Pathophysiology Final Exam Review Updated, Exams of Nursing

Download Pathophysiology Final Exam Review Updated and more Exams Nursing in PDF only on Docsity! 1 Pathophysiology Final Exam Review Hypopituitarism Etiology o Congenital, genetic disease o Destruction of the gland (surgery/ radiation) o Tumor/ mass lesions o Pituitary infection o Deficiency of hypothalamic hormones Disorders of the posterior pituitary ADH • ADH: peptide synthesized by cells in the hypothalamus -> transported along a neural pathway -> store in pituitary • Nerve impulses causes stored ADH to be released into circulation based on serum osmolality (so based on what your body needs) o Too much concentration – you hold pee to balance ▪ Very sweet juice, you dilute it with water so you hold it in o Too little concentration- you let it out ▪ Unsweetened juice, you pee it out to make it sweet Exerts effects on tubular cells of the kidney to cause reabsorption of water Osmolality is how concentrated or diluted the serum is Sensitive changes in blood pressure and can lead to the release of ADH Abnormal synthesis of ADH because of trauma, stress, severe pain, nausea and certain medications You can check for osmolality on a blood test Usually 280-310 osm/L Isotonic – 300 Lactate ringers, normal saline 0.9% Hypertonic – above 300 Hypotonic- less than 300 Trigger is higher the osmolality the higher the concentration 2 Secretes ADH and ADH vasoconstricts and keeps fluid on board Comes from posterior pituitary SIADH vs DI Diabetes insipidus Insipidus –no flavor SIADH (syndrome of inappropriate ADH) Super increased ADH ADH (regulates H2O) and vasoconstriction Deficiency Excessive secretion Serum osmolality ↑blood very concentrated ↓blood very diluted Urine osmolality ↓ ↑ Urine output High urine output (diluted) 5-24 L per day Low urine output Fluid volume status Deficit Overload Sodium level Hypernatremia Hyponatremia • Diabetes insipidus is a disorder of the posterior lobe of the pituitary • Vasodepressor • Diabetes insipidus are unable to concentrate their urine and excretes large volumes of urine o CNS component to it because of something in the ADH ex: head trauma, surgery • When kidneys don’t respond to ADH • Drugs that cause DI- electrolyte disorders… • We can evaluate antidiuretic hormone levels along with osmolality of the urine • If you can’t excrete urine it stays in the tissue o Polyuria: lots of urine o Sodium is low because there is a lot of fluid o Syndrome of ADH is a result of brain tumors • Brain tumors can start secreting hormones o -surgery o -temperature changes Disorders of the thyroid • Thyroid releases T3 and T4 5 6 lOMoAR cPSD|4971631 ▪ B cells make antibodies against TSH receptors and the antibodies stimulate TSH o Adenoma □ tumor o Thyroid storm o Iodine- containing agents Autoantibodies get produced Low TSH levels because of negative feedback loop Negative feedback loop would close off anterior pituitary Goiter- can involve entire gland and can develop nodules and may produce signs of thyroidtoxosis Glands can be so enlarged that it puts pressure on other organs or masses Signs and symptoms • Increase in oxygen consumption • Use of metabolic fuels • Tissues exposed to high level of circulating thyroid hormone • Increase SNS activity o Increased HR, palpitations o Shortness of breath, fine muscle tremor o Heat intolerance o Excessive sweating o Muscle gramps in the GI tract ▪ Diarrhea ▪ Listen for hyperactive bowel sounds o Thin hair/ skin o Nervousness, anxiety Hyperthyroidism: Graves Disease • Autoimmune disorder • Abnormal stimulation of thyroid by thyroid-stimulating antibodies • Cytokine-mediated responses causes o Exophthalmos □ Results in cytokine and develop abnormal tissue in the eyes that push the eyeballs out and corneal ulcerations o Goiter Weight loss o Anxiety o S/S hyperthyroid o Seen in ages 20-40 years old 7 10 lOMoAR cPSD|4971631 o Increased in women o Thyroid is destroyed o Can develop goiter because of immune mediated destruction of the thyroid gland Clinical manifestations • Hypometabolic state o Weakness, fatigue, weight gain o Cold intolerance / dry skin o Mental sluggishness o Puffy face, edema o Brittle hair o Slowed GI motility □ Constipation o Mental dullness, lethargy o Hoarse voice o Bradycardia, decreased CO Hypothyroidism: myxedema coma Pathophysiology • Carbon dioxide retention • Fluid and electrolyte imbalance • Hypothermia Clinical manifestations • Coma, cardio vascular collapse • Hypoventilation • Hyponatremia • Hypoglycemia Lactic acidosis • Unable to metabolize sedatives • Hypothermia Disorders of the adrenal gland HPA Axis • Aldosterone: retention of water and sodium and excretes potassium • Adrenal medulla makes epi and norepi Disorders of adrenal function • Control of adrenal cortical function Aldosterone (principal mineralocorticoid) ▪ Function in sodium, potassium, and water balance 11 12 lOMoAR cPSD|4971631 o Cortisol (hydrocortisone [major glucocorticoid]) ▪ Aid in regulating the metabolic functions of the body and in controlling the inflammatory response ▪ Essential for survival in stress situations • If you don’t have it you can’t respond to stress and die ▪ Regulated by negative feedback loop by ACTH o Androgens (chief sex hormone) Disorders of adrenal cortex: adrenal insufficiency • Primary o Patho: disorder caused by destruction of adrenal gland o Addisons disease • Secondary o Patho: disorder of the HPA system Addison’s disease • Adrenal cortical hormones are deficient • ACTH levels are elevated (lack of feedback inhibition) • Etiology: hemorrhage, AIDS, drugs, metastatic cancer • R/T primary mineralocorticoid deficiency, glucocorticoid deficiency and hyperpigmentation from increased ACTH levels • NO CORTISOL AND NO ALDOSTERONE Autodestruction of the adrenal gland A lot of the gland has to be destroyed for you to see sings Causes bronze pigmentation of the skin because of increased ACTH levels Addison’s disease: clinical manifestations • Mineralcorticoid deficiency o Decreased sodium, decreased CO, increased K ▪ Due to lack of aldosterone o Dehydration ▪ Sulfa drugs? o Weakness, fatigue o CV collapse Orthostasis ▪ Low volume • Glucocorticoid deficiency (sugar) o Hypoglycemia 15 16 ↑Ca⁺ PTH inhibited Calcium deposited into bones increased in the bone • Clinical manifestations o Altered fat metabolism ▪ Buffalo hump ▪ Moon face o Muscle weakness/wasting o Abdominal fat o Purple striae o Osteoporosis o Derangements in glucose metabolism □ Elevated o Gastric acid secretion o Hypokalemia o Hirsutism, mild acne, and menstrual irregularities Cushings needs bananas because they are high in potassium and the person is low in potassium Cancers can produce tumors from there the organ is not at Very thin extremities because of protein breakdown Poor wound healing o Increased glucogenesis/ hyperglycemia o Nitrogen, CHO, mineral metabolism altered; increased total body fat □ Truncal obesity, moon face, buffalo hump o Hypokalemia; hypernatremia, hypervolemia o Hypertensive Disorders of parathyroid hormone: normal ▪ Parathyroid hormone is secreted by the parathyroid ▪ Located on dorsal surface of the thyroid ▪ If you take out the thyroid check the parathyroid because of location ▪ Dominated regulator of parathyroid is calcium concentration in the plasma o Responds to changes in calcium levels ▪ Parathyroid hormones take calcium from the bones and takes it into the blood ▪ Phosphorus does not affect calcium but indirectly works with it ▪ Higher the phosphorus, the lower the calcium o Inversely proportional ▪ Phosphorus ↓Ca⁺ PTH increased Calcium mobilized from bone and released into blood decreased in the bone and goes into the blood bones break 17 binds with calcium 20 protein and go into the liver 21 • Increases breakdown of proteins into amino acids for use in gluconeogenesis • Increases conversion of amino acids into glucose precursors • Promotes glycogen breakdown • Increases the amount of fatty acids available • Glucose uses fats Other hormones affecting blood glucose • Catecholamine’s o Epi and norepi o Help to maintain blood glucose levels during periods of stress □ Increase blood glucose during times of fight or flight • Growth hormone o Increases protein synthesis in all cells of the body, mobilizes fatty acids from adipose tissue, and antagonizes the effects of insulin o In periods of fasting when glucose and insulin levels fall, growth hormone increases • Glucocorticoids o Critical to survival during periods of fasting and starvation o Stimulate gluconeogenesis by the liver o Increases the level of blood glucose Diabetes mellitus • Common chronic disease • Requires lifelong behavioral and lifestyle changes • Collaborative approach • Nurse’s role as part of team: o Plan, organize, coordinate care o All about managing diabetes at HOME Major public health issue • Abnormality in blood glucose regulation and nutrient storage o Absolute deficiency of insulin- type 1 o Resistance to actions of insulin – type 2 □ Either makes in small amounts or makes in adequate amounts but there is a resistance in the receptors • Affects 23.6 million (7.8% of population) • 57 million have “pre-diabetes” • Nursing role o Prevention o Education Diabetes mellitus • Pre-diabetes o Impaired fasting plasma glucose and impaired glucose tolerance □ 8 hours fasting for blood glucose testing o Have glucose levels that don’t meet the levels of diabetes but too high to be considered normal o Will lead to type 2 o We can restrict calories and put them on weight loss programs and exercise o 22 Higher than 126 is when we say you are diabetic 25 • Chronic hyperglycemia can induce beta cell desensitization (glucotoxicity) 26 • Chronic elevation of free fatty acids can cause toxicity to beta cells (lipotoxicity) • Amyloid deposition in the beta cell can cause dysfunction 27 Type 1 Type 2 Metabolic syndrome Hyperglycemia in patients with type 2 diabetes is frequently associated with o 30 ▪ Not metabolizing food properly 31 Glycosuria – sugar in the urine Intracellular dehydration leads to thirst Eating a lot but not losing weight Low bp High HR – fast, thready pulse Clinical manifestations of hyperglycemia • Weight loss or gain • Recurrent blurred vision o Changes behind the eye retina • Fatigue • Paresthesia o Tingling/ numbness • Skin infections o Bacteria loves sugar • Dehydration -> o Hemoconcentration o Hypovolemia o Hyperviscosity ▪ Blood gets thick o Hypoperfusion ▪ Slow because blood cannot get to the proper places because it’s thick o Hypoxia (especially to brain cells) If you can’t send glucose, you start to see altered levels of consciousness Diagnostic testing • Fasting blood glucose o At least 8 hours o Under 100 o Around 120- impaired fasting glucose o Above 126 is considered diabetic • Casual blood glucose test o Blood drawn randomly • Oral glucose test o Give patient 75g of glucose solution o Draws blood later (4 hours) • Capillary blood tests and self- monitoring of capillary blood glucose levels o Go to health care center • Glycosylated hemoglobin testing o HbA1c • Urine tests 32 DM management • Insulin o Short acting o Intermediate acting o Long acting • Dietary • Exercise • Weight loss • Education • Pancreas or islet cell transplantation Acute complications of diabetes Diabetic ketoacidosis (DKA) • Characteristics o Hyperglycemia (>250 mg/dL) ▪ Urinates a lot ▪ Very thirsty o Ketosis (+ urine and serum ketones) ▪ Hyposmolarity o Metabolic acidosis (low serum bicarbonate, low pH) ▪ Acidosis is the problem and the ph is low so respiratory takes over to get rid of the acid and increases the rate and depth of breathing in attempt to get rid of CO2 ▪ Breath is acetone scented • Life threatening • Primarily affects type 1 DM o Stress, infection • Pee a lot and it will be clear • Dehydration from peeing so much • Will lead to electrolyte imbalance • Decreased bicarb o Low bicarb- acidic o High bicarb- alkalotic Hyperosmolar hyperglycemic state (HHS) • Characterized by o Hyperglycemia (>600mg/dL) o Hyperosmaolarity (plasma osmolarity >320) ▪ Normal labs are about 280-300 • Lab dependent o Dehydration o Absence of ketoacidosis ▪ Non ketonic- still have some action from insulin o Depression of sensorium ▪ Altered level of consciousness • May occur with type 2 DM Hypoglycemia • Not enough food Too much insulin • Sweating • Shaking • Altered mental status 35 • Women affected nearly three times more commonly than men during early adulthood (< 40 years) 36 • Incidence is equal in puberty and after age of 40 • Incidence is higher in men after age 50 • Lambert-Eaton myasthenic syndrome (don’t stress) o Can be considered an autoimmune disorder o Develops in association with neoplasms (small-cell carcinoma of the lungs) Generation of nerve impulses from the neurons and it happens across the synapse These impulses are transmitted by neurohumoral transmitters Acetylcholine is the important neurotransmitter Acetylcholine gets released from the axon terminal and bind to receptor on the motor neuron Acetylcholine causes the muscles to contract Myasthenia gravis is an antibody mediated attack on the receptors and affects communication between the neuron and the innervated muscle. Tends to peak in early adulthood • Definition o Disorder of transmission at the neuromuscular junction that affects communication between the motor neuron and the innervated muscle cell o They can’t control muscle alignment • Pathophysiology o Autoimmune disease caused by antibody-mediated loss of acetylcholine receptors in the neuromuscular junction Three mechanisms underlie the loss of functional acetylcholine receptors: ACTH doesn’t get transmitted properly 1. Complement-mediated injury to postsynaptic muscle membrane 1. Injury 2. Accelerated acetylcholine receptor degradation by receptor specific antibodies 1. Doesn’t take the ACTH 3. Blockade of the receptor by antibodies attached to the acetylcholine-binding sites 1. Blocks it Every time acetylcholine is released, you have decreased amplitude of the transmitters Tends to be more central but can be distal Trigger/Inciting Factor o Unclear, but evidence implicates thymic 37 abnormalities 40 • Worsening of parkinsons o By a virus ▪ Side effect of therapy with antipsychotic drugs which block dopamine receptors ▪ Toxic reaction to a chemical agent ▪ Outcome of severe carbon monoxide poisoning • Clinical Manifestations o Tremor o Rigidity o Bradykinesia/slowness of movement o Cognitive dysfunction o Failure to express emotion o Orthostatic hypotension o Drool when they eat which can lead to nutritional problems o Can lead to aspiration pneumonia □ Food/fluid goes into lungs Diagnosis • Physical assessment, HPI • Rule out other etiology • PET scan • Dopamine challenge o Give them dopamine and they get better Nursing interventions • Fall prevention • Aspiration precautions • Monitoring of vital signs Upper motor neuron disorders: multiple sclerosis Definition • Demyelinating disorder characterized by inflammation and selective destruction of CNS myelin Peripheral nervous system is spared o If it gets bad then it spreads to the peripheral Etiology • Most common demyelinating disease • Age of onset: 20-40 years • Women affected twice as frequently as men • A lot end up paralyzed Autoimmune disorder. You need a myelin sheath. The sheath helps with smooth movements. Without it you will have decreased transmission with movement. Immune system and environmental factors lead to the cause such as a being predisposed and a virus. Mainly seen in women. Could be hormonal element in the midlife age group Lesion plaque forms and the myelin sheath breaks down and leads to problems with muscle movement Lesions commonly affected by MS are optic nerve, visual fields, speech, swallowing, muscle strength, gait, coordination, balance, 41 Affects -brain stem, cerebellum (balance), matter white with some grey 42 Common type is relapse remitting Acute exacerbation, recovery and then a relapse During relapse PTO is very important Symptoms lasts days to weeks and then resolves. Depression, mood swings, loss of memory • Demyelination of nerve fibers in white matter of the brain, spinal cord and optic nerve • Lesions of MS macroscopically visible throughout the white matter (plaques) o Predilection for optic nerves o Brain stem, cerebellum and spinal cord white matter Oligodendrocytes are decreased in number or absent Secondary progressive- Numbness, burning, tingling, gradual deterioration with or without relapsing Primary- near continuous deterioration without relapse/remission Primary is the worst Gradual deterioration, Subsequent superimposed relapses More central nervous systems- young, female, maybe hormonal component, premenopausal Diagnosis • MRI • Also by clinical history of exacerbations Nursing Interventions 45 Classification of Brain Attacks • Ischemic strokes o Caused by an interruption of blood flow in a cerebral vessel and are the most common type of stroke, accounting for 70–80% of all strokes. • Hemorrhagic strokes o Caused by bleeding into brain tissue, usually from a blood vessel rupture caused by hypertension, aneurysms, arteriovenous malformations, head injury, or blood dyscrasias o Spontaneous rupture that causes hematoma, edema Ischemic is more common interruption of blood flow TIA- transient ischemia- you don’t develop the infarction at the time but you can recover and have a stroke later on Resolves within 24 hours. No physiologic changes will show on a scan A thrombus tends to happen locally and the patient will develop collateral circulation Ischemic Brain Attacks • Thrombus o Most common (large or small vessels) o Atherosclerosis • Embolic o Cardiogenic ▪ Came from the heart ▪ Small emboli that form in the heart and can go to the brain o Frequent site: MCA • TIA o Warning sign o Resolves within 24 hours o Causes are same as ischemic stroke Hemorrhagic Stroke • Most frequent fatal stroke: intracerebral hemorrhage Results in: o Hemorrhage into brain tissue o Intraventricular hemorrhage o Cerebral Edema o Compression of brain contents o Spasm of adjacent blood vessels • Predisposing factors o Age 46 o Hypertension o Aneurysm o Trauma o Tumors o AV malformations o Coagulopathy TIME FRAME IS IMPORTANT • Clinical manifestations o Sudden in onset o Focal o One-sided o Weakness of face/arm/leg o Unilateral numbness o Vision loss in one eye or to one side o Language disturbance o Slurred speech o Unexplained imbalance • Specific stroke signs depend on vascular territory compromised Locate which artery is being affected Collateral circulation- new channels that form for circulation Numbess on one side or vision loss on one side In a TIA these symptoms resolve quickly on their own Diagnosis • CT scan • MRI • H & P Nursing Interventions • Safe environment • Monitor ABC’s • Medication administration • Aspiration precautions Urinary tract infections (UTI) • The second most common bacterial infection seen by health care providers • Etiology o Gram Negative Bacteria ▪ E-coli ▪ Staphylococcus saprophyticus ▪ Proteus mirabilis, Klebsiella pneumoniae, Enterobacter, Pseudomonas o Gram-positive ▪ Staphylococcus aureus, group B streptococcus ▪ Complicated UTIs Lower- cystitis- bladder Upper- pyelonephritis- more serious, can cause renal damage 47 Commonly caused by e-coli (found in the GI tract), not wiping correctly or washing hands can lead to contamination • Bacteria usually enter through the urethra Host defenses include: o Washout phenomenon ▪ Urine washes out the bacteria o Protective mucin layer ▪ Coating barrier that prevents against bacterial invasion o Local immune responses and IgA ( body fluids) o Normal bacterial flora ▪ Lactobacillus in urethra of women ▪ Men: prostatic fluid protects urethra ▪ IgA protects against infections in urethra Most enter through the urethra or blood stream in immunocompromised patients. Small portions of the urethra has bacteria in distal end Urethra is sterile in the middle Normal flora especially in women protect against infections Very hormonal based Harder for men to get UTI because of the longer urethra and prostatic fluid that protects the urethra Risk factors • Anatomical or structural factors • Sexual activity • Delayed postcoital urination o Pee after sex to flush out bacteria • Impaired voiding o Neuro problems, stress continence, reflux of urine • Catheters & other urinary instrumentations • Constipation • Reduction of estrogen • Diabetes o Because of sugar in the urine and sugar helps bacteria grow Estrogen plays a role in promoting normal mucosal structures Lack of estrogen can be a lack of mucosa and discharge Urinary catheters can lead to UTI Signs and symptoms • Dysuria o Pain during urination • Urgency • Frequency • With acute cystitis (infection of the bladder): o Hematuria 50 Usually not symptomatic. Mainly found in men over 65 who already have enlarged prostate. Environmental – high fat diets, processed meats, a lot of dairy (causes inflammation), is familial deposition Prostate cancer: prevention • Screening: • General: PSA/DRE Age 50-75 • Family History: Age 40-45 • PSA controversy • Diet • Medication PSA is controversial and needs to be looked over time Diagnosis prostate CA • History and physical • Biopsy • MRI • Blood test for serum creatinine (urine clearance) and prostate-specific antigen (PSA) Prostate cancer prevention: • Men die earlier than women – women don’t have a prostate lol • One issue is lack of screening and • health maintenance • Prostate cancer and enlargement very • common • Early diagnosis can prevent future • morbidity and mortality • Visit doctor or urologist regularly KNOW SIGNS AND SYMPTOMS BPH looks like cancer Benign prostatic hyperplasia (BPH) • Nodules have compressed the urethra to a narrow slit • Decreasing testosterone levels can decrease the prostate growth Age related, nonmalignant, periurethral (surrounding urethra) Benign prostatic hyperplasia • Urinary Retention Renal Impairment • Urinary Tract Infection • Gross Hematuria 51 o Lots of blood in the urine and you can see it • Bladder Stone • Bladder decompensation- affects the way the bladder works • Overflow incontinence as a result of • retention Symptoms look similar Tend to develop stones in the bladder. When stones develop in the bladder the pain is not the same as kidney stones Diagnosis of BPH • history • digital rectal examination • urinalysis • blood test for serum creatinine and prostate- specific antigen Kidney stone formation • Supersaturation of one or more salts o Presence of a salt in a higher concentration than the volume able to dissolve the salt • Precipitation of a salt from liquid to solid state o Temperature and pH • Growth into a stone via crystallization or aggregation Other factors affecting stone formation: o Crystal growth-inhibiting substances o Particle retention o Matrix • Stones: o Calcium oxalate or calcium phosphate o Struvite stones 15% and form in alkaline urine □ Tend to relate to UTI o Uric acid stones Calcium salts, uric acid stone, phosphate stones, cysteine Type of stone a person develops is based on the pH and ions present Calcium obsolete- crystal From nuclei and tend to start growing Most of the stones you see are calcium stones 80-85% and tend to be patients that have increased calcium in the blood Too many calcium supplements does not help An acidic environment is not favorable for UTI, stones form in an acidic environment 52 How do you know what kind of stone? – Strain the urine and the stones sit on the strain and are sent to the lab Clinical manifestations • Severe abdominal or Flank Pain • Frequency and Dysuria • Oliguria and Anuria with obstruction • Hematuria • Nausea • Hydronephrosis (fluid starts backing up) Flank pain Unilateral so block the ureter on one side Lasers help Pain is highest priority Kidney stones diagnosis • Manifestation o Renal colic • Evaluation o History o Stone and urine analysis o o Spiral Intravenous pyelogram (IVP) or kidney, ureter, bladder x-ray (KUB) abdominal CT or Ultrasound o Urine Culture o Cystoscopy Prevention • Low calcium diet • Protein restriction (struvite stone) • Sodium intake of 3 to 4g/d recommended • Avoid intake of oxalate containing food (eg strawberries, spinach, peanuts, wheat bran) • Fluid intake 1 to 2 L daily IgE- eosinophils- allergic reactions Class description IgG Newborns, placenta IgA Body Secretions: mucus, saliva IgM Forms natural antibodies such those ABO blood IgD B lymphocytes 55 Photosensitivity – blisters from the sun due to exposure. They need to limit their exposure to the sun Western blot test- HIV specific test Viral load increases and CD-4 count decreases CD4 is normally at a million When less than 200 you have AIDS HAART- cocktail med that work in the replication of the virus With HIV you want to monitor the CD4 count because you don’t want it to get too low You want a high CD4 load and a low viral load CMV- cytomegalovirus Pernicious anemia- specific type of b12 anemia. Lack of b12. They don’t have the intrinsic factor so they can’t absorb b12. You need injections. Tingling in the extremities is a big sign. Red beefy tongue. Iron deficiency- fatigue, palpitations, dyspnea, brittle hair and nails, agular chelosis (cracks on the sides of the lips) Neuro deficit is only for B12. None of the anemias have high or extra color. Aplastic anemia affects all the blood lines. Chronic anemia- IBD because of chronic inflammation can lead to bleeding. Hyperplas Hypertrop Metaplasia Dysplasia Atrophy 56 ia hy Increase in the number of cells in an organ or tissue- responds to a stimulus and stops when the stimulus is removed. Breast enlargement during pregnancy are examples of physiologic hyperplasia. The regeneration of the liver after a partial hepatectomy is an example of compensator y hyperplasia. An increase in cell size and with an increase in tissue mass. Physiological hypertrophy: The increase muscle mass relating to exercise. Pathological hypertrophy: Disease conditions and may be adaptive. Adaptive: Thickening of the urinary bladder from long-continued obstruction of urinary flow. Compensatory: When one kidney is removed, the remaining one will enlarged to compensate for the loss. Reversible change in which one adult cell type replaces another adult cell type. More mature cells become replaced by immature cells EX: adaptive substitution of stratified squamous epithelial cells for the ciliated columnar epithelial cells in the trachea and large airways of a habitual cigarette smoker. (Barrett’s esophagus) Deranged cell growth of a specified tissue, results in a vary in size, shape, and organs Potentially reversible is underlying cause is removed. This is a strong precursor of cancer The decrease in cell size. Physiological atrophy: When you don’t use your muscles they get smaller and this is usually reversible. Pathological Atrophy: This has to do with a disease which causes the cell size to shrink. Causes: 1. Disuse 2. Denervation 3. Loss of endocrine stimulation 4. Inadequate nutrition 5. Ischemia Adaptive and reversible 57 Megaloblastic, and different anemias Iron Deficiency Anemia Megaloblastic Anemia Aplastic Anemia Chronic Disease Anemia Iron deficiency anemia is a Microcytic anemia, smaller size. You also have hypochromic meaning the color is less. You have a decrease in H&H (Decrease in hemoglobin and hematocrit) you will have: increase RR, you will also be dizzy. Iron deficiency anemia is usually related through chronic blood loss from the stool. Usually related to the GI tract. Iron cannot be recycled. The other things that patients will exhibit is cracked lips. Large hemorrhoids can cause iron deficiency anemi a o Vitamin b12 deficiency o Folic Acid deficiency With Vitamin b12 deficiency and folic: you still tend to have a normal hemoglobin, but the RBC have a shorter half-life. They live less than the average individual ”MEGA” meaning bigger, and enlarged RBC. MCV is greater. LARGE RBC • Vitamin b12: help with the transmission of nerve symptoms. o Will have a tingling sensation in hands and feet. o NEUROLOGIC SYNDROME o Schilling Test: done for vitamin B 12 deficiency. It can be able to tell you if your body is absorbing the correct amount of b12. This test makes sure there is intrinsic factor which is needed for production of b12. Aplastic Anemia: Anemia that occurs from chronic conditions. Chronic kidney disease, erythropoietin is produced here. RBC will be impaired. Crohn’s, ulcerative colitis, and inflammatory bowel diseases will cause chronic anemia. Your bone marrow . is not working . u ctio Result in rnedu of everythingse RBC WBC, platelets. Yo need bone marrow transplant. d Radiation can cau this,s Chemicals, etc.. a CBC valuesA are low, but size an hemoglobin content of RBC’ are normal, Aplastic Anemi IS CAUSED BY STEM CELL DEFICIENC Y 60 o They will have ketone present in the urine o They will have lactic acid buildup. o What precipitates this? Patient has no idea that they have this. Body cannot keep up with metabolic demands. The lack of lipids. Ketones will store. You have no glucose; the body relies on lipids which is why they have ketones in the urine. You need some source of energy. o DKA! Metabolic acidosis! Difference between 1 & 2 diabetes Patho/manifestations for MS à Patho Manifestations Diagnosis Demyelination of nerve fibers in white matter of the brain (CENTRAL NERVOUS SYSTEM), spinal cord and optic nerve causes temporary, repetitive or sustained interruption in conduction of nerve o Pain from spasticity o Abnormal gait, ataxia à o Bladder and sexual dysfunction o Vertigo à Common demyelinating disorder, not curable but treatment can slow progression Women affected twice as frequently than men, most prominent in European Americans w/ an age onset of 20-40 y/o o MRI- lesions or white matter plaques o Oligodendrocytes are decrease in number absent o Lumbar Puncture for CSF (clonal IgG bands present)- high impulses Inflammation occurs 61 à Fatigue, described as a generalized Pre-renal, intra-renal and Post renal failure Pre-renal Intra-renal Post-renal Unknown etiology, possibly autoimmune or genetic basis or childhood viral infection Considered a type 4 hypersensitivity reaction Relapse/ remitting o Nystagmus o lowenergy feeling not related depression o Dysarthria: Speech à Disturbance o Mood swings, depression, OR any emotional upsets o Euphoria, apathy, forgetfulness, loss of memory o VISION is AFFECTED around plaques as well as in normal tissue; astrocytes (gliosis) appear in lesions and scar tissue forms, replacing axons and leading to permanent disability. The term gliosis leads to the term sclerosis which means scarring Characterized by exacerbations and remissions over many years in several different sites in the CNS Initially, there is normal or nearnormal neurologic function between exacerbations. As the disease progresses, there is less improvement between exacerbations Corticosteroids are used, plasmapheresis level of antibodies o Muscle testing 62 Right sided heart failure Left sided heart failure Decreased blood flow to the kidney A sharp decrease in urine output is a sign of prerenal failure. Causes of prerenal failure are; Hypovolemia Hemorrhage Dehydration Excessive loss of G.I. tract fluids Excessive loss of fluid to burn injury Decreased vascular filling, anaphylactic shock, septic shock HF and cardiogenic shock Decreased renal Disorders that disrupt the structures in the kidney The main cause of intrarenal failure are ischemia associated with pre- renal failure, toxic insult to the tubular structures of the nephron and Intratubular obstruction. Causes include: Acute tubular necrosis Prolonged renal ischemia Exposure to toxic drugs Intratubular obx Acute renal disease Disorders that interfere with the elimination of urine from the kidney. Due to increased urine not being able to be excreted due to obx, retrograde pressure occurs throughout the tubules and nephrons which ultimately damages the nephrons. Prostatic hyperplasia is the most common underlying problem. Causes include: Bilateral ureteral obx Bladder outlet obx perfusion Signs for right/ left heart failure