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patho
patho final review
| Question | Answer |
|---|---|
| hormones function | regulation of metabolism, fluid/electrolyte, growth, reproduction, stress response, blood glucose |
| how to hormones travel in the body | travel in blood to target cells with specific receptors |
| HPA | hypothalamic pituitary axis from hypothalamus -> releasing/inhibiting hormones -> anterior pituitary |
| anterior pituitary secretes what hormones | TSH ACTH GH prolactin LH FSH |
| posterior pituitary function | store/release ADH and oxytocin made in hypothalamus |
| negative feedback | main pattern of regulation in the body think in thyroid function |
| negative vs positive feedback | negative main pattern (ie. thyroid hormone) positive feedback is rare (ie oxytocin) |
| ACTH | adrenocorticotropic hormone stimulates cortex of adrenal glands to secrete cortisol |
| negative feedback loop of thyroid hormones | high T3/T4 leads to reduction of TSH production low T3/T4 leads to stimulation and increase of TSH production |
| how does positive feedback work | rising level of hormone cause another gland to release hormone stimulating to first hormone |
| oxytocin positive feedback loop | posterior pituitary release oxytocin (pressure on cervix from fetal head on stretch receptors) oxytocin intensify uterine contraction increased contraction = more pressure on cervix more contraction repeat until baby is delivered |
| hormones of stress | CRH ACTH cortisol catecholamines (epinephrine, norepinephrine, dopamine) |
| stages of GAS | alarm resistance exhaustion |
| catecholamines | neurotransmitters including dopamine, norepinephrine, epinephrine induce response in organs for fight or flight response |
| how does stress response work | stress stimulate hypothalamus secrete CRH -> CRH stimulate pituitary secreting ACTH -> ACTH stimulates adrenal cortex secreting cortisol additional catecholamine response by SNS |
| CRH | produced by hypothalamus stimulate pituitary gland to secrete ACTH |
| cortisol | hormone that increases metabolism and regulate glucose for energy also works as antiinflammatory |
| alarm stage of GAS | fight or flight response blood to vital organs (heart/brain/lung) more alert skeletal muscle activation blood away from nonvital organs (skin/GI) |
| SIADH | syndrome of inappropriate ADH caused by excess ADH = water retention w/o extra sodium = dilutional hyponatremia |
| ADH | antidiuretic hormone (aka vasopressin) signal kidney to reabsorb water |
| symptoms of SIADH | N/V headache confusion cramp seizure/coma |
| key labs signs for for SIADH | low serum Na (hyponatremia) low serum osmolality concentrated nurine |
| diabetes insipidus | too little ADH central vs nephrogenic |
| central vs nephrogenic diabetes insipidus | central = no ADH is made nephrogenic = kidney ignores ADH |
| symptoms of diabetes insipidus | polyuria polydipsia dehydration risk of hypovolemic shock |
| key labs of diabetes insipidus | dilute urine -> low specific gravity and low urine osmolality |
| mnemonic for SIADH and DI | SI stands for "soaked inside" DI stands for "dry inside" |
| graves disease | autoimmune hyperthyroidism |
| hyperthyroidism | TSH receptors are overstimulated => excess T3/T4 sometimes d/t excessive iodine intake |
| hyperthyroidism clinical signs | weight loss heat intolerance tachycardia tremor anxiety diarrhea goiter exophthalamos |
| hashimotos | autoimmune hypothyroidism |
| hypothyroidism | too little TSH from thyroid damage, iodine deficiency, autoimmune disease |
| signs of hypothyroidism | fatigue weight gain cold intolerance constipation dry skin/coarse hair bradycardia myxedema goiter |
| myxedema | severe form of hypothyroidism skin swelling and thickening -> can lead to myxedema coma |
| hypothyroidism labs | high TSH low FT4 in primary hypothyroidism |
| hyperthyroidism labs | low TSH high T3/T4 increased radioactive iodine (when eating too much iodine) |
| cushing vs addison | cushing = too much cortisol addison = too little cortisol/aldosterone |
| cushing syndrome | too much cortisol |
| causes of cushing syndrome | long term steroid pituitary tumor (increased ACTH) adrenal tumor ectopic ACTH |
| signs of cushing syndrome | moon shaped face/buffalo hump truncal obesity think skin poor wound healing hyperglycemia infection mood change |
| addison disease | too little cortisol (often with aldosterone deficiency) |
| causes of addison disease | damage to adrenal cortex (usually autoimmune destruction) |
| signs of addison disease | hyperpigmented skin weakness weight loss hypotension hyponatremia/hyperkalemia dehydration poor stress tolerance |
| Addison's disease crisis | aka adrenal crisis see severe hypotension and shock life threatening condition |
| insulin | anabolic hormone promotes glucose, potassium, phosphate and magnesium intake in cells promote glycogen/protein/fat synthesis |
| type 1 DM | autoimmune destruction of beta cells (absolute insulin deficiency) |
| T1 DM signs | classic Ps = polyuria, polydipsia, polyphagia weight loss fatigue |
| polydipsia | excessive thirst |
| polyuria | excessive urine production |
| polyphagia | excessive hunger |
| DMT1 treatment | exogenous insulin |
| type 2 DM | insulin resistance (with insulin deficiency) strong link to obesity and inactivity |
| type 2 DM complications | usually asymptomatic in beginning can cause CVD, neuropathy, nephropathy, retinopathy |
| gestational diabetes | glucose intolerance in pregnancy due to pregnancy related insulin resistance |
| risk of gestational diabetes | macrosomnia neonatal hypoglycemia maternal progression to DMT2 |
| pancreatic alpha cells | secrete glucagon |
| pancreatic beta cells | secrete insulin |
| pancreatic delta cells | secrete somatostatin and gastrin -> regulate alpha/beta cell function by suppressing insulin/glucagon/pancreatic polypeptide production |
| glucagon function | mobilize glycogen from liver and suppress insulin secretion maintain blood glucose between meals |
| islets of langerhans | part of pancreas made up of alpha, beta and delta cells |
| endocrine function of pancreas | insulin/glucagon hormone secretion -> regulate blood glucose level affect distant target |
| exocrine function of pancreas | production and release of digestive enzymes (amylase/lipase/proteases) aid food digestion -> local delivery |
| hypoglycemia causes | too much insulin not enough food exercise illness |
| hypoglycemia signs | tachycardia tremor sweating pallor anxiety confusion |
| tx for hypoglycemia | fast acting carbs when awake glucagon for severe cases |
| DKA | diabetic ketoacidosis (usually d/t DMT1) fat breakdown d/t insulin deficiency -> ketone byproduct -> metabolic acidosis |
| signs of DKA | polyuria dehydration kussmaul respiration fruity breath abdominal pain |
| significant labs for DKA | glucose >250 low bicarbonate low pH high anion gap ketone present |
| hyperglycemia hyperosmolar state (HHS) | usually DMT2 extremely high blood sugar levels and severe dehydration without significant ketosis |
| HHS symptoms | neurologic symptoms which can progress to coma confusion altered consciousness seizures |
| Dawn phenomenon | early morning hormones leading to high AM glucose no nighttime low sugar state (no somogyi) |
| somogyi effect | nighttime hypoglyemia with rebound high AM glucose after counter regulatory hormones |
| difference between dawn phenomenon and somogyi | both have high AM glucose dawn = no nighttime hypoglycemia somogyi = nighttime hypoglycemia |
| aging definition | Gradual, time-dependent, irreversible structural changes that reduce physiologic reserve and stress tolerance |
| senescence definition | Post-maturational processes that weaken homeostasis and increase vulnerability to illness and injury |
| life expectency | age where 50% of population expected to survive |
| life span | max human life length (abt 100 years) |
| what causes aging | a multifactorial result of changes in: - genetic programming - lifelong exposures - accumulated damages |
| cellular changes of age | telomere shortening (limit cell division) DNA damage/reduced DNA repair increased apoptosis waste product accumulation cellular atrophy/hypertrophy w/ impaired mitosis |
| outward appearing changes of age | thinner/less elastic skin (wrinkles + sagging) and pigment change thinning/graying hair height loss, stooped posture, kyphosis |
| immunologic changes of age | thymus (main immune organ) shrink T-cell function decline = more autoimmunity and infection |
| somatic mutation theory | damage to DNA and impaired repair = cellular dysfunction over time |
| free radical theory | reactive Oxygen species cause oxidative damage (lipid proteins and DNA) |
| neuroendocrine changes of age | change in hormone and nervous system influence aging ie HPA |
| immunosenescence | immuno (immune) + senescence (post maturation deteroriation) reduce thymus + T-cell function chronic low grade inflammation (inflammaging) + more auto immunity slow wound healing |
| fluid + electrolyte in aging | decrease renal function and GFR impaired thirst perception and altered Na/H2O handling higher risk of dehydration/electrolyte balance easy dehydration or hyper/hyponatremia with less classic symptoms |
| neurologic changes of aging | decrease brain volume, neurons, synapses and myelin slower nerve conduction and altered neurotransmitter level difference in cognition/sensation/motor response |
| normal vs abnormal neuro changes in aging | mild slowing/memory change = normal sudden confusion/major memory loss/focal deficit = abnormal (delirium, stroke or dementia) |
| mobility and MSK change in aging | sarcopenia joint degeneration (osteoarthritis) bone loss (osteoporosis/vertebral compression/kyphosis) gait instability |
| sarcopenia | loss of muscle mass and strength sarco meaning muscle |
| neuro/mobility change consideration in older adults | treat every older adult at fall risk until shown otherwise |
| cardiovascular change in old age | decreased arterial elasticity and increased after load left ventricular hypertrophy + increased atherosclerosis higher risk of HTN/ischemia/arrhythmia/HF |
| respiratory change in old age | loss of elastic recoil and capillary density in lung less efficient gas exchange higher risk of O2 desaturation in illness/exertion |
| CV/respiratory consideration in old age | older adults have lower physiological reserve tire easily decompensate faster accumulate drug effects more easily |
| nutritional change in aging | decreased appetite alter taste/smell oral change increased risk of protein/micronutrient deficiency |
| undernutrition | contribute to frailty, muscle loss, impaired immunity, poor wound healing and anemia |
| elimination in aging | bowel = slower motility/constipation, higher sensitivity to food/meds bladder = decrease capacity/incomplete emptying or incontinence |
| nutrition/elimination considerations in old age | ask about appetite, weight change, bowel habit and continence -> clue about overall health |
| osteoporosis | imbalance of bone resorption and formation = low bone density and high fracture risk |
| osteoporosis risk factors | age female (esp menopause) low calcium/vit D FHx smoking/EtOH inactivity meds (steroids) |
| osteoporosis manifestations | fracture vertebral compression fracture hip fracture height loss kyphosis |
| osteoporosis tx | weight bearing exercise + Ca/Vit D intake fall prevention medications (bisphosphonates) |
| alzheimer disease | progressive neurodegenerative dementia of beta-amyloid plaques, tau angles, neuroinflammation, neuronal loss, and brain atrophy (esp hippocampus/cortex) |
| early vs middle alzheimers | early = short term memory loss and slight difficulty with complex task middle = disorientation, language/behavior change, impaired ADL |
| late alzheimers | severe cognitive and physical dependence |
| RN role in alzheimers | safety (prevent wandering/falls/choking/med error) communication routine support/educate caregiver |
| apoptosis vs necrosis | programmed cell death vs uncontrolled cell death |
| humoral immunity | antibody mediated immunity |
| cell mediated immunity | T-cell response cytotoxic T-cell = directly kill pathogen helper T-cell = activate other WBC |
| type I hypersensitivity reaction | IgE mediated hypersensitivity basically allergies |
| type II hypersensitivity reaction | IgG/IgM mediated hypersensitivity autoimmune (ie. hemolytic anemia, Ab attacks RBCs or Grave's Dz) |
| type III hypersensitivity reaction | immune complex (antibody+antigen) deposits ie. lupus |
| type IV hypersensitivity reaction | T-cell mediated causing delayed reactions w/ possible inflammatory response ie. contact dermatitis |
| primary vs secondary immunodeficiency | primary = congenital/from birth secondary = acquired (ie. HIV) |
Created by:
sleepingbear