term) Androgens Adrenal Medulla: SNS NTs Epinephrine Norepinephrine Thyroid: Thyroid hormone: increases metabolic rate; necessary for fetal & infant growth & development Calcitonin: ↓ Ca2+ & phosphate levels in the blood Parathyroid: PTH: ↑ Ca2+ & phosphate levels in the blood Pancreas: Insulin: ↓ blood glucose; facilitates glucose transport across cell membranes Glucagon: ↑ blood glucose; stimulates glycogenolysis & glyconeogenesis Describe the role of the hypothalamus and pituitary gland in regulating pituitary control of endocrine function. hypothalamus → centrally located in the brain → COORDINATING CENTER ○ receives neural input r/t emotion, pain, body temperature…& communicates to the rest of the endocrine system via hormonal cascade ○ releases “releasing” or “inhibiting” hormones pituitary gland (aka hypophysis) → connected to the floor of the hypothalamus → MASTER GLAND ○ directly communicates with the ‘coordinating center’ by blood & nerves ○ its hormones control the functions of many target glands & cells ○ anterior pituitary → TSH, ACTH, GH ○ posterior pituitary → ADH Identify the role of growth hormone including consequences of hypo- or hyper-secretive states. Growth Hormone (GH) → necessary for growth & contributes to the regulation of metabolic functions ○ cartilage growth ○ linear bone growth → direct action on the epiphyseal growth plates ○ increased protein synthesis → lean muscle mass development ○ increased size and function of body organs GH deficiency → endocrine disorder leading to short stature pituitary Dwarfism ○ ↑ subcutaneous fat in the abdominal area ○ immature facial features ○ delayed dentition ○ underdeveloped nasal bridge ○ ↓ BMD & lean muscle mass GH excess → endocrine disorder leading to tall stature, or pituitary Gigantism ○ when this occurs in adulthood, after the epiphyses of long bones have fused, the condition is referred to as acromegaly ○ in children → excessive skeletal growth & tall stature ○ in adults: enlargement of small bones of hands & feet broad & bulbous nose protruding jaw slanting forehead cartilaginous structures become enlarged (larynx & respiratory tract) enlargement of virtually every organ → ex. development of HTN d/t cardiomegaly Discuss alterations in structure or function, identify compensatory mechanisms, clinical manifestations, risk factors, and treatments for: Thyroid hormone (TH) → increases metabolism & protein synthesis & is necessary for growth & development ○ Metabolic rate: lipids are mobilized from adipose tissue catabolism of cholesterol by liver increased absorption of glucose from GI tract ○ Cardiovascular fxn: ↑ O2 consumption (d/t increased metabolic rate)  ↑ vasodilation, blood volume, CO, & ventilation enhanced HR & contractility w/o a rise in BP (vasodilation offsets ↑ CO) ○ Gastrointestinal fxn: ↑ motility & gastric secretions ↑ appetite weight loss Thyroid [TRH → TSH → T4 & T3] Hypothyroidism: deficient Hyperthyroidism: excessive production of TH production of TH General behavior mental & physical sluggishness, restlessness, irritability, anxiety, fine somnolence tremors Cardiovascular ↓ CO, bradycardia ↑ CO, tachycardia, palpitations GI constipation, decreased appetite diarrhea, increased appetite Temperature tolerance cold intolerance heat intolerance Skin & hair decreased sweating; coarse & dry skin increased sweating; thin & silky, & hair velvety skin & hair General features myxedematous features (generalized exophthalmos (in Graves disease) puffiness) Acute State Myxedema coma Thyroid storm Causes of primary: thyroidectomy Grave’s disease (destruction or dysfunction iodine deficiency → Goiter adenoma of the thyroid of thyroid gland) development thyroiditis Hashimoto’s radiation Treatment lifetime, levothyroxine high-calorie diet low-calorie beta-blockers radiation ***let’s think about primary and secondary causes together Goiters → can occur in hypo-, eu-, or hyper-thyroid states ○ NURSING CONSIDERATION: dysphagia & respiratory status  Adrenal Cortical Hormones → aldosterone (mineralcorticoid) & cortisol (glucocorticoid) ○ Aldosterone (RAAS & K+ levels) → regulate K+ & Na+ levels and water balance ○ Cortisol (CRH → ACTH → cortisol) → glucose metabolism, protein metabolism, fat metabolism, anti-inflammatory action Adrenal Cortical Addison Disease: AC insufficiency Cushing Disease: hypercortisolism hyperpigmentation, hypotension, buffalo “hump,” “moon face,” truncal hypoglycemia, poor tolerance to stress, obesity, abdominal striae, amenorrhea, fatigue, anorexia, GI upset, polyuria osteoporosis, HTN, HF, w/retention of K+ hyperglycemia, Na+ retention & hypokalemia, “roid rage” Priorities ↑ K+ levels → cardiac arrhythmias → ↓ Ca2+ absorption, ↑ risk of infection, elevated T-waves; fluid volume deficit fluid volume overload Causes tumors of adrenal gland small cell lung carcinoma secreting ACTH or CRH iatrogenic Treatment “Add a -sone” → surgery hydrocortisone or irradiation fludrocortisone pharmacological therapy ↑ Na+ in diet Acute crisis Addisonian crisis → triggered by minor illness or stress DM: Contrast the hormones glucagon & insulin. Insulin → promotes cellular uptake of glucose & storage of glucose as glycogen or fat → pulls from circulation → lowers blood sugar ○ inhibits lipolysis Glucagon → stimulates gluconeogenesis (creates more glucose from glycogen stores in the liver) → glucose released into circulation → raises blood sugar Metabolism = balance b/w anabolism & catabolism Discuss alterations in structure or function, identify compensatory mechanisms, clinical manifestations, risk factors, and treatments for the following key abnormal conditions: DM 1: ○ considered autoimmune → targeted destruction of pancreatic beta cells → absolute insulin deficiency ○ often r/t a genetic predisposition ○ insulin-dependent; childhood onset DM II: ○ majority of cases of DM (90-95%) ○ heterogenous; lifestyle-dependent → overweight/obese, sedentary, smoking, high-fat diet; there is also a strong genetic component ○ insulin-resistant, deranged secretion of insulin, increased glucose production by the liver can have high, normal, or low insulin levels; type II is simply characterized by the decreased ability of insulin to act effectively on target tissues Metabolic Syndrome: constellation of abnormalities caused by insulin resistance ○ visceral obesity ○ high levels of triglycerides ○ low levels of HDLs ○ HTN ○ systemic inflammation (indicated by ↑ CRP) Discuss the acute complications of diabetes mellitus. hypoglycemia: ○ headache, difficulty problem solving, coma, seizures, anxiety, tachycardia, sweating, & constriction of blood vessels (PALE, COOL, CLAMMY) ○ 15g carbohydrate snack or oral glucose tab, recheck blood glucose in 15 mins  ○ if pt is unconscious → glucagon 1 mg IM or subcut, then have them ingest complex carb after recovery (sweet potatoes, oatmeal, or whole grain bread) ○ important to know that this state can mimic alcohol intoxication Contrast DKA & r: DKA (greater association w/ DM I) HHS (greater association w/ DM II) rapid onset ( 300 > 600 Differentiating hyperglycemia, ketones present in urine hyperglycemia, hyperosmolarity, manifestations & blood, GI upset (metabolic acidosis), dehydration, seizures, reversible paralysis fruity breath, Kussmaul’s Both polyuria, polydipsia, polyphagia, weight loss, blurred vision, headache, weakness, orthostatic hypotension, mental status changes Treatment correct fluid/electrolyte imbalance; when similar to DKA, yet greater focus on blood glucose approaches 250, D5W is fluid administration added to fluid therapy, insulin drip Considerations watch that potassium level Discuss the chronic complications of DM. Microvascular: ○ neuropathy ○ retinopathy ○ nephropathy Macrovascular: ○ CAD ○ peripheral vascular disease ○ diabetic foot ulcers ○ infections Renal & Genitourinary: Review Starling Forces *related to how fluid moves into & out of tissues, how the kidneys are absorbing & getting rid of fluid… Starling/Pressure forces: ○ hydrostatic → pressure that pushes fluid away capillary hydrostatic: dependent on arterial & venous blood pressure (factors that ↑ BP, will also ↑ hydrostatic pressure) interstitial hydrostatic: dependent on tissue & lymphatic drainage efficiency opposes filtration if + promotes filtration if - ○ oncotic/osmotic → pressure that pulls fluid towards plasma oncotic: dependent on osmotically active particles in the blood Main contributor = albumin = most abundant plasma protein & is given as an IV colloid solution to expand blood volume promotes reabsorption interstitial oncotic: dependent on protein leakage into the interstitium or tissue injury promotes filtration Colloid: a mixture where tiny particles are dispersed throughout a continuous medium ○ milk ○ detergent ○ blood ○ smoke FLUID SHIFTS: it’s all about the net filtration pressure (NFP) ○ plasma → interstitial examples: Edema in HF: ↑ capillary hydrostatic pressure d/t elevated venous pressure Localized edema w/inlammation or injury: ↑ capillary permeability d/t inflammatory mediators like histamine Hypoalbuminemia w/liver disease or malnutrition: ↓ capillary oncotic pressure d/t low plasma protein levels ○ interstitial → plasma examples:  Albumin infusion for hypovolemia: ↑ plasma oncotic pressure d/t exogenous albumin administration (important treatment for burns to restore circulating volume) Use of diuretics for edema: ↓ capillary hydrostatic pressure as excess fluid is removed from circulation Osmotic diuretic (mannitol) administration for ↑ ICP: increases plasma osmolarity, drawing H2O into vascular space, but prevents water reabsorption in the renal tubules, promoting diuresis Discuss alterations in structure or function, risk factors, clinical manifestations, and selected treatments for the following conditions: Renal Calculi/Nephrolithiasis (“kidney stones”): ○ most common cause of upper urinary tract obstruction ○ Contributing factors: supersaturated urine w/ stone components: calcium salts ○ hypercalcemia ○ high doses of Vitamin D ○ immobilization ○ hyperparathyroidism ○ intestinal bypass surgery struvite (magnesium ammonium phosphate) ○ UTIs uric acid ○ gout ○ high protein diet ○ diabetes ○ metabolic syndrome ○ chronic diarrhea or malabsorption cystine (amino acid) ○ hereditary disorder ○ Clinical manifestations: PAIN acute, intermittent, & excruciating in the flank & upper outer quadrant of the abdomen on affected side; can radiate to lower abdomen  deep, dull ache in the flank or back exaggerated by drinking large amounts of fluid hematuria nausea/vomiting fever and chills if infection accompanies obstruction ○ Treatments: fluids, pain management medications: tamsulosin → relax ureteral muscles dutasteride & tamsulosin procedures/surgeries prevention? Urinary Tract Infections ○ bacterial infection of the urinary tract, usually caused by E. coli ○ affects the bladder (cystitis) or urethra, w/ potential progression to the kidneys (pyelonephritis) ○ Risk factors: female anatomy (shorter urethra), menopause d/t pH changes sexual activity (recommend peeing after intercourse) catheterization, urinary retention, or structural abnormalities blockages–kidney stones or enlarged prostate diabetes or immunosuppression ○ Clinical manifestations: look at the difference based on location dysuria (painful urination), urinary frequency/urgency suprapubic pain or pressure cloudy, malodorous urine fever & systemic symptoms if infection progresses ○ Treatment: short-course or broad-spectrum abx → need to finish complete course evaluation for structural issues prevention: adequate hydration, post-coidal voiding, & cranberry supplementation Glomerulonephritis: ○ inflammation of the glomeruli, impairing filtration ○ leads to proteinuria, hematuria, azotemia, reduced GFR, oliguria, HTN, & potential kidney failure ○ can be acute or chronic ○ Risk factors: infection autoimmune diseases (SLE, DM…) ○ Clinical manifestations:  hematuria (cola-colored urine) & proteinuria edema (periorbital, lower extremities) HTN fatigue & oliguria (no urine production) azotemia → waste products & toxins remain in circulation & can accumulate ○ Treatment: acute → symptomatic support chronic → scarring → given dialysis to remove toxins medications: ACE inhibitors → reduce pressure/blood flow through kidneys corticosteroids → reduces inflammation & scarring Pyelonephritis (aka upper UTI): ○ infection of the renal parenchyma and pelvis, typically ascending from the lower urinary tract ○ ○ Risk factors: untreated or recurrent UTI (apply the same risk factors) ○ Clinical manifestations: chronic or severe → reduced concentrating ability → more dilute urine = low specific gravity Differentiate between acute kidney injury (AKI) and chronic kidney disease (CKD). Kidney Labs: (Cr/BUN increase when kidneys are stressed; GFR decreases) Creatinine ○ normal range: 0.6-1.2 mg/dL ○ waste product of muscle metabolism; freely filtered in the glomeruli Blood urea nitrogen (BUN) ○ normal range: 8-20 mg/dL ○ urea is the end product of protein metabolism  ○ influenced by protein intake, GI bleeding, & hydration status (if BUN is high, but Cr is normal → indicates another issue like dehydration) ○ approximately ⅔ of renal function must be lost before a significant rise in BUN level occurs eGFR (estimated glomerular filtration rate) ○ measured clinically using mathematical formula ○ measures kidney function ○ decreases with kidney disease & age ○ normal range: 90-120 mL/min Acute Renal Failure/Acute Kidney Injury (ARF/AKI): abrupt loss of kidney function (over hours or days) ○ reduced GFR, accumulation of nitrogenous waste products (creatinine & urea), & disturbances in fluid, electrolyte, and acid-base balance ○ typically reversible w/timely intervention ○ Causes: prerenal: decreased perfusion–hypovolemia, HF, sepsis intrarenal: damage to kidneys–acute tubular necrosis, glomerulonephritis acute tubular necrosis = most common cause → destruction of tubular epithelial cells d/t nephrotoxic drugs or low BP postrenal: obstruction–stones, tumors, enlarged prostate ○ Stages: oliguric → fluid and waste retention/accumulation; reduced GFR uremic symptoms: n/v, confusion, fatigue hyperkalemia, metabolic acidosis diuretic → gradual increase in UO; often exceeding 3-5 L/day; increased GFR polyuria; risk of hypovolemia & dehydration hypokalemia & hyponatremia recovery → return to normal or near-normal renal function can take months Chronic Kidney Disease (CKD): progressive, long-term decline in kidney function lasting 3 mos or longer ○ irreversible structural damage & persistent reduction in GFR (< 60 mL/min) ○ permanent & often progressive w/o treatment ○ Causes: Leading cause = Diabetes mellitus Second-leading cause = HTN chronic glomerulonephritis, polycystic kidney disease, recurrent infections, autoimmune diseases (SLE) ○ Stages:  Renal insufficiency (moderate CKD–stages 3 &4; eGFR b/w 15-59 mL/min) Renal failure/End-Stage (ESRD–stage 5; eGFR 40 years old ○ family hx ○ obesity ○ cardiovascular disease ○ type 2 DM ○ lack of exercise ○ ED Prostate gland enlargement: ○ often d/t hormonal changes (higher proportion of estrogen & accumulation of DHT) ○ compresses the urethra, leading to partial or complete obstruction ○ Clinical manifestations: weak stream, hesitancy postvoid dribbling frequency of urination nocturia Increased smooth muscle tone: ○ hyperplasia of smooth muscle & connective tissue exacerbates urethral compression & urinary obstruction Detrusor instability & impaired bladder contractility: ○ increased resistance to urine flow increases workload of the bladder, leading to detrusor muscle hypertrophy & reduced compliance ○ ○ Clinical manifestations:  straining to urinate prolonged urination sensation of incomplete emptying urinary urgency & frequency, occasional urge incontinence, double-voiding Important lab marker: Prostate-specific antigen (PSA) ○ elevated in both BPH & prostate cancer