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Goulds Ch 10, 11, 16
| Question | Answer |
|---|---|
| Blood circulates through the body and functions to | Transport oxygen and nutrients to all tissues, Remove waste products of cellular metabolism, Play a critical role in the body’s defenses/immune system, and serve in maintaining body homeostasis |
| Hematocrit refers to | the proportion of cells (essentially the erythrocytes) in blood and indicates the viscosity of the blood |
| All blood cells originate from the | red bone marrow |
| In the adult, red bone marrow is found in the | flat and irregular bones, ribs, vertebrae, sternum, and pelvis |
| A common site for a bone marrow aspiration for biopsy is | The iliac crest in the pelvic bone |
| The various blood cells develop from | a single stem cell during the process of hemopoiesis or hematopoiesis |
| The life span of a normal RBC is | approximately 120 days |
| An individual’s blood type (e.g., ABO and Rh group) is determined by | the presence of specific antigens on the cell membranes of that person’s erythrocytes. |
| Blood Dyscrasias are | disorders of the cellular components of the blood |
| Anemias reduce oxygen transport in the blood because of | a decrease in hemoglobin content. |
| The low hemoglobin level may result from | declining production of the protein, a decrease in the number of erythrocytes, or a combination of these factors |
| Anemias may be classified by | typical cell characteristics such as size and shape (morphology) or by etiology (e.g., the hemolytic anemias). |
| The oxygen deficit leads to a sequence of events: | Less energy is produced in all cells; cell metabolism and reproduction are diminished |
| Compensation mechanisms to improve the oxygen supply include | tachycardia and peripheral vasoconstriction. |
| General signs of anemia include | fatigue (excessive tiredness), pallor (pale face), dyspnea (increased effort to breathe), and tachycardia (rapid heart rate) |
| Decreased regeneration of epithelial cells causes the digestive tract to become | inflamed and ulcerated, leading to stomatitis (ulcers in the oral mucosa), inflamed and cracked lips, and dysphagia (difficulty swallowing); the hair and skin may show degenerative changes |
| Severe anemia may lead to | angina (chest pain) during stressful situations if the oxygen supply to the heart is sufficiently reduced. Chronic severe anemia may cause congestive heart failure. |
| Anemias may also occur when | there is a deficiency of a required nutrient, bone marrow function is impaired, or blood loss/excessive destruction of erythrocytes occurs |
| Iron Deficiency Anemia Pathophysiology | Insufficient iron impedes the synthesis of hemoglobin, thereby reducing the amount of oxygen transported in the blood .This results in microcytic (small cell), hypochromic (less color) erythrocytes owing to a low concentration of hemoglobin in each |
| Iron deficiency anemia Etiology: | Dietary intake of iron, Chronic blood loss, Duodenal absorption of iron may be impaired, Severe liver disease . In the form of iron deficiency anemia associated with some infections and cancers, iron is present but is not properly used |
| Signs and Symptoms of Anemia | Pallor of the skin and mucous membranes , Fatigue, lethargy, and cold intolerance , Irritability, brittle hair and spoon-shaped and ridged nails, Stomatitis and glossitis, Menstrual irregularities, Delayed healing, Tachycardia, dyspnea, syncope |
| Pernicious Anemia–Vitamin B12 Deficiency (Megaloblastic Anemia) are characterized by | very large, immature, nucleated erythrocytes. |
| Pernicious anemia usually results from | a deficit of folic acid (vitamin B9) or vitamin B12 (cyanocobalamin). Vitamin deficiencies usually develop gradually. |
| Pathophysiology of Pernicious anemia is | caused by the malabsorption of vitamin B12 owing to a lack of intrinsic factor. The most common cause of vitamin B12 deficiency is malabsorption, which may result from an autoimmune reaction, particularly in older individuals; from chronic gastritis |
| Signs and Symptoms of Pernicious Anemia | Basic manifestations of anemia, In addition, the following : The tongue is typically enlarged, red, sore, and shiny, digestive discomfort, often with nausea and diarrhea, tingling or paresthesia in the extremities or loss of muscle coordination |
| Aplastic Anemia Pathophysiology | Aplastic anemia results from impairment or failure of bone marrow, leading to loss of stem cells and pancytopenia, which is decreased numbers of erythrocytes, leukocytes, and platelets in the blood |
| Etiology of Aplastic anemia | In approximately half of the cases the cause is unknown or idiopathic. Myelotoxinsthat damage the bone marrow., Viruses, particularly hepatitis C,. Autoimmune disease, Genetic abnormalities such as myelodysplastic syndrome (MDS) or Fanconi anemia |
| Signs and Symptoms of Aplastic Anemia | In a majority of cases, the onset is insidious. Anemia (pallor, weakness, and dyspnea), Leukopenia, such as recurrent or multiple infections, Thrombocytopenia petechiae—flat, red, pinpoint hemorrhages on the and a tendency to bleed excessively |
| Hemolytic anemias result from | excessive destruction of RBCs, or hemolysis, leading to a low erythrocyte count and low total hemoglobin |
| Hemolytic anemias etiology | have many causes, including genetic defects affecting structure, immune reactions, changes in blood chemistry, the presence of toxins in the blood, infections such as malaria, transfusion reactions, and blood incompatibility in the neonate |
| Sickle Cell Anemia athophysiology | an inherited characteristic leads to the formation of abnormal hemoglobin, hemoglobin S (HbS) When this altered hemoglobin is deoxygenated, to “sickle” shape, leading to thrombus formation and repeated multiple infarctions |
| Sickle Cell Etiology | The gene for HbS is recessive and is common in individuals from Africa and the Middle East. In homozygotes, most of the normal hemoglobin (hemoglobin A) is replaced by HbS, resulting in clinical signs of sickle cell anemia |
| Signs and Symptoms of Sickle Cell | do not appear until the child is about 12 months of age, when fetal hemoglobin has been replaced by HbS. Severe anemia causes pallor, weakness, tachycardia, and dyspnea. Hyperbilirubinemia is indicated by jaundice, Splenomegaly is common in young people |
| Vascular occlusions and infarctions In sickle cell lead to | periodic painful crises and permanent damage to organs and tissues. Ulcers on the legs and feet, areas of necrosis in the bones or kidneys, or seizures or hemiplegia resulting from cerebral infarctions (strokes). Pain can be intense. |
| In sickle cell Occlusions in the smaller blood vessels of the hands or feet cause | hand-foot syndrome. Pain and swelling are often early signs in children. |
| In sickle cell, Growth and development in children | are delayed. Late puberty is common. Tooth eruption is late, and hypoplasia is common. Intellectual development is usually impaired. |
| In sickle cell Congestive heart failure may develop owing to | constant efforts to improve the supply of oxygen and the increased peripheral resistance caused by the obstructions. |
| In sickle cell Frequent infections occur because of | when the damaged spleen can no longer adequately filter the blood, the presence of necrotic tissues, and poor healing capabilities. Pneumonia is a common cause of death in children. Infections tend to cause more sickling, and a vicious cycle develops. |
| Thalassemia Pathophysiology | This anemia results from a genetic defect in which one or more genes for hemoglobin are missing or variant. |
| Etiology of Thalassemia | Thalassemia is the most common genetic disorder in the world. |
| Signs and Symptoms of Thalassemia | The usual signs of anemia and increased hemolysis are present, The child’s growth and development are impaired. Hyperactivity in the bone marrow leads to invasion of bone and impairs normal skeletal development. Heart failure develops |
| Spontaneous bleeding or excessive bleeding following minor tissue trauma often indicates | a blood-clotting disorder. |
| Warning Signs of Excessive Bleeding and Possible Blood-Clotting Disorders | Persistent bleeding from the gums or repeated nosebleeds, Petechiae, Frequent purpura and ecchymoses, More persistent bleeding, hemarthroses, hemoptysis, hematemesis, Blood in fecesoften black (tarry) or occult (hidden), Anemia |
| Excessive bleeding has many causes: | Thrombocytopenia may be caused by acute viral infections in children or autoimmune reactions in adults . Human immunodeficiency virus (HIV) infection, hepatomegaly and splenomegaly, and certain drugs also lead to thrombocytopenia. Chemotherapy, radiation |
| Hemophilia A Pathophysiology | is a deficit or abnormality of clotting factor VIII and is the most common inherited clotting disorder. The defect causing hemophilia A is transmitted as an X-linked recessive trait |
| Signs and Symptoms of Hemophilia A | Prolonged or severe hemorrhage occurs following minor tissue trauma. Persistent oozing of blood after minor injuries and hematomas is common. Spontaneous hemorrhage into joints (hemarthrosis. Blood may appear in the urine (hematuria) or feces because of b |
| von Willebrand Disease Pathophysiology | This is the most common hereditary blood clotting/bleeding disorder. |
| Von Willebrand disease is caused by | a deficiency of the von Willebrand factor, a clotting factor that helps platelets clump and stick to the walls of blood vessels where damage has occurred. |
| Signs and Symptoms of Von Willebrand Disease | typically include the following: Skin rashes, Frequent nosebleeds, Easy bruising, Bleeding of the gums, Abnormal menstrual bleeding |
| Disseminated Intravascular Coagulation Pathophysiology | is a condition, often life-threatening, that involves both excessive bleeding and excessive clotting. Clotting may be induced by the release of tissue thromboplastin or by injury to the endothelial cells, causing platelet adhesion. The process causes mult |
| Etiology of Disseminated Intravascular Coagulation | A variety of disorders can initiate DIC. It may result from an obstetric complication such as toxemia, amniotic fluid embolus, or abruptio placentae, in which tissue thromboplastin is released from the placenta, infection or carcinomas |
| Signs and Symptoms Of Disseminated Intravascular Coagulation | Obstetric patients usually manifest increased bleeding, whereas cancer patients tend to have more thromboses. More often, hemorrhage is the critical problem |
| Thrombophilia Pathophysiology | Thrombophilia refers to a group of inherited or acquired disorders that increase the risk of developing abnormal clots in the veins or arteries. |
| Abnormal clotting events can result in | conditions such as deep venous thrombosis, pulmonary embolism, or peripheral vascular disease. |
| Etiology of Inherited thrombophilias are | a result of mutations in the genes responsible for producing the coagulation proteins in the blood. Acquired thrombophilias commonly occur during events such as surgery or injury, or in individuals with medical conditions that allow for an increase of the |
| Signs and Symptoms of thrombophilia | The signs and symptoms of an abnormal clotting event are not specific and can affect any organ or system in which the clot may lodge and cut off the blood supply. In cases in which the clot lodges in the heart or vessels of the lung, the result can be a m |
| Myelodysplastic Syndrome pathophysiology | term used for diseases that involve inadequate production of cells by the bone marrow. It excludes disorders such as aplastic anemias and deficiency dyscrasias. |
| Etiology of Myelodysplastic diseases | may be idiopathic, or can often occur following chemotherapy or radiation treatment for other cancers. Several different types are described, including anemias and pancytopenias, in which all cell types are reduced. |
| Polycythemia Pathophysiology | Primary polycythemia, or polycythemia vera, is a condition in which there is an increased production of erythrocytes and other cells in the bone marrow. It is considered a neoplastic disorder. |
| Signs and Symptoms of Polycythemia Vera | The patient appears plethoric and cyanotic, with the deep bluish red tone of the skin and mucosa resulting from the engorged blood vessels and sluggish blood flow. Hepatomegaly, an enlarged liver, and splenomegaly are present. Pruritus is common. Blood p |
| Pathophysiology of leukemias | group of neoplastic disorders involving the WBCs Leukocytes appear undifferentiated, immature, nonfunctional cells that multiply uncontrollably in the bone marrow, and large quantities are released as such into the general circulation As the numbers of le |
| Acute leukemias are characterized by | a high proportion of very immature, nonfunctional cells (blast cells) in the bone marrow and peripheral circulation; the onset usually is abrupt, with marked signs and complications. Chronic leukemias have a higher proportion of mature cells (although the |
| Etiology of Chronic leukemias are | more common in older people |
| Etiology of acute leukemias occur | primarily in children and younger adults. |
| Signs and Symptoms of acute leukemia is | Infection, Severe occurs because of thrombocytopenia. Signs of anemia develop as the erythrocyte count drops. Bone pain is severe and steady, continuing during rest. The lymph nodes, spleen, and liver are often enlarged and may cause discomfort. If leukem |
| Signs and symptoms of Chronic leukemia | tends to have a more insidious onset, with milder signs, and may be diagnosed during a routine blood check. Early signs include fatigue, weakness, and frequent infections. |
| Atherosclerosis Pathophysiology | the presence of atheromas, plaques consisting of lipids, cells, fibrin, and cell debris, often with attached thrombi, which form inside the walls of large arteries, Low-density lipoprotein. It is a major factor contributing to atheroma formation |
| Signs and Symptoms of atherosclerosis | Increasing fatigue and weakness in the legs develop as blood flow decreases. Intermittent claudication, is a key indicator. Initially pain subsides with rest Sensory impairment may also be noted as paresthesias. Peripheral pulses distal to the become weak |
| Aortic Aneurysms Pathophysiology | a localized dilatation and weakening of an arterial wall. |
| Etiology of Aortic Aneurysms | Common causes are atherosclerosis, trauma (particularly car accidents), syphilis and other infections, and congenital defects. Hypertension is present in half of patients diagnosed with aortic aneurysms. |
| Signs and Symptoms of Aortic Aneurysms | frequently asymptomatic for a long period of time until they become very large or rupture. Abdominal aneurysms are sometimes detected as palpable pulsating masses with bruits (abnormal sounds). Rupture occasionally leads to moderate bleeding, but most oft |
| Varicose VeinsPathophysiology | Varicosities are irregular dilated and tortuous areas of the superficial or deep veins. The most common location is the legs, but varicosities are also found in the esophagus (esophageal varices) and the rectum (hemorrhoids). |
| Varicose veins in the legs etiology | may develop from a defect or weakness in the vein walls or in the valves. Long periods of standing during which the pressure within the vein is greatly elevated can also lead to varicosities. |
| Etiology of Varicose Veins | A familial tendency to varicose veins is probably related to an inherent weakness in the vein walls. The superficial leg veins are frequently involved because there is less muscle support for these veins. Valves may be damaged by trauma, intravenous admin |
| Signs and Symptoms of Varicose Veins | Superficial varicosities on the legs appear as irregular, purplish, bulging structures. |
| Thrombophlebitis refers to | an inflammation in a vein that leads to the development of a thrombus or clot. The platelets adhere to the inflamed site, and a thrombus develops. |
| Phlebothrombosis refers to | a thrombus forms spontaneously in a vein without prior inflammation, although inflammation may develop secondarily in response to thrombosis. |
| Thrombophlebitis etiology | stasis of blood or sluggish blood flow, which is often present in people who are immobile, Endothelial injury, which may have arisen from trauma, chemical injury, intravenous injection, or inflammation, is another factor, or increased blood coagulation, w |
| The lymphatic system consists of | lymphatic vessels, lymphoid tissue, which includes the palatine and pharyngeal tonsils, lymph nodes, the spleen, and the thymus gland. |
| The lymphatic system functions to | return excess interstitial fluid and protein to the blood, to filter and destroy unwanted material from the body fluids, and to initiate an immune response. |
| The spleen has many functions: | defense, hematopoiesis, and red blood cell (RBC) and platelet destruction, as well as serving as a reservoir for blood. As part of the body’s defense, the blood passes through the spleen, where macrophages remove microorganisms from the blood and destroy |
| The thymus plays a critical role in the immune response to infections. | the final site of lymphocyte development before birth; and the secretion of hormones after birth that enable lymphocytes to develop into mature T cells. The role of the thymus is extremely important as part of the immune mechanism of the body. |
| Lymphadenopathy pathophysiology | the most common disease of the lymphatic system, is an inflammation or infection of lymph nodes. |
| Etiology of lymphadenopathy | Infections can be caused by both bacteria and viruses, such as streptococcus, human immunodeficiency virus (HIV), and organisms associated with skin wound infections. Cancer can also cause severe inflammation of the nodes. |
| Symptoms of lymphadenopathy | typically manifests as swollen lymph nodes and is a common sign of another disease. |
| Lymphomas pathophysiology | malignant neoplasms involving lymphocyte proliferation in the lymph nodes. The two main disorders, Hodgkin lymphoma and non-Hodgkin lymphoma, actually a group of lymphomas, are differentiated by lymph node biopsy. |
| Etiology of lymphomas | Specific causes of lymphomas have not been identified, but there is a higher incidence in adults who received radiation treatments during childhood. |
| Pathophysiology of Hodgkin disease | a type of lymphoma starting in lymphocytes. The disease can start almost anywhere, but most often it originates in lymph nodes in the upper part of the body. |
| Symptoms of Hodgekin Lymphoma | initially involves a single lymph node, frequently in the neck area Later the cancer spreads to adjacent nodes and then to organs via the lymphatics. The atypical cell used as a marker for diagnosis of Hodgkin lymphoma is the Reed–Sternberg cell, a giant |
| A common system used for staging Hodgkin lymphoma is the | Ann Arbor staging system, which uses the diaphragm as the differential landmark. |
| The Ann Arbor staging system generally defines a stage I cancer as | affecting a single lymph node or region |
| The Ann Arbor staging system defines a stage II cancer as | affecting two or more lymph node regions on the same side of the diaphragm or in a relatively localized area. |
| The Ann Arbor staging system defines a Stage III cancer involves | nodes on both sides of the diaphragm and the spleen. |
| The Ann Arbor staging system defines a Stage IV | diffuse extralymphatic involvement such as bone, lung, or liver |
| Signs and Symptoms of Hodgekin Lymphoma | The first indicator is usually an enlarged lymph node, often cervical, that is painless and nontender. Later, splenomegaly and enlarged lymph nodes at other locations may cause pressure effects; for example, enlarged mediastinal nodes may compress the eso |
| Non-Hodgkin Lymphomas pathophysiology | Non-Hodgkin lymphomas are similar to Hodgkin lymphoma only in some ways. About 80% of the cases involve B lymphocytes. |
| Symptoms of Non Hodgekin lymphoma | The initial manifestation is an enlarged, painless lymph node. The clinical signs, staging, and treatment are similar to those for Hodgkin lymphoma. Non-Hodgkin lymphoma is distinguished by multiple node involvement scattered throughout the body and a non |
| Multiple Myeloma or Plasma Cell Myeloma Pathophysiology | a neoplastic disease of unknown etiology involving the plasma cells (mature B lymphocytes involved in production of antibodies). An increased number of malignant plasma cells replace the bone marrow and erode the bone Blood cell production is impaired, as |
| Signs and Symptoms of Multiple Myeloma | The onset is usually insidious and the malignancy well-advanced before diagnosis. Frequent infections related to impaired production of antibodies may be the initial sign. Pain, related to bone involvement, is common and is present at rest. Pathologic fra |
| Lymphedema Pathophysiology | is a condition in which the tissues in the extremities swell because of an obstruction of the lymphatic vessels and the subsequent accumulation of lymph. |
| Lymphedema Etiology | The most common form of the disorder is congenital and may involve not only the vessels but the lymph nodes as well. Another condition can also be caused by blockage of the lymph vessels by infestation of parasitic worms. This specific form of lymphedema |
| Signs and Symptoms of lymphedema | The extremities swell as the lymph accumulates. The swelling may initially be soft, but as the condition progresses, the extremity affected may become firm, painful, and unresponsive to treatment. Chronic lymphedema may lead to frequent infections, result |
| Elephantiasis (Filariasis) pathophysiology | This is a type of lymphedema caused primarily by an infestation and blockage of the lymph vessels of the extremities by a parasitic worm called filaria. |
| Etiology of Elephantiasis | The parasitic worms infest the small lymph vessels, blocking lymph flow and resulting in significant swelling of the affected extremity. In severe cases the swelling can be so pronounced that the extremity may resemble an elephant’s limb, giving this diso |
| Signs and Symptoms of elephantiasis | Extreme swelling of the legs, breasts, or genitalia, Thickening of the subcutaneous tissue, Frequent infections, Skin ulcerations, Fever |
| Castleman disease refers to | a group of inflammatory disorders. It is a rare illness that involves the overgrowth of lymphoid tissue. |
| Castleman disease unicentric | affects only a single lymph node |
| Multicentric castleman disease | affects multiple lymph nodes and tissue and may lead to a severe weakening of the immune system. |
| Unicentric manifestations include: | Difficulty breathing or eating because of fullness or pressure in the chest or abdomen, A large lump in the neck, armpit, or groin, Unexplained weight loss and anorexia, Persistent cough |
| Multicentric manifestations include: | Fever and night sweats Nausea and vomiting leading to a loss of appetite and resulting in weight loss, Weakness and overall fatigue, Enlarged spleen, liver, or peripheral lymph nodes in the neck, groin, or armpits |
| Hypothalamic-releasing hormones produced from | Hypothalamus |
| Hypothalamic-releasing hormones Effects | Sends stimuli to anterior pituitary to release specific hormone |
| Hypothalamic-inhibiting hormones produced from | Hypothalamus |
| Hypothalamic-inhibiting hormones Effects | Decrease release of specific hormone by anteriorpituitary |
| Growth hormone (somatotropin) produced from | Pituitary—anterior lobe (adenohypophysis) |
| Growth hormone effects | Stimulates protein synthesis |
| Adrenocorticotropic hormone produced from | Adenohypophysis |
| Adrenocorticotropic hormone effects | Stimulates adrenal cortex to secrete primarily cortisol |
| Thyroid-stimulating hormone produced from | Adenohypophysis |
| Thyroid-stimulating hormone Effects | Stimulates thyroid gland |
| Follicle-stimulating hormone produced from | Adenohypophysis |
| Follicle-stimulating hormone Effects | Women: stimulates growth of ovarian follicles and estrogen secretion; men: stimulates sperm production |
| Luteinizing hormone produced from | Adenohypophysis |
| Luteinizing hormone Effects | Women: stimulates maturation of ovum and ovulation; men: stimulates secretion of testosterone |
| Prolactin produced from | Adenohypophysis |
| Prolactin Effects | Stimulates breast milk production during lactation |
| Antidiuretic hormone produced from | Pituitary—posterior lobe (neurohypophysis) |
| Antidiuretic hormone Effects | Increases reabsorption of water in kidney |
| Oxytocin produced from | Neurohypophysis |
| Oxytocin effects | Stimulates contraction of uterus after delivery, Stimulates ejection of breast milk during lactation |
| Insulin produced from | Pancreas-Beta cells |
| Insulin effects | Transport of glucose and other substances into cells, Lowers blood glucose level |
| Glucagon produced from | Pancreas—alpha cells |
| Glucagon Effects | Glycogenolysis in liverIncreases blood glucose level |
| Parathyroid hormone produced from | parathyroid gland |
| Parathyroid effects | Increases blood calcium level by stimulating bone demineralization and increasing absorption of calcium in the digestive tract and kidneys |
| Calcitonin produced from | Thyroid gland |
| Calcitonin effects | Decreases release of calcium from the bone to lower blood calcium level |
| T3, T4 produced from | Thyroid gland |
| T3, T4 Effects | Increases metabolic rate in all cells |
| Aldosterone produced from | Adrenal cortex |
| Alosterone effects | Increases sodium and water reabsorption in the kidney |
| Cortisol produced from | Adrenal cortex |
| Cortisol Effects | antiinflammatory effects and decreases immune response. Catabolic effect on tissues; stress response |
| Norepinephrine produced in | Adrenal medulla |
| Norepinephrine Effects | General vasoconstriction |
| Epinephrine produced from | Adrenal medulla |
| Epinephrine effects | Stress response;Visceral and cutaneous vasoconstriction. Vasodilation in skeletal muscle, Increases rate and force of heart contraction, Bronchodilation |
| The release of hormones from glands is most frequently controlled by | a negative feedback mechanism For example, as levels of blood glucose increase, the secretion of insulin increases, thus increasing movement of glucose into the cells and lowering the level in the blood. |
| The most common cause of endocrine disorders is | the development of a benign tumor, or adenoma. Adenomas may be secretory, causing excess hormone, or they may have a destructive effect on the gland, causing a hormonal deficit. |
| Diabetes mellitus is caused by | a relative deficit of insulin secretion from the beta cells in the islets of Langerhans or by the lack of response by cells to insulin (insulin resistance). To simplify the text, insulin deficit is used to cover both decreased secretion of the hormone and |
| Etiology of Type 1 Diabetes | the insulin deficit results from destruction of the pancreatic beta cells in an autoimmune reaction, resulting in an absolute deficit of insulin in the body and therefore requiring replacement therapy. Acute complications such as hypoglycemia or ketoacido |
| Type 2 Diabetes Mellitus This abnormality may involve decreased pancreatic beta cell production of insulin, increased resistance by body cells to in | decreased effectiveness of insulin or a relative deficit of insulin. |
| Type 2 diabetes may be controlled by | adjusting the need for insulin by Regulating dietary intake, Increasing the use of glucose, such as with exercise, Reducing insulin resistance, Stimulating the beta cells of the pancreas to produce more insulin |
| Etiology of Type 2 | metabolic syndrome, a complex of several pathophysiologic conditions marked by obesity, cardiovascular changes, and significant insulin resistance owing to increased adipose tissue . Individuals with metabolic syndrome often have developed vascular or oth |
| Gestational diabetes pathophysiology | may develop during pregnancy and disappear after delivery of the child |
| Symptoms of Diabetes | Initial Stage: decreased transportation and use of glucose in many cells of the body.hyperglycemia, glucosuria, polyuria, dehydration, polydipsia, polyphagia, Progressive Effects: if the insulin deficit is severe or prolonged, the process continues to dev |
| Hypoglycemia (Insulin Shock) Pathophysiology | Hypoglycemia is precipitated by an excess of insulin, which causes a deficit of glucose in the blood. It usually occurs in patients with type 1 diabetes mellitus, often quite suddenly, following strenuous exercise, an error in dosage, vomiting, or skippin |
| Hypoglycemia Signs and Symptoms | Poor concentration, Slurred speech, Lack of coordination and staggering gait; persons with hypoglycemia are sometimes assumed to be intoxicated with alcohol, Increased pulse, Pale, moist skin, Anxiety, Tremors |
| Diabetic Ketoacidosis Pathophysiology | As indicated earlier, DKA results from insufficient insulin, which leads to high blood glucose levels and mobilization of lipids. It is more common in patients with type 1 diabetes mellitus. Ketoacidosis usually develops over a few days and may be initiat |
| Signs and Symptoms of Diabetic Ketoacidosis | The signs and symptoms of DKA are related to dehydration, metabolic acidosis, and electrolyte imbalances. Signs of dehydration include the following: Thirst, Dry, rough oral mucosa, Warm, dry skin, Rapid but weak and thread pulse, Low blood pressure a |
| Macroangiopathy with Diabetes | Myocardial infarction, Cerebrovascular accident, Peripheral vascular disease (ischemia, gangrene, and amputation affecting the legs), Atherosclerosis in large arteries related to hyperlipidemia, hypertension, and degenerative changes in the intimal layer |
| Microangiopathy in Diabetes | Diabetic nephropathy, Chronic renal failure, Retinopathy, Microaneurysms, neovascularization, and fibrosis Leads to blindness, Neuropathy in the central nervous system and peripheral nerves |
| Infections in diabetes | Infections are more common and tend to be more severe in diabetics, probably because of the vascular impairment, which decreases tissue resistance, the delay in healing because of insulin deficit, and the increased glucose levels in body fluids that suppo |
| Hypoparathyroidism leads to | hypocalcemia, or low serum calcium levels. |
| Hypoparathyroidism manifestations | Hypocalcemia affects nerve and muscle function in different ways. Low serum calcium levels result in weak cardiac muscle contractions, but also increase the excitability of nerves, leading to spontaneous contraction of skeletal muscle. This causes muscle |
| Hyperparathyroidism may be caused by | an adenoma, hyperplasia, or secondary to renal failure. |
| Hyperparathyroidism causes | hypercalcemia, or high serum calcium levels. Hypercalcemia leads to forceful cardiac contractions The most serious effects of hyperparathyroidism occur in the bone tissue. Increased PTH causes calcium to leave the bone, leading to osteoporosis, weakening |
| The most common cause of pituitary disorders are | Benign adenomas. |
| Effects of Benign adenomas | The effect of the mass as it enlarges and causes pressure in the skull. Signs of pressure on brain tissues include increasing headaches, seizures, and drowsiness. Visual defects such as hemianopsia are common because of pressure on the adjacent optic chia |
| Dwarfism, or short stature, may be caused by | a number of factors, one of which is a deficit of GH |
| Gigantism, or tall stature, results from | excess GH before puberty and fusion of the epiphyses. |
| Acromegaly refers to | the effects of excess GH secretion in the adult, usually by an adenoma. The bones become broader and heavier, and the soft tissues grow, resulting in enlarged hands and feet, a thicker skull, and changes in the facial features |
| Diabetes Insipidus Pathophysiology | results from a deficit of ADH. This deficit may originate in the neurohypophysis. |
| Etiology for Diabetes Insipidus | Head injury or surgery may cause a temporary condition. In some cases, the condition is considered to be nephrogenic, when the renal tubules do not respond to the hormone. The latter may be genetic or linked to electrolyte imbalance or drugs. |
| Signs and Symptoms of Diabetes Insipidus | Polyuria with large volumes of dilute urine, Thirst, eventually causing severe dehydration |
| Inappropriate Antidiuretic Hormone Syndrome Pathophysiology and etiology | also called syndrome of inappropriate ADH, is caused by excess ADH, which causes retention of fluid. In some cases, the additional ADH is temporary, triggered by stress, or may be secreted by an ectopic source |
| Signs and Symptoms of Inappropriate Antidiuretic Hormone | The signs are related to severe hyponatremia, which causes mental confusion and irritability. |
| Thyroid Disorders Pathophysiology | Endemic goiter may affect large groups of people in a specific geographic area. It is a hypothyroid condition that occurs in regions where there are low iodine levels in the soil and food , TSH causes hyperplasia of the gland and can promote goiter format |
| Toxic goiter is | a hyperthyroid condition resulting from hyperactivity of the thyroid gland, perhaps caused by excessive stimulation by TSH, which produces a large nodular gland. |
| Hyperthyroidism (Graves Disease) Pathophysiology | Graves disease occurs more frequently in women older than 30 years of age and is related to an autoimmune factor. |
| Signs and Symptoms of Graves Disease | Exophthalmos is evident by the presence of protruding, staring eyes and decreased blink and eye movements. Thyrotoxic crisis, or thyroid storm, is an acute situation in a patient with uncontrolled hyperthyroidism, usually precipitated by infection or surg |
| Hypothyroidism pathophysiology | is easily treated by replacement doses of thyroid hormone |
| Etiology of Graves Disease | Hashimoto thyroiditis is a destructive autoimmune disorder. |
| Myxedema, severe hypothyroidism in adults | (myxedema refers to the nonpitting edema manifested as facial puffiness and a thick tongue); myxedema coma refers to acute hypothyroidism resulting in hypotension, hypoglycemia, hypothermia, and loss of consciousness, a life-threatening complication occur |
| Cretinism | untreated congenital hypothyroidism, may be related to iodine deficiency during pregnancy or may be a developmental defect. |
| Cushing syndrome is caused by | an excess of glucocorticoids (e.g., hydrocortisone or cortisol). The mechanism for the excess amount of hormone and the effect on related hormones depends on the cause. Excess glucocorticoids may result from various conditions: Adrenal or Pituitary adenom |
| Typical changes associated with Cushing syndrome include | a moon face and a heavy trunk , (buffalo hump), Fragile skin, hirsutism,osteoporosis delayed healing,gluconeogenesis and insulin resistance,hypertension, edema, and possible hyperkalemia, Suppression of inflammatory response |
| Addison disease refers to | a deficiency of adrenocortical secretions, the glucocorticoids, mineralocorticoids, and androgens. |
| Addison disease etiology | An autoimmune reaction is the common cause. The gland may be destroyed by hemorrhage with meningococcal infection or by viral, tubercular, or histoplasmosis infections. Destructive tumors may also cause hypoactivity. |
| The symptoms of Addison disease | usually develop slowly, Decreased blood glucose levels, Poor stress response, Fatigue, Low blood pressure, Weight loss and decreased appetite, Hyperpigmentation, Frequent infections, Low serum sodium concentration,hypotension,high potassium levels |
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