– steady state of internal balance, regulated by nutrient concentration, O2 & CO2, waste products, pH, water, salt & electrolytes, volume & pressure, temp Flashcards

Question

Describe the 4 buffering systems in the body

Answer 1

Carbonic acid Buffer changes brought about by causes other than fluctuation in CO2 generated H2CO2 – lactic acid, loss of HCL due to vomiting Protein buffer Primarily important intracellularly Excellent because they contain both acidic/basic groups that can give/take up H+ Hemoglobin buffer- Most H+ generation from CO2 at tissue becomes bound to Hb Phosphate buffer- Important intracellularly and in urine

Answer 2

Increased waist circumference : men >40 in, Women >35 in Plasma triglycerides ≥ 150 mg/dl HDL-C : men <40, women <50 BP ≥130/85 Fasting plasma glucose ≥100 mg/dl

Answer 3

Modifiable Hyperhomocysteinemia, dyslipidemia HTN, smoking, obesity, DM, sedentary lifestyle, stress, alcohol Nonmodifiable Increasing age, male gender/women after menopause, genetic predisposition, black/Asian

Answer 4

Initiating event – endothelial damage ** Oxidation of LDL is central to the development of atherosclerotic plaque Injury to endothelium causing endothelial dysfunction & inflammation. Inflammatory cytokines release 🡪 draw monocytes Monocytes adhere to damaged endothelium, migrating between endothelial cells into intima. Monocytes 🡪 macrophages releasing enzymes & toxic oxygen free radicals causing more damage leading to oxidation of LDL Macrophages that engulf oxidized LDL🡪 foam cells🡪 fatty streaks

Answer 5

Stable angina Short lasting chest pain that many radiate , commonly mistaken for indigestion -associated with pallor, diaphoresis, dyspnea -caused by gradual luminal narrowing and hardening of arterial walls -relieved by rest & nitrates Prinzmental angina Chest pain due to transient ischemia occurs exclusively at rest -caused by vasospasm of coronary artery w/wo atherosclerosis -cyclic pattern of occurrence -results from hyperactivity of SNS, increased ca+ influx in arterial smooth muscle, impaired prod. Prostaglandin/thromboxane Silent/asymptomatic - presence of regional abnormality in left ventricular sympathetic afferent innervation - metabolic dysfunction in DM -following CABG/cardiac transplant -following ischemic nerve injury by MI Unstable angina Reversible myocardial ischemia & is a harbinger of impending infarction. -symptoms with no apparent trigger -long duration and cannot be relieved by nitrates. -caused by rupture of plaque in coronary artery

Answer 6

Left Sided HF Systolic/diastolic ventricular dysfunction ↓ left ventricular emptying & abnormal diastolic relaxation ↑ volume & pressure in left ventricle, atrium ↑ volume in pulmonary veins & pulmonary capillary bed Pulmonary edema ↑ pulmonary vascular resistance Right ventricular failure CM- external & nocturnal dyspnea, blood-tinged sputum, cough, cyanosis, fatigue Right Sided HF most common cause is left side HF , in the absence of LHF, it is caused by COPD, cystic fibrosis, ARDS ↑ pulmonary vascular resistance ↓ right ventricular emptying ↑ volume & pressure in right ventricle, atrium & great veins ↑ volume in systemic venous circulation ↑ capillary pressure resulting in peripheral edema

Answer 7

a.) Blood Volume: the higher the blood volume, the greater the amount of work is needed for the heart to pump blood through the circulatory system; ↑Blood Volume = ↑Blood Pressure b.) Overall Compliance: the elastic characteristics of the vessels contribute to the overall pressure in the vessels; the more elastic the blood vessels are, the lower the blood pressure is; ↑Blood Vessel Elasticity=↓Blood Pressure c.) Cardiac Output(CO): this is related to heart rate and stroke volume; ↑H.R. and Stroke Volume= ↑C.O= ↑B.P. d.) Peripheral Resistance: the resistance of the arteries is related to the overall compliance characteristic; ↑Peripheral Resistance = ↓Overall Compliance = ↑Arterial Blood Pressure

Answer 8

Classification of blood pressure (see table) WNL <120 mmgHg and < 80 mmHg Pre-HTN 120-129 or. <80 Stage 1 HTN 130-139 or. 80-89 Stage 2 HTN >140 or. > 90

Answer 9

Primary HTN Upper body obesity, family history , advancing age, sleep apnea, black race, high sodium intake, low intake of K+, Ca++, Mg++, smoking, alcohol Pregnancy, Diabetes, psychological stress, dylipidemia Secondary HTN Renal disease : renal artery stenosis, renal failure Adrenal disease : cushing syndrome, pheochromocytoma Thyroid disease

Answer 10

Modulates vascular tone, influences salt & water retention by kidneys

Answer 11

Cardiogenic: -Decreased CO -Tissue hypoxia -Adequate -intravascular volume -Associated w MI, HF, dysrhythmias, acute valvular dysfunction, massive PE Hypovolemic: -Loss of whole blood(hemorrhage), loss of plasma(burns), -Interstitial fluid (DM, DI, emesis, diarrhea, sweating) -Intravascular volume decreased by 15% Neurogenic: Massive vasodilation(decreased SVR)- parasympathetic overstimulation, sympathetic under stimulation - trauma to spinal cord/medulla -interruption of O2 supply/glucose to medulla -bradycardia Anaphylactic: Hypersensitivity reaction -vasodilation, relative hypovolemia, decreased tissue perfusion, impaired cellular metabolism Septic: Infection>bacteremia>SIRS Ends with multiple organ dysfunction syndrome. Most common sources of infection are: lungs, Urinary tract, GI, wounds, indwelling vascular catheters

Answer 12

The normal values for PCO2 is 35-45, and for PO2 it’s between 80-100mmHg

Answer 13

Hypoxemia ↓ PaO2 (oxygenated arterial blood) Caused by _ decrease oxygen content (high alt.), hypoventilation (COPD), diffusion abnormalities (edema), abnormal ventilation perfusion ration(asthma), pulmonary shunt (RDS) Hypercapnia - ↑ CO2, hypoventilation, results in acid base imbalance dysrhythmia, high level results in coma Caused by : decreased drive to breathe, inadequate ability to respond to ventilatory stimulation Hypoventilation - inadequate aveolar ventilation due to pulmonary mechanics or neuro control. -CO2 removal unable to keep pace with CO2 prod. (hypercapnia) Hyperventilation -alveolar ventilation that exceeds metabolic demands, hypocapnia -occurs with anxiety, acute head injury, conditions that cause insufficient oxygenation of blood Dyspnea unable to get enough air Associated with disturbances of: ventilation, gas exchange, ventilation-perfusion, increased WOB, lung diseases

Answer 14

Presence of air in pleural space caused by rupture in visceral pleura/parietal pleura. Neg, pressure destroyed Open- Tension (life threatening) – associated with decreased venous return & CO (hypoxemia, dyspnea, hypotension) Spontaneous & Secondary – pain, tachypnea, mild dyspnea

Answer 15

ARDS can be described as acute lung inflammation with alveolocapillary injury; the steps in the causes are.. (1)Decreased surfactant(which impairs the compliance of the lungs) (2)Endothelial Damage(which increases alveolocapillary membrane permeability, which will lead to pulmonary edema (3)Vasoconstriction(ventilation-perfusion mismatching) ***THE ROLE OF NEUTROPHILS IS CENTRAL TO THE DEVELOPMENT OF ARDS, because they release many inflammatory mediators like Cytokines, and these mediators can then damage the alveolocapillary membranes, which will increase membrane permeability. These mediators can also cause vasoconstriction.

Answer 16

All 3 of these Chronic Obstructive Pulmonary diseases are characterized by difficult expiration that results in increased force required to expire, and slowed emptying of the lungs. Asthma and Chronic Bronchitis are similar in that they involve impaired ciliary function, excess mucus production, and bronchospasms. Emphysema differs from them both, because it’s NOT due to any excess mucus, there’s no bronchospasms involved, nor impaired ciliary function. Instead, it involves changes to lung tissues which leads to reduced air flow, which then causes difficulty breathing, and then a reduction in elastic recoil.. Asthma is caused by … o a hyperactive immune response to an inhaled allergen that will end up activating Eosinophils, B-cells that prod. IgE antibodies that will crosslink onto IgE receptors of Mast cells in the airway and the Mast cells will release mediators o There’s then, an immediate phase where mast cell-released mediators open up tight junctions, allowing antigens to enter mucosa and activate mucosal mast cells and Eosinophils that will end up releasing more mediators. When this happens, this can cause either 1 of 3 things→ (1)Bronchospasm (2)Inc. Vascular Permeability, which will allow for more cells to come in and release additional mediators(ex: neutrophils, eosinophils, basophils, etc) (3)Increase in mucous production oThere’s a Late phase where recruited leukocytes release more mediators, there’s factors(esp. from Eosinophils) that cause damage to the epithelium and further mucus production. *Eosinophils play a key role by slowing ciliary beating, disrupting mucosal integrity, and causing epithelial damage. Chronic Bronchitis is caused by… o Inflammation of the Bronchi due to irritants such as smoke, air pollution, etc oBronchial swelling occurs, there’s excess mucus production, a chronic productive cough, bronchospasm, impaired ciliary function Emphysema is caused by… oAbnormal permanent enlargement of airways and the destruction of alveolar walls oObstruction is from changes in lung tissues, and NOT because of mucous production and inflammation oMajor mechanism is decreased air flow due to loss of elastic recoil from difficult expiration and hyperinflation

Answer 17

Pulmonary Edema: when there’s excess water in the lungs; due to lack of lymphatic drainage, lack of balance between capillary hydrostatic and capillary oncotic pressure, and a lack of capillary permeability. Pulmonary Embolism: this is an occlusion of a portion of the pulmonary vascular bed by an embolus(most common is a thrombi that’s been dislodged from deep veins in the calf); risk is higher for those who have disorders that promote blood clotting, frequent complication of hospitalization. Pulmonary Hypertension: The cause for PRIMARY pulmonary HTN is unknown, but in Secondary form of pulmonary HTN causes can be→ COPD, interstitial lung diseases, congenital or acquired heart diseases(ex: mitral stenosis, L Heart failure), or recurrent pulmonary emboli

Answer 18

The pH: ranges from 4.5-8 usually, and it may indicate whether or not there is a urinary tract or a kidney infection Specific Gravity: tells you how dilute the urine is/the urine concentration; if it’s not dilute that usually means that you’re not drinking enough fluids. Protein: can indicate Glomerular disease; trace to 4+ and detects albumin levels; the larger the amount of protein you have the more it may indicate a kidney issue. Blood: may detect myoglobin and also Glucose; may be a sign of renal damage, kidney stones, infection, cancer; RBCs in blood show sign of kidney disease, blood disorder, underlying condition like a blood disorder Glucose: sugar doesn’t usually show up in your urine, so if it does that means you’re at risk for Diabetes. Ketones: are a sign of diabetes Nitrite: bacteria that can convert nitrate into nitrite; may indicate that there is a U.T.I present Leukocyte Esterase:detects the presence of WBCs; might be a sign of infection Urine Microscopy: In urine microscopy, cells are reported as a number per high-power field; there are usually casts involved in urine microscopy and casts are tube-shaped proteins that usually indicate kidney disorders and crystals indicate kidney stones; in the casts you can see RBCs, WBCs, bacteria & yeast, and crystals; the types of casts are usually Hyaline, Granular, Waxy, RBC, and WBC oHyaline= has Tamm-Horsfall(a protein produced by renal tubular cells of Kidney); one of the most abundant proteins; the development of hyaline casts often suggests a diminished or slow urine flow, which might be a result of excessive exercise, use of diuretic drugs, fever, or acute vomiting; could indicate kidney damage or dysfunction oGranular= usually pathologic; indicate Acute Tubular Necrosis oWaxy= broad, formed in tubules of kidneys that have become dilated and atrophic because of chronic disease; waxy casts are non-specific and can be observed in a wide variety of acute and chronic kidney diseases. However, they indicate a certain degree of slowing in urine formation and, therefore, possibly more advanced kidney disease. oRBCs= if there’s more than 2-3 per High Power Field(HPF), then it’s considered pathologic; a sign of Glomerulonephritis WBCs= seen in Pyelonephritis (sudden and severe inflammation of kidney due to bacterial infection)

Answer 19

Pre-renal: refers to things involving blood flow TO the kidney; you get reduced perfusion due to inadequate blood volume and C.O. along with significant vasodilation; can be due to G.I. losses(ex: vomiting, G.I suctioning, diarrhea, G.I. bleeding); can be due to renal losses(ex: Na+/H2O imbalances from diarrhea, osmotic diuresis, D.M); can be due to skin/resp. losses(ex: burns); movement of fluid into interstitial tissue; crush injuries, acute pancreatitis, internal hemorrhaging. Intrinsic: involving issues within the kidney itself; most common problem with kidneys(makes up 65% of renal failures) o Can have Acute Tubular Necrosis(ATN) which is caused by ischemia after it being in a prolonged prerenal state or Nephrotoxicity(from drugs or pigments); Acute tubular Necrosis leads to tubular damage in Proximal Tubule or ascending limb of Henle and is usually irreversible; Clinical Manifestations: oliguric(dec. urine output) or non-oliguric, presence of granular casts on urinalysis oCan have Acute Interstitial Nephritis(AIN) which is an inflammation of interstitial tissue accompanied by tubular dystrophy; typically see edema of interstitial tissue, infiltration of lymphocytes, or tubular cell damage(in chronic interstitial nephritis you get fibrosis and atrophy of the tubulointerstitial tissue) oCan have Renovascular disease which is often due to renal infarction/red. blood supply, renal vein thrombosis(blood clot), renal artery occlusion; must be bilateral to cause renal failure Postrenal: describes flow FROM/OUT of the kidneys; makes up the lowest % of renal failure; obstruction most involve both kidneys to cause renal failure; caused by Benign Prostatic Hypertrophy(BPH), tumor, kidney stones, papillary necrosis, clots, or uteral/pelvic tumor; elevated pressures in your vessels results in adaptive dilation; if obstruction isn’t relieved it can cause nephron destruction or scarring

Answer 20

risk factors for Kidney Stones are: (1)Crystalloid Concentration(↑Ca+, ↑Oxalate, ↓Urine volume); (2)Promoters(↑Uric Acid production, and pH) (3)Inhibitor deficiencies(↓Citrate, ↓Mg) (4)Infections (urease splitting organisms) (5)Anatomical anomalies

Answer 21

The most common cause of Acute Tubular Necrosis is Ischemia(usually occurs after a prolonged prerenal state)

Answer 22

Number one indicator of the progression of Chronic Kidney Disease(CKD) is Proteinuria; the most common complication of CKD is Hypertension.

Answer 23

The risk factors for the progression of CKD is Proteinuria, HTN, Tubulointerstitial fibrosis on biopsy, Hyperlipidemia, smoking, Analgesic abuse, and Ethnicity

Answer 24

Chronic Kidney DIsease(CKD): the presence of kidney damage or decreased blood level of kidney function for at least 3 months.

Answer 25

Hypertension: if there’s decreased excretion of Na+ and H2O it can lead to HTN and it can contribute to dev. of Chronic Heart Failure(CHF). -Hyperkalemia : kidneys lose ability to secrete K+; decrease K+ intake so it doesn’t build -Renal osteodystrophy: decreased production of Vitamin D; decreased gut absorption of Ca+; Hypocalcemia; retention of “toxic” metabolites(ex:Osteomalacia, impaired bone growth in children)

Answer 26

Erythropoiesis is basically regulated w/ the hormone Erythropoietin in a negative feedback loop. Basically, when the blood O2 levels begin to decrease, the Kidney cells will detect this drop. In response, the kidney cells will signal the kidney to increase its production of EPO and release it into the blood. This then increased bone marrow and then, now, we get increased RBC production. Overall, tissue hypoxia in the kidneys causes erythropoietin release that stimulates proliferation of erythrocytes.

Answer 27

Microcytic: unusually small RBCs; Macrocytic: unusually large RBCs; Hypochromic: decrease in HgB concentration, so there’s not enough pigment that carries O2; Hyperchromic: high HgB concentrations, so there’s too much pigment that carries O2; Anisocytosis: RBCs that are of unequal size; Poikilocytosis: RBCs in varying shapes(i.e. sickle shape, oval, teardrop)

Answer 28

They help to constrict damaged blood vessels, form hemostatic plugs in injured blood vessels(blood clots), provide substances that accelerate blood clotting(factors III, Factors XIII).

Answer 29

Aplastic Anemia:is a red. in RBCs, WBCs, and platelets from bone marrow suppression; Clinical Manifestations are usually: S.O.B, rapid H.R, headache, fever, tiredness; can be autoimmune disorders directed at blood stem cells; can be idiopathic or from total body radiation, can be familial, or from infections(ex: HIV, Hepatitis) Pernicious Anemia: there’s a slow onset, but by the time of diagnosis symptoms are severe; characterized by B12 deficiency(usually cause of gastritis or absence of intrinsic factor needed to absorb B12 or can be cause of genetics); Clinical Manifestations are usually: weakness, fatigue, paresthesias, ataxia, sore throat, red tongue, low HgB, high Hematocrit, High MCV, low B12. Folate Deficiency Anemia: Characterized by a deficiency in Folate which is essential for DNA and RNA synthesis; Pathophysiology is low serum folate; Clinical Manifestations are: similar to pernicious anemia, severe chelosis(swollen red patches at mouth corners), and stomatitis(inflamed and sore mouth) Hemolytic Anemia: Hemolysis/destruction of RBCs by way of the immune response(ex: transfusion rxn), trauma(ex; prosthetic heart valve, blood clot disorder), infection(ex: bacterial, viral), drugs,/chemicals, physical(ex: burns, radiation)or via genetics(ex: sickle cell anemia); Hematocrit and Hemoglobin levels are low and there’s a low amount of reticulocytes(immature RBCs); Clinical Manifestations are typically: hemolysis, reticulocytosis, anemia, aplastic crisis(sudden cessation of bone marrow activity), infection(loss of splenic function), pain episodes, hand-foot syndrome(swelling of hands and feet), stroke, acute chest syndrome(dyspnea, chest pain, fever, vision problems, delayed growth, inc. risk for preterm and low weight babies) Iron Deficiency Anemia: deficient iron intake or when the demand for iron exceeds the supply of it(usually due to deficient iron intake, blood loss via G.I. bleed, metabolic iron deficiency, insufficient delivery of iron to bone marrow); Pathophysiology is: Stage 1(body iron stores depleted), Stage 2(iron transport to bone marrow is diminished; iron deficient erythropoiesis); Stage 3(small HgB deficient cells enter the circulations resulting in manifestations); Clinical Manifestations are: weakness, fatigue, S.O.B, paleness, more advanced clinical manifestations(ex: brittle nails, tongue abnormalities, stomatitis/mouth swelling, dysphagia/difficulty swallowing, neurologic conditions). Idiopathic Thrombocytopenia: in general Thrombocytopenia is when platelet count is below 150,000; oAcute idiopathic occurs more frequently in children and lasts 1-2 months, and it’s usually 2ndary to an infection(usually viral); Pathophysiology is that it occurs w/o Lupus and is assoc. w/ an inc. in antigens in the blood and the antigens form a complex w/ circulating antibodies oChronic Idiopathic is most common in women between 20 & 40 and is progressive; Pathophysiology is that Ig antibodies are directed to platelet glycoproteins and antibody-coated platelets are then recognized and removed by macrophages in the spleen -Clinical Manifestations for both Acute and Chronic Idiopathic are petechiae and purpura which may progress to major hemorrhage and cause symptoms like wt. loss, fever, and headaches) - Thrombotic Thrombocytopenia:an occlusion of arterioles and capillaries by aggregated platelets; Pathophysiology is platelet depletion, organ ischemia, assoc. w/ dysfunction of the plasma metalloprase ADAMTS14(enzyme responsible for cutting willebrand factor into smaller molecules and defects in this enzyme cause large molecular wt. von willebrand factor on cell surface–which results in aggregates of platelets which can form vessel occlusions) -Clinical Manifestations: severe thrombocytopenia(<20,000), hemolytic anemia, ischemia(which most likely involves CNS side effects), kidney failure, fever, and you’ll see an inc. in LDL and LDH. - Thrombocythemia: when the platelet count exceeds >600,000 oEssential(Primary): thrombopoietin levels are increased oSecondary: Splenectomy(spleen doesn’t remove platelets from circulation) or inflammatory conditions(excessive prod. of cytokines causes an inc.in thrombopoietin) - The Clinical Manifestations for Thrombocythemia are: arterial or venous thrombosis, ischemia, nervous system may be involved(headache, dizziness, paresthesias, stroke, visual disturbances), myocardial and renal arteries may be involved D.I.C: an acquired clinical syndrome involving widespread activation of clotting; you get multiple clots that disrupt blood flow to the organs–resulting in multi-organ failure; clotting results in consumption of platelets and platelet clotting factors leading to severe bleeding. oStep 1 of D.I.C→ endothelial injury, tissue injury, inflammation oStep 2 of D.I.C→ release of large amounts of tissue factor oStep 3 of D.I.C→ Tissue Factor initiates clotting cascade leading to production of thrombus, which leads to the production of Fibrin, which leads to the formation of a fibrin clot. -there’s platelet activation that leads to a microvascular thrombosus, ischemia, necrosis. Then, these things can cause impaired organ perfusion leading to end organ failure. The kinin system gets activated, followed by activation of the complement system, which leads to increased permeability of vessels, and then Hypotension and shock can soon follow oStep 4 of D.I.C→ factors like Tissue Necrosis Factor induce inhibitors that prevent the synthesis of Plasma, so you get diminished Fibrinolysis ability and, therefore, can’t destroy fibrin oStep 5 of D.I.C→ these fibrin products trigger cytokine release from monocytes, and this can result in further damage to the endothelium and cause further Tissue Factor release. oStep 6 of D.I.C→ consumption of platelets and clotting factors leads to hemorrhage. Clinical Manifestions of D.I.C: bacterial, viral, or parasitic infections, tissue damage, inflammation, neoplastic disorders, C.V. disorders, fat embolism, liver cirrhosis, P.E, hypothermia, placental abruption

Answer 30

Sickle cell anemia is caused by a glutamine to valine substitution; genetics can cause a mutation of HBB gene(which codes for B-Hemoglobin), and the mutation of that gene ends up calling for the nucleotide change from Thymine to Adenine; you get inflammation which causes abnormal erythrocyte membrane and the presence of chronic hemolysis which ends up triggering an inflammatory response and endothelial dysfunction. HbAs= sickle cell trait; HBSS=sickle cell disease; HbAA=normal child/adult Lost of splenic function usually because of infection is associated with sickle cell anemia, and pain is the most common symptom of sickle cell anemia/disease; can get aplastic crisis(sudden cessation of bone marrow activity), hand-foot syndrome(swelling of hands-feet), stroke, vision problems, delayed growth,

Answer 31

Negative feedback works to restore homeostasis by correcting the disruption in it. In the case of hormones, it helps to keep the thyroid hormone within its normal range.

Answer 32

Hypothyroidism: associated with the impairment of thyroid hormone output that leads to a hypometabolic state; some of the most common causes of Hypothyroidism are→ Hashimoto’s disease(blocks autoantibodies to the TSH receptor), large resection of the thyroid gland, radioactive iodine therapy, iodine deficiency; The clinical manifestations in children/during fetal dev.is cretinism(retardation of physical and intellectual growth as well as impaired skeletal growth/brain development), in adults it’s myxedema(slowed mental and physical activity; initial symptoms are fatigue, lethargy, cold intolerance, apathy; sleep apnea may develop; peripheral edema cause of accumulation of mucopolysaccharides); DIagnosed by having increased TSH levels, and lowered T4, and presence of antithyroid peroxidase antibodies in the serum(usually if they have Hashimoto’s Disease) Hyperthyroidism: Primary causes of hyperthyroidism are→ Grave’s Disease, hyperfunctional multinodular goiter, hyperfunctional adenoma/benign tumor, thyroiditis(inflammation of thyroid that causes inc. in thyroid release), thyroid cancer; Secondary causes of Hyperthyroidism are→ TSH-secreting pituitary adenoma; common clinical presentations of thyroid disease are: palpitations, fatigue, wt. loss, tremors, excessive sweating, and heat intolerance. Typically cardiac symptoms are an early hallmark of hyperthyroidism o Graves’ Disease: an autoimmune disease initiated by igG antibodies against specific domains of the TSH receptor(TSH binds to receptor and stimulates inc. release of thyroid hormones and the TSH stimulates more cells and more cells=more thyroid); you get hyperfunctioning diffuse hyperplastic goiter A.K.A overworked, spread out over a large area, enlarged goiter, ophthalmopathy(enlarged eyes), dermopathy(late characteristic where you have specks/pittings of edema); since Graves disease is an autoimmune disorder, the actions of these igG antibodies can’t be regulated by negative feedback of thyroid hormone; Diagnosed by labs showing→ decreased TSH levels, elevated T3 and T4

Answer 33

Insulin and glucagon are hormones that work together to maintain glucose homeostasis in the body. Insulin is secreted by the pancreas in response to elevated blood glucose(usually following a meal). Insulin lowers blood glucose by increasing glucose uptake in muscle and adipose tissue and by promoting glycolysis and glycogenesis in liver and muscle. Glucagon, on the other hand, is secreted by the pancreas when blood glucose levels drop. Glucagon raises blood glucose levels by stimulating glycogenolysis (breakdown of glycogen) and gluconeogenesis (synthesis of glucose from non-carbohydrate sources) in the liver.

Answer 34

Type 1 (IDDM) -lack of insulin due to reduced B-cell mass from genetic susceptibility, autoimmunity, & environmental factors. Non/immune CM- hyperglycemia, glycosuria, polyuria ,polydipsia , polyphagia ,weight loss, ketoacidosis, diabetic coma Type 2 (NIDDM) -nonspecific symptoms of fatigue, pruritus, recurrent infections, visual changes, paresthesia Increased risk of cardiovascular disease Causes – obesity & sedentary lifestyle Insulin resistance: ↓number of insulin receptors, impaired signaling, decrease synthesis and/or translocation of GLUT-4 in muscle & fat cells. - Increase in hepatic gluconeogenesis Insulin deficiency: hyperglycemia —>reduced insulin secretion-decreased GLUT-2 transporter, absence of oscillations of insulin secretion

Answer 35

a.) Fasting Blood Sugar→ <110 mg/dL c.)LDL→ <100 b.) Hemoglobin A1c→ <5.7% d.) HDL→ >45 for men and >55 for women

Answer 36

Cushing’s Disease/Syndrome: elevated cortisol (hypercortisolism). majority have a pituitary adenoma/benign tumor which secretes excess ACTH, loss of normal feedback inhibition by cortisol (i.e. the ACTH secreted by the tumor is not regulated by increased cortisol levels); most common cause of Cushing’s Syndrome is prolonged use of glucocorticoids; other cause include→ 1) ectopic ACTH-secreting tumors 2) Cortical-secreting adrenal tumors oClinical Manifestations of Cushing’s Disease→ Weight gain is the most common feature and often the initial symptom – related to accumulation of adipose tissue in the trunk, facial, and cervical areas (i.e. moon face, buffalo hump). Other manifestations include… 1. Glucose intolerance due to cortisol-induced insulin resistance, increased gluconeogenesis and increased glycogen storage. Cortisol antagonizes the action of insulin in peripheral tissues. 2. Muscle wasting, specifically in the muscle of the extremities, due to excess protein catabolism and decreased muscle protein synthesis (causes muscle weakness). 3. Increased bone resorption, inhibits bone formation, decreases intestinal calcium absorption, and increases renal calcium excretion – osteoporosis and fractures. 4. Hypercalciuria and renal stone formation 5. Glucocorticoid excess inhibits fibroblasts, leading to loss of collagen and connective tissue. Thinning of the skin, abdominal striae, easy bruisability, poor wound healing, and frequent skin infections. 6. Hyperpigmentation – associated with high levels of ACTH (results in a bronze color) 7. Hypertension (75-85%) – increased vascular sensitivity to catecholamines leading to vasoconstriction and hypertension. 8. Suppression of the immune system – increased susceptibility to infections, especially fungal infections (poor wound healing). 9. Alterations in mental status (irritability and depression to severe psychiatric disturbances). 10. Females – increased hair growth, acne, and oligomenorrhea due to increased adrenal androgen levels. 11. Men – decreased testosterone secretion – decreased libido, loss of body hair, and impotence. - Addison’s Disease: a decrease in the Aldosterone secretion from the Adrenal glands; there are idiopathic and secondary pathophysiology for Addison’s disease; o If it’s Idiopathic it’s usually the result of an autoimmune disease where there’s antibodies specifically targeting cells of the Adrenal Cortex, there’s a defect in immune surveillance mechanisms and so there becomes a deficiency in immune-suppressor cells.There can also be atrophy of the cortex o If it’s Secondary, there’s low to absent ACTH levels which leads to a decrease in cortisol secretions from the adrenal cortex.( In this type of hypocortisolism, aldosterone levels are normal); there’s inadequate adrenal stimulation, adrenal atrophy occurs, then dec. in the synthesis of corticosteroids; Usually what triggers secondary development of Addison’s Disease is (1)exogenous administration of glucocorticoids (2)surgical removal of ACTH/cortisol-secreting hormone (3)pituitary hypofunction (4)pituitary removal (5)ACTH deficiency oClinical Manifestations of Addison’s Disease: Symptoms usually begin gradually. Some common ones are→ (1)weakness (2)fatigue (3)anorexia (4)wt. loss (5)nausea (6)diarrhea (7)orthostatic hypotension (8)hyperpigmentation (8)Females – loss of pubic and axillary hair (due to decreased adrenal hormones)

Answer 37

Children: trauma, congenital defects, sequelae of chronic illness(pathological condition resulting from a prior disease, injury, or attack) Adolescents: growth delay, epiphyseal injuries, bone lesions Adults: imbalance of bone modeling, trauma, repetitive stress, cumulative load (important mechanism contributing to musculoskeletal injury and pathology), pregnancy Mature Adults: bone loss, joint degeneration, neurological/sensory changes, falls, drug therapy

Answer 38

Osteoblasts: bone formation : assists w calcification, help concentrate nutrients in the matrix Osteoclasts: bone resorption

Answer 39

- The purpose of bone remodeling is to replace old bone tissue w/ new bone tissue and is a type of preventative maintenance process. Typically it takes about 3-4 months. - Stage 1(Resting Phase): period of rest during bone formation - Stage 2(Activation): pre-osteoclasts are attracted to remodeling sites - Stage 3(Resorption): osteoclasts dig out a cavity - Stage 4(Reversal): mononuclear cells appear on the bone surface - Stage 5(Formation): osteoblasts lay down new bone til’ resorbed bone is completely replaced.

Answer 40

- Synovial joints are made up of five classes of tissues. These include bone, cartilage, synovium, synovial fluid, and tensile tissues composed of tendons and ligaments. - The synovial joint is also called the “diarthrodial joint” and is formed by three basic components: the joint cavity, the joint(articular) cartilage, and the joint capsule. - oJoint cavity- Synovial fluid is a viscous fluid that fills the synovial cavity and acts as a lubricant for smooth movement of bone - oJoint(Articular) Cartilage- covers the surfaces of articulating bones; the smooth and slippery lubricated surface of the articular cartilage is what covers the ends of bones, allowing the sliding of bones at the joint without rubbing each other - oJoint Capsule- is composed of a synovial membrane layer lining up the joint cavity and a fibrous layer(the fibrous connective tissues are what help to connect muscles to bones) and it surrounds the joint;

Answer 41

- Step 1: a fracture occurs/there’s a disruption to the periosteum and blood vessels - Step 2: there’s bleeding at the site, which leads to the inflammatory response and eventual clot formation - Step 3: necrosis starts to happen along the fracture line - Step 4: there’s the activation of bone-forming cells - Step 5: Osteoblasts start to synthesize collagen and bone matrix, and then bone remodeling eventually occurs - The healing of a fracture can be divided into three phases: inflammatory phase, reparative phase, and remodeling phase. The inflammatory phase is the first stage of healing and begins immediately upon fracture. A blood clot forms allowing the influx of inflammatory cells to the wound area. This is followed by a cytokine cascade that brings repair cells into the fracture gap. The reparative phase begins with the formation of a soft callus made up of fibroblasts and chondroblasts. The soft callus then hardens into a hard callus made up of osteoblasts and chondroblasts. The remodeling phase involves the replacement of woven bone with compact bone

Answer 42

Osteoporosis: increased loss of bone mass -imbalance between bone resorption & formation -menopausal changes -calcium deficiency -vertebral fractures most common, complications -pulmonary embolism, pneumonia Risk- age, lack of physical, inadequate calcium & vitamin d, excessive alcohol, smoking -Sprains/strains -Rhabdomyolysis: Rhabdomyolysis: a complication of severe muscle trauma oPathophysiology→ traumatic crushing of muscle, obstruction of blood supply to muscle, excessive muscle strain or activity, thermal injury, electrical oClinical Manifestations→ principle manifestation is myoglobinuria(dark urine), large levels of muscle enzymes in serum, pain and tenderness of affected muscle, serum electrolyte alterations(ex: large levels of K+/Hyperkalemia); complications can be renal failure, tachycardia, cardiac dysrhythmias, metabolic and respiratory acidosis, temperature elevation -Osteoarthritis : inflammation of synovial joints: loss & damage of articular cartilage, thickening of joint capsule, subchondral bone changes -effects primarily load bearing areas CM-pain (may be referred), stiffness, swelling, limited ROM -Rheumatoid arthritis : A systemic autoimmune diseases that causes chronic inflammation in multiple joint; synovial membrane is usually the first to be effected oPathophysiology→ an antigen activates CD4 helper T-cells and most likely b-cells; the T-cells express RANKL–which wlll promote osteoclast formation and lead to bony erosion; inflammatory cytokines induce enzymatic breakdown of cartilage and bone oClinical Manifestations→ gradual onset, fever, fatigue(systemic manifestations of inflammation), joints become painful and tender and stiff, joint swelling, loss of R.O.M, joint deformity, rheumatoid nodules, systemic symptoms -Gout: a byproduct of protein metabolism that normally assists with removal of nitrogen waste from the body; at low levels it’s an antioxidant, but at high levels it’s a pro-oxidant and causes inflammatory changes oPathophysiology→ inflammatory response to uric acid production, resulting in high levels of uric acid in the blood and other body fluids; uric acid concentration exceeds 6.8mg/dL and ends up crystallizing and forms insoluble complexes of urate that deposit in connective tissue; crystallization happens in synovial fluid which triggers an inflammatory response by macrophages; these macrophages then phagocytize urate crystals–forming an inflammasome(protein complex that regulates immunity); inflammasomes convert inactive interleukins into their active form–prolonged accumulation results in joint damage; Urate crystals trigger the acute inflammatory response oClinical Manifestations→ hyperuricemia(high level of uric acid); recurrent attacks of monoarticular arthritis, MSU deposits in and around the joints; renal disease/uric acid stones The clinical stages are.. (1)Asymptomatic hyperuricemia (2)Acute gouty arthritis (3)Tophaceous gout(severe gout)

Answer 43

Thrombotic stroke: arterial occlusions caused by thrombi in the arteries supplying the brain/intracranial vessels - Development linked to atherosclerosis,arthritis, increased coagulation, dehydration ,hypotension, prolonged vasoconstriction Embolic stroke: involves fragments that break away from a thrombus formed outside the brain(heart, aorta, carotid, thorax); involves small vessels & obstructs at a bifurcation/other point of narrowing - Atrial fibrillation major conditions associated , others include MI, endocarditis, rheumatic heart disease Hemorrhagic stroke : intracranial hemorrhage - HTN, ruptured aneurysms, arteriovenous malformations, bleeding into tumor Transient ischemic attacks: focal ischemic cerebral neurologic deficits brain angina), deficit lasting <1hr, causes are same as ischemic stroke. Warning of impending stroke

Answer 44

Generalized seizures - Involve neurons bilaterally , often no local onset, usually originate from subcortical/deep brain focus - Consciousness is always impaired/lost - Tonic, clonic, myoclonic Focal seizures - Involve neurons unilaterally, often have a local onset and usually originate from cortical brain tissue - LOC may/may not occur, may become Geraldine’s and lasts <2mins – simple or complex

Answer 45

Sudden change in membrane potential of a group of neurons: defect in GABA, channel abnormalities, abnormalities in excitatory transmission -if uninvited, excitation neurons spread to contra lateral cortex and subcortical areas-basal ganglia, thalamus, brain stem -tonic phase: phase of muscle contraction once spread to subcortical area o brain ,associated w LOC -clonic phase : phase of alternating contraction & relaxation of muscles, which begins as inhibitory muscles begin to inhibit cortical excitation

Answer 46

Nociceptor impulses are transmitted by specialized skin receptors ro spinal cord thru A & C fibers stimulation of large fibers trigger cells to “close gate “, which decreases transmission of impulses, & diminishes pain perception stimulation of small fibers “ opens the gate”, enhances pain perception

Answer 47

Substance P= activates ascending pathways Glutamate = AMPA, NMDA

Answer 48

Mechanical – cutting, crushing, pinching. Thermal -temp extremes (esp. heat) Polymodal- respond to all kinds of damaging stimuli including irritating chemicals released from injured tissues (all can be senitized by prostaglandins)

Answer 49

Responsible for inhibition of afferent pain signals *** Efferent neurons form synapses with structures in medulla that inhibit pain, impulses are transmitted back thru spinal pain to dorsal horn to block transmission of nociceptive impulses

Answer 50

1st – A (myelinated fibers Fast (30 m/sec), occurs on stimulation of mechanical & thermal nociceptors, carry well localized sharp pain sensations 2nd -C fibers (unmyelinated) Slow (12 m/sec), on stimulation of polymodal nociceptors, diffuse aching/burning sensations, poorly localized Activated by chemicals like bradykinin & capsaicin Unpleasant , persists for longer time

Answer 51

Pain threshold: the point at which a stimulus is perceived as pain. Perceptual dominance: intense pain at one location may cause an increase in threshold in another location. Pain tolerance: duration of time/instensity of pain that an individual will endure before initating overt pain responses. Influenced by – cultural perception, expectations, role, physical & mental health. Referred pain: present in area distant from its point of origin, supplied by the same spinal segment as actual site of pain Somatic pain: pain with a cause (MI) Psychogenic pain : no known physical cause, not imaginary

Answer 52

CD4 - normal >500 - immunocompetency, predicts progression Viral load - measures amount of circulating virus, reflects viral prod in all cells. - increased in infection & associated w progression.

Answer 53

Initial/early stage - Immune responds quickly & symptoms disappear in 2 weeks - HIV antibody test becomes positive w/in 4-6weeks after infection, avg 30 days (seroconversion) Chronic HIV - Contrast pattern of viral production-CD4 destruction - Lasts for several years without symptoms, eventually body’s immune system is developed and individual develops symptoms – lymphadenopathy, skin problems Advanced stage/AIDS - Labs indicate severe immunosuppression – CD4 <200 cells - One or more of 26 AID conditions: opportunistic definitions, neoplasticism disease, neurologic manifestations

Answer 54

Thrush/candida/yeast in mouth, esophagus, vagina Pneumocystis pneumonia (PCP): - life threatening if untreated, symptoms of fever, dry cough, SOB, fatigue, weight loss; prophylaxis recommended when CD4 ≤ 200 cells -Cytomegalovirus (CMV) - most commonly affects eyes causing retinitis and blindness Eye symptoms- floating spots in eye, hazy vision, blurred/blind spots GI- diarrhea, loss of appetite Mycobacterium Adium Complex (MAC) - affects lungs & intestines; severe when spread to organs like BM, liver & spleen . Symptoms of weight loss, stomach pain, diarrhea, fever , night sweats, fatigue -rarely occurs when CD4>100 cells, prophylaxis when CD4<50 cells Toxoplasmosis- - caused by parasites that infects CNS from animal feces & uncooked meat. Symptoms of confusion, seizures, headaches, numbness, coma Prevention - don’t change cat litter, wear gloves when gardening, & fully cook all meats & eggs

Answer 55

-GERD: · reflux of chyme from stomach to esophagus Risk- obesity, H. Pylori Relaxation/weakness of lower esophageal sphincter, increased abdominal pressure, delayed gastric emptying (Ulcers), hiatal hernia - CM: heartburn, upper abdominal pain w/in 1hr of eating, symptoms worsen when lying down/increase in intra-abdominal pressure -Gastritis : inflammatory disorder of gastric mucosa lining from drugs (NSAIDS), alcohol, H. Pylori -Peptic ulcer disease -Ulcerative colitis -Crohn’s disease

– steady state of internal balance, regulated by nutrient concentration, O2 & CO2, waste products, pH, water, salt & electrolytes, volume & pressure, temp Flashcards

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