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exams 2 study guide Flashcards

1
Q

wha is pernicious anemia

A
  • Caused by a LACK of INTRINSIC FACTOR made by the gastric parietal cells which is required for vitamin B12 absorption

so basically the body cannot absorb vitamin b12 leading to =
- vitamin B12 deficiency

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2
Q

when can pernicious anemia also occur

A
  • after GI surgery (i.e., gastrectomy, gastric bypass, small bowel resection involving the ileum)
  • In strict vegetarians since most of vitamin B12 come from meat
  • Excessive alcohol or smoking
  • More common in elderly than in younger patients*
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3
Q

what are some typical anemia symptoms

A
  • Neurologic manifestations due to nerve demyelination
  • Loss of appetite, abdominal pain, beefy red tongue (atrophic glossitis), icterus, splenic enlargement
  • Treatment
    Parenteral or high oral doses of vitamin B12

Often unrecognized in older adults due to subtle, slow onset and presentation

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4
Q

what is the Neurologic manifestations due to nerve demyelination of pernicious anemia

A

Weakness, paresthesias of feet and hands, ↓ vibratory and position senses, ataxia, muscle weakness, and impaired thought processes

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5
Q

what are some treatment for pernicious anemia

A
  • Parenteral or intranasal administration of Vit B12 is the treatment of choice
  • Patients will die in 1-3 years without treatment
  • Long-standing neuromuscular complications may not be reversible
  • Increasing dietary cobalamin does not correct this anemia if intrinsic factor is lacking or if there is impaired absorption in the ileum
    Dose: 1000 mg of cobalamin IM daily for 2 weeks and then weekly until the Hgb is normal, then monthly for life
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6
Q

Common causes of Folic Acid Deficiency Anemia (absence of neurological problems)

A
  • dietary deficiency (leafy greens, citrus fruits)
  • Malabsorption syndromes ( celiac disease, chron’s disease, small bower resection)
  • Increased requirement (i.e., pregnancy
  • drugs
  • alcohol abuse and anorexia
  • loss during hemodialysis
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7
Q

what is celiac disease

A
  • genetic autoimmune disease
  • people can’t eat gluten because it will damage their small intestine
  • Gluten is a protein found in wheat, rye bread, and barley. It may also be in other products like vitamins and supplements, hair and skin products, toothpastes, and lip balm
  • affects each person differently and can occur in digestive system or other parts of the body
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8
Q

treatment of celiac disease

A

glutten free diet

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9
Q

other characteristics of celiac disease

A
  • One person might have diarrhea and abdominal pain, while another person may be irritable or depressed.
  • Irritability is one of the most common symptoms in children.
  • Some people have no symptoms.
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10
Q

what is Folic Acid Deficiency

A
  • Serum folate level is low but vit b12 is normal
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11
Q

treatment of folic acid deficiency

A

We can treat them by replacement therapy or eat the food with larger amount of folic acid

  • In malabsorption states or with chronic alcoholism, up to 5 mg per day may be required.
  • During diagnostic studies, the gastric analysis is positive for hydrochloric acid.
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11
Q

treatment of folic acid deficiency

A

We can treat them by replacement therapy or eat the food with larger amount of folic acid

  • In malabsorption states or with chronic alcoholism, up to 5 mg per day may be required.
  • During diagnostic studies, the gastric analysis is positive for hydrochloric acid.
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12
Q

what are Iron Deficiency Anemia

A
  • Most common type of anemia worldwide
  • Nutritional iron deficiency
  • Metabolic or functional deficiency
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13
Q

Symptomatic hemoglobin level for iron deficiency anemia

A

Symptomatic @ Hgb 7-8 g/dl

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14
Q

Progression of iron deficiency causes:

A
  • Brittle, thin, coarsely ridged, spoon-shaped nails

- A red, sore, painful tongue

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15
Q

treatment goal of iron deficiency anemia

A

Treat underlying disease that is causing reduced intake or absorption of iron

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16
Q

how to replace iron in iron deficiency anemia

A
  • Nutritional therapy
  • Oral iron supplements if adequate nutrition
  • Transfusion of packed RBCs
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17
Q

what is normocytic anemia

A

Anemia resulting from blood loss may be caused by either acute or chronic problems

  • It means you have normal-sized red blood cells, but you have a low number of them
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18
Q

Acute blood loss occurs as a result of

A

Acute blood loss occurs as a result of sudden hemorrhage

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19
Q

Sources of chronic blood loss are similar to?

A

those of iron-deficiency anemia

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20
Q

how does the body respond when acute blood loss is gradual

A
  • the body maintains its blood volume by slowly increasing the plasma volume, but then the number of RBCs is significantly DIMINISHED
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21
Q

Causes of sudden hemorrhage/ acute blood loss

A
  • Trauma
  • Complications of surgery
  • Conditions or diseases that disrupt vascular integrity
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22
Q

conditions that disrupt vascular intergrity

A
  • Hypovolemic shock
  • Compensatory increased plasma volume with diminished O2 -carrying RBCs
  • Hypovolemic shock is an emergency condition in which severe blood or other fluid loss makes the heart unable to pump enough blood to the body
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23
Q

Some causes of chronic blood loss:

A

Bleeding ulcer
Hemorrhoids
Menstrual and postmenopausal blood loss

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24
Q

Management of chronic blood loss involves

A

Identifying the source
Stopping the bleeding
Providing supplemental iron as needed

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25
Q

complications of blood transfusions

A
  • Fluid overload
  • Blood-borne infection
  • Exposure to donor leukocytes
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26
Q

what is blood transfusion

A

Not linked into one baseline hemoglobin level but recommended for people with hematocrit level of < 30

  • Benefits/risks weighed
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27
Q

blood transfusion reactions

A
  • Incompatibility, Major - - Acute hemolytic transfusion reaction
  • Febrile reaction
  • Allergic reaction
  • Hypocalcemia
  • Bleeding
  • Hypothermia – ventricular dysrhythmias
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28
Q

Laboratory Tests for Red Blood Cells

A
  • Red blood cell count (RBC)
  • Percentage of reticulocytes (normally approximately 1%)
  • Hemoglobin (grams per 100 mL of blood)
  • Hematocrit
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29
Q

what is Red blood cell count (RBC)

A

measures the total number of red blood cells in 1 mm3 of blood

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30
Q

what is Percentage of reticulocytes (normally approximately 1%)

A

Provides an index of the rate of red cell production

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31
Q

what is Hemoglobin (grams per 100 mL of blood) test

A

Measures the hemoglobin content of the blood

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32
Q

what is Hematocrit test

A

Measures the volume of red cell mass in 100 mL of plasma volume

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33
Q

what is Sickle Cell Disease

A

Inherited structural abnormality in the hemoglobin

  • Crystal-like, elongated, rigid cell causes occlusion in the microcirculation
  • Sickling in response to cold, dehydration, hypoxia, infection, and acidosis
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34
Q

Clinical presentation

of sickle cell disease

A
  • Severe bone pain
  • Microinfarcts in many organs, leading to cardiomegaly, renal failure, and chronic leg ulcers
  • Pulmonary infarction leading to HTN and possible ARDS
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35
Q

Treatment of Sickle Cell Crisis

A
  • Oxygen administration
  • Aggressive intravenous fluid hydration
  • Prompt treatment of infection with broad-spectrum antibiotics
  • RBC transfusions are not usually required
  • Pain control with around-the-clock narcotics
  • Folic acid supplementation
  • Hydroxyurea
  • Hematopoietic stem cell transplantation (HSCT) is promising towards finding a cure for Sickle Cell Disease
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36
Q

Aging and Red Blood Cells

A

Reduction in hematopoietic progenitors

  • Reduced production of hematopoietic growth factors
  • Inhibition of erythropoietin
  • Inflammatory cytokines interfere with erythropoietin interaction with its receptors.

-erythropoitin is a hormone. hematopoeiten is the process

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37
Q

what is Polycythemia Vera

A

A condition in which the red blood cell mass is increased.

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38
Q

what is Relative polycythemia:

A

results from a loss of vascular fluid and is corrected by replacing the fluid

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39
Q

what is Primary polycythemia:

A

a proliferative disease of the bone marrow with an absolute increase in total red blood cell mass accompanied by elevated white cell and platelet counts

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40
Q

what is Secondary polycythemia

A

is caused by other disease processes that induce hypoxia. For these, the underlying cause is treated. These include: chronic heart and lung disease, living at high altitude, sleep apnea.

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41
Q

examples of conditions that leads secondary polycepthemia

A
  • chronic heart
  • lung disease
  • living at high altitude
  • sleep apnea
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42
Q

Polycythemia Manifestations

A

Variable and related to an increase in RBCs, hemoglobin level, and hematocrit with increased blood volume and viscosity

  • Splenomegaly
  • Depletion of iron
  • Disrupted cardiac output
  • Hypertension
  • Decreased cerebral blood flow
  • Venous stasis
  • Thromboembolism and hemorrhage
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43
Q

Treatment of Polycythemia

A
  • Prevention of thrombosis
  • Therapeutic serial phlebotomy
  • Treatment with hydroxyurea
  • Watch for progression to acute leukemia
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44
Q

what are Leukemias

A

Malignant neoplasms arising from the transformation of a single blood cell line derived from hematopoietic stem cells

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45
Q

Classifications of leukemia according to cell lineage

A
  • Lymphocytic (lymphocytes)

- Myelocytic (granulocytes, monocytes)

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46
Q

what are Chronic Leukemias

A

Malignancies involving the proliferation of well-differentiated myeloid and lymphoid cells

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47
Q

Types of chronic leukemia

A
  • Chronic lymphocytic leukemia (CLL)

- Chronic myelogenous leukemia (CML)

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48
Q

what leukemias involve the pluripotent myeloid stem cells in bone marrow and interfere with the maturation of all blood cells.

A
  • Acute myelogenous (myeloblastic) leukemia (AML)

- Chronic myelogenous leukemia (CML)

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49
Q

what leukemias involve immature lymphocytes and their progenitors in the bone marrow, the spleen, lymph nodes, CNS, and other tissue.

A
  • Acute lymphocytic (lymphoblastic) leukemia (ALL)

- Chronic lymphocytic leukemia (CLL)

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50
Q

what is Thrombocytopenia

A

Results from a decrease in platelet production, increased sequestration of platelets in the spleen, or decreased platelet survival

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51
Q

types of thrombocytopenia

A
  • Drug-induced thrombocytopenia
  • Idiopathic thrombocytopenic purpura
  • Thrombotic thrombocytopenic purpura
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52
Q

in vitamin K deficiency,

A

the liver produces inactive clotting factor resulting in abnormal bleeding.

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53
Q

Manifestations of Thrombocytopenia

A

Mucous membranes
Nose, mouth, gastrointestinal tract, and uterine cavity
Commonly occurs in small vessels
Petechiae—pinpoint purplish-red spots
Seen almost exclusively in conditions of platelet deficiency
Purpura—purple areas of bruising

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54
Q

Hemorrhagic telangiectasia

A

An uncommon autosomal dominant disorder characterized by thin-walled, dilated capillaries and arterioles

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55
Q

Vitamin C deficiency (scurvy) bleeding

A

Results in poor collagen synthesis and failure of the endothelial cells to be cemented together properly, causing a fragile wall

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56
Q

what is Cushing disease

A

Causes protein wasting and loss of vessel tissue support because of excess cortisol

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57
Q

what is Senile purpura

A

(bruising in elderly persons)

- Caused by the aging process

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58
Q

Five Stages of Hemostasis

A
  • Vessel spasm
  • Formation of the platelet plug
  • Blood coagulation or development of an insoluble fibrin clot
  • Clot retraction
  • Clot dissolution
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59
Q

what is Thrombosis

A

the inappropriate formation of clots within the vascular system

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60
Q

what is Bleeding

A

Failure of blood to clot in response to appropriate stimulus

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61
Q

Vascular Constriction

A
  • Vessel spasm constricts the vessel and reduces blood flow. It is a transient event that usually lasts minutes or hours.
  • Vessel spasm is initiated by endothelial injury and caused by local and humoral mechanisms.
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62
Q

Clot Retraction and Dissolution

A

The process involves the interaction of substrates, enzymes, protein cofactors, and calcium ions that circulate in the blood or are released from platelets and cells in the vessel wall.

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63
Q

another name for Disseminated intravascular coagulopathy (DIC)

A

Known as the “clotting-bleeding syndrome”

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64
Q

facts about Disseminated intravascular coagulopathy (DIC)

A

Clotting cascade is triggered, causing widespread systemic intravascular clotting
- ITS LIMITED, WHEN USED UP CAUSES MICROCLOTS

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65
Q

release of kinins

A

increases vascular permeability and causes hypotension and shock

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66
Q

Fibrin and fibrinogen breakdown causes

A

increase in fibrin degradation products and D-dimers

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67
Q

what activates Disseminated intravascular coagulopathy (DIC)

A
  • Burns
  • Bacterial endotoxins (especially gram-negative)
  • Heat stroke
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68
Q

conditions associated with Disseminated intravascular coagulopathy (DIC)

A
  • Obstetric conditions
  • Cancers
  • Infections
  • Shock
  • Trauma or surgery
  • Low-flow states
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69
Q

treatment of Disseminated Intravascular Coagulation DIC

A
  • Treat the causative factor
  • Correct hypotension, hypoxemia, and acidosis
- Medications
Heparin
FFP
Platelets 
Cryoprecipitate
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70
Q

what are Infectious Mononucleosis

A

Self-limited lymphoproliferative disorder

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71
Q

Causes and Characteristics

of mononucleosis

A
  • Caused by the B-lymphocytotropic EBV, a member of the herpes virus family; transmitted in saliva
  • Characterized by fever, generalized lymphadenopathy, sore throat, and the appearance in the blood of atypical lymphocytes and several antibodies
  • Highest incidence in adolescents and young adults
  • Treatment is symptomatic and supportive.
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72
Q

what is Hodgkin disease

A

Lymphoma arises in a single node or chain of nodes.

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73
Q

what is Non-Hodgkin disease

A

Lymphoma originates at extranodal sites and spreads to anatomically contiguous nodes.

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74
Q

Reed-Sternberg cells are derived from?

A

B lymphocytes

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75
Q

Reed-Sternberg cells are present in what disease

A

Hodgkin disease

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76
Q

Stage A of Hodgkin Disease

A

Lack constitutional symptoms

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77
Q

Stage B of Hodgkin Disease

A
  • (40% of persons with Hodgkin disease)

- Significant weight loss, fevers, pruritus, or night sweats

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78
Q

Advanced Stages of hodgkin disease

A
  • Fatigue and anemia

- Liver, lungs, digestive tract, and CNS may be involved.

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79
Q

Low-grade lymphomas of Non-Hodgkin Lymphomas

A

Predominantly B-cell tumors

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80
Q

Intermediate-grade lymphomas of Non-Hodgkin Lymphomas

A

Include B-cell and some T-cell lymphomas

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81
Q

High-grade lymphomas Non-Hodgkin Lymphomas

A

Largely immunoblastic (B cell), lymphoblastic (T cell), Burkitt, and non-Burkitt lymphomas

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82
Q

Staging of Non-Hodgkin Lymphomas Disease

A
  • Bone marrow biopsy
  • Blood studies
  • Chest and abdominal CT scans
  • Nuclear medicine studies
  • Cytologic examination of the cerebrospinal fluid
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83
Q

Treatment for Hodgkin and NHL

A
  • Radiation

- Combination chemotherapy

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84
Q

Non-Hodgkin Lymphomas Disease treatment ONLY

A
  • Adjuvant radiation therapy

- Monoclonal antibodies

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85
Q

what is Multiple Myeloma

A

A plasma cell dyscrasia characterized by expansion of a single clone of immunoglobulin-producing plasma cells and a resultant increase in serum levels of a single monoclonal immunoglobulin or its fragments

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86
Q

main site involved in Multiple Myeloma

A
  • The bones and bone marrow
  • Proliferation and activation of osteoclasts that lead to bone resorption and destruction
  • Pathologic fractures
  • Hypercalcemia
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87
Q

what is Pleural effusion:

A

abnormal collection of fluid in the pleural cavity

  • Transudate or exudate, purulent (containing pus), chyle, or sanguineous (bloody)
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88
Q

Spontaneous Pneumothorax

A

Occurs when an air-filled blister on the lung surface ruptures

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89
Q

what is Traumatic Pneumothorax

A

Caused by penetrating or nonpenetrating injuries

  • accidents airbag hitting chest, hard hit on chest, blow, stabbing, gunshot
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90
Q

what is Tension Pneumothorax

A

occurs when the intrapleural pressure exceeds atmospheric pressure

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91
Q

types of fluid in pleural effusion

A
  • Transudate
  • Exudate
  • Purulent drainage (empyema)
  • Chyle
  • Blood
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92
Q

what is Atelectasis

A

The incomplete expansion of a lung or portion of a lung

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93
Q

causes of atelectasis

A
  • Airway obstruction
  • Lung compression such as that occurs in pneumothorax or pleural effusion
  • Increased recoil of the lung due to loss of pulmonary surfactant
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94
Q

types of atelectasis

A
  • Primary = present birth

- Secondary = Develops in the neonatal period or later in life

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95
Q

what is transudative pleural effusion

A
  • occurs due to increased hydrostatic pressure or low plasma oncotic pressure

LOW IN PROTEIN AND LDH

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96
Q

examples of transudative pleura effusion

A
  • CHF
  • cirrhosis
  • nephrotic sundrome
  • pulmonary edema
  • Hypoalbuminemia
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97
Q

what is exudative pleural effusion

A

occurs due to inflammation and increased capillary permeability

HIGH IN PROTEIN AND LDH

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98
Q

examples of exudative pleural effusion

A
  • pneumonia
  • viral infection
  • pe
  • autoimmune
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99
Q

what is Asthma

A

A chronic inflammatory disease of the airways that causes hyperresponsiveness, mucosal edema, and mucus production

AFFECTS THE AIRWAYS

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100
Q

Genetic Factors Involved in the Pathophysiology of Asthma

A
  • Atopy
  • Early versus late phase

Atopy refers to the genetic tendency to develop allergic diseases

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101
Q

Factors Involved in the Pathophysiology of Asthma

Environmental

A

Viruses
Allergens
Occupational exposure

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102
Q

Contributing Factors to an Asthmatic Attack

A

-Allergens
-Respiratory tract infections
Exercise
Drugs and chemicals
Hormonal changes and emotional upsets
Airborne pollutants
Gastroesophageal reflux

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103
Q

Classifications of Asthma Severity

A

Mild intermittent

Mild persistent

Moderate persistent

Severe persistent

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104
Q

Status asthmaticus

A
  • Bronchospasm not reversed by usual measures
  • Life-threatening

does not respond to regular treatment

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105
Q

Clinical manifestations of asthma

A
  • Asymptomatic between attacks

- Chest constriction, expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachycardia, tachypnea

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106
Q

what is tuberculosis

A

World’s foremost cause of death from a single infectious agent

  • Tuberculosis (TB) usually involves the lungs, but any organ can be infected including brain, kidneys, and bones

DRUG-RESISTANT FORMS

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107
Q

M. tuberculosis hominis (human tuberculosis)

A
  • Airborne infection spread by minute droplet nuclei harbored in the respiratory secretions of persons with active tuberculosis
  • Living under crowded and confined conditions increases the risk for spread of the disease
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108
Q

Bovine tuberculosis

A
  • Acquired by drinking milk from infected cows; initially affects the gastrointestinal tract
  • Has been virtually eradicated in North America and other developed countries
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109
Q

The major factors that contributed to the resurgence of TB were

A
  • high rates of TB among patients with HIV infection

- the emergence of multidrug-resistant (MDR) strains of M. tuberculosis

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110
Q

Positive Tuberculin Skin Test

A

Results from a cell-mediated immune response

  • Implies that a person has been infected with M. tuberculosis and has mounted a cell-mediated immune response
  • Does not mean the person has active tuberculosis
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111
Q

what is emphysema

A
  • Enlargement of air spaces and destruction of lung tissue

Types: centriacinar and panacinar

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112
Q

what is Chronic Obstructive Bronchitis

A

Obstruction of small airways

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113
Q

Characteristics of Pulmonary Emphysema

A 
Smoking history
Age of onset: 40 to 50 years
- Often dramatic barrel chest
- Weight loss
Decreased breath sounds
Normal blood gases until late in disease process
Cor pulmonale only in advanced cases
Slowly debilitating disease
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114
Q

characteristics of pathophysiology of chronic bronchitis

A
  • enlarged submucosal gland
  • inflammation of epithelium
  • mucous plug
  • mucus accumaltion
    hyperinflation of alveoli
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115
Q

what is Bronchiectasis

A

Permanent dilation of the BRONCHI and BRONCHIOLES

- Weight loss and anemia are common

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116
Q

manifestations of Bronchiectasis

A 
Atelectasis 
Obstruction of the smaller airways 
Diffuse bronchitis 
Recurrent bronchopulmonary infection
Coughing; production of copious amounts of foul-smelling, purulent sputum; and hemoptysis
Weight loss and anemia are common.
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117
Q

what is Cystic Fibrosis

A

An autosomal recessive disorder involving fluid secretion in the exocrine glands and the epithelial lining of the respiratory, gastrointestinal, and reproductive tracts

118
Q

Manifestations of Cystic Fibrosis

A 
Pancreatic exocrine deficiency
Pancreatitis
Elevation of sodium chloride in the sweat
Excessive loss of sodium in the sweat
Nasal polyps
Sinus infections
Cholelithiasis
119
Q

Acute Respiratory Distress Syndrome

A

A number of conditions that produces pathologic lung changes that include diffuse epithelial cell injury with increased permeability of the alveolar–capillary membrane

120
Q

Occupational Lung Diseases

A
  • Pneumoconioses
    The inhalation of inorganic dusts and particulate matter
    Hypersensitivity diseases
  • The inhalation of organic dusts and related occupational antigens
  • Byssinosis: cotton workers; has characteristics of the pneumoconioses and hypersensitivity lung disease
121
Q

Causes of Acute Respiratory Distress Syndrome

A
  • Aspiration of gastric contents
  • Major trauma (with or without fat emboli)
  • Sepsis secondary to pulmonary or nonpulmonary infections
  • Acute pancreatitis
  • Hematologic disorders
  • Metabolic events
  • Reactions to drugs and toxins
122
Q

what is pneumonia

A

Respiratory disorders involving inflammation of the lung structures (alveoli and bronchioles)

123
Q

infectious agents of pneumonia

A

such as bacteria and viruses

124
Q

Noninfectious agents of pneumonia

A

gastric secretions aspirated into the lungs

125
Q

Factors Facilitating Development of Pneumonia

A

An exceedingly virulent organism
A large inoculum = culture
Impaired host defenses

126
Q

Classifications of Pneumonias

A
  • According to the source of infection = community or hospital acquired
  • According to the immune status of the host = whether they are immunocompentent or immunocompromise
127
Q

Cor Pulmonale

A
  • Right heart failure resulting from primary lung disease and long-standing primary or secondary pulmonary hypertension
  • Involves hypertrophy and the eventual failure of the right ventricle
  • Manifestations include the signs and symptoms of the primary lung disease and the signs of right-sided heart failure.
128
Q

normal pH range

A

7.35 - 7.45 is NORMAL

  • pH less than 7.35 = acidic
  • pH greater than 7.45 = alkalotic
129
Q

example of Respiratory acidosis

A

hypoventilation = pH is low

130
Q

Respiratory alkalosis example

A

hyperventilation = pH is high

person breathing too fast

131
Q

PCO2 range

A

35 – 45

below 35 = respiratory akalosis

above 45 = repiratory acidic

132
Q

HCO3 (metabolic) ranges

A

22-26

below 22 = metabolic acidic

above 26 = metabolic akalosis

133
Q

Functions of the Digestive System

A
  • Production of enzymes and hormones
  • Storage and synthesis of vitamins
  • Dismantling and reassembling of food
  • Entrance of nutrients, vitamins, minerals, electrolytes, and water through the gastrointestinal tract
  • Collection and elimination of wastes
134
Q

what is digestion

A

Digestion is the process of dismantling foods into their constituent parts. Digestion requires hydrolysis, enzyme cleavage, and fat emulsification.

135
Q

what is absorption

A

Absorption is the process of moving nutrients and other materials from the external environment of the GI tract into the internal environment.

136
Q

Signs and Symptoms Common to Gastrointestinal Disorders

A
  • Anorexia = LOSS OF APETITE
  • Nausea = feeling like throwing up
  • Vomiting
  • Gastrointestinal bleeding
137
Q

what is retching

A
  • feeling like throwing up but nothing coming. Just brushing your teeth and bruch goes towards throat
  • Retching consists of the rhythmic spasmodic movements of the diaphragm, chest wall, and abdominal muscles.
138
Q

Anorexia, Nausea, Retching, and Vomiting responses to GI disorders

A

These responses are protective to the extent that they signal the presence of disease and, in the case of vomiting, remove noxious agents from the GI tract.

  • They can also contribute to impaired intake or loss of fluids and nutrients.
139
Q

Swallowing

A
  • Depends on the coordinated action of the tongue and pharynx
    These structures are innervated by cranial nerves V, IX, X, and XII.
140
Q

Dysphagia

A

Difficulty in swallowing = narrowing of the esophagus

141
Q

Odynophagia:

A

Painful swallowing

142
Q

Achalasia

A

Failure of the esophageal sphincter to relax. The place btween the end of the esophagus and the opening of the stomach

143
Q

Infection with H. pylori

A
  • Thrives in an acid environment of the stomach
  • Disrupts the mucosal barrier that protects the stomach from harmful effects of its digestive enzymes
  • Colonize the mucus-secreting epithelial cells of the stomach.
  • Produce enzymes and toxins that have the capacity to interfere with the local protection of the gastric mucosa against acid.
  • Produce intense inflammation.
  • Elicit an immune response.
144
Q

Major Causes of Gastric Irritation and Ulcer Formation

A

Aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs)
- on’t take NSAIDs on empty stomach cus it can cause gastric inflammation

NSAIDS Irritate the gastric mucosa and inhibit prostaglandin synthesis

145
Q

Acute Gastritis

A
  • A transient inflammation of the gastric mucosa

- Most commonly associated with local irritants such as bacterial endotoxins, alcohol, and aspirin

146
Q

Chronic Gastritis

A
  • Characterized by the absence of grossly visible erosions and the presence of chronic inflammatory changes
  • Leads eventually to atrophy of the glandular epithelium of the stomach
147
Q

Autoimmune gastritis

A

body recognize itself as foreigh and start producing against in or attacking it

148
Q

what is Peptic Ulcer

A

Ulcerative disorders that occur in areas of the UPPER gastrointestinal tract that are exposed to acid–pepsin secretions

149
Q

what are common in peptic ulcers

A

Spontaneous remissions and exacerbations

150
Q

what are common in peptic ulcers

A

Spontaneous remissions and exacerbations

151
Q

causes of peptic ulcer

A
  • H. pylori
  • Aspirin = if you take them on an empty stomach
  • Age
  • Warfarin
  • Smoking
152
Q

Complications of Peptic Ulcer

A

Hemorrhage
Obstruction
Perforation

153
Q

what is Hemorrhage from peptic ulcer

A

Caused by bleeding from granulation tissue or from erosion of an ulcer into an artery or vein

154
Q

Obstruction peptic ulcers

A

Caused by edema, spasm, or contraction of scar tissue and interference with the free passage of gastric contents through the pylorus or adjacent areas

155
Q

Perforation peptic ulcer

A

Occurs when an ulcer erodes through all the layers of the stomach or duodenum wall

156
Q

Hematemesis

A
  • Blood in the vomitus

- May be bright red or have coffee ground appearance

157
Q

Melena & Hematochezia

from GI bleeding

A

blood in stool

melena = tarry black stool
hematochezia = bright red stool

MAY BE OCCULT(HIDDEN) = CAN APPEAR NORMAL

158
Q

Zollinger-Ellison syndrome

A

rare digestive disorder that results in too much gastric acid

159
Q

Symptoms of Diverticulitis

TREATMENT=EAT MORE FIBER

A

pouches in the large intestine

  • Pain in the lower left quadrant
  • Nausea and vomiting
  • Tenderness in the lower left quadrant
  • A slight fever
  • An elevated white blood cell count
160
Q

Viral Infection

of the intetstine

A

Rotavirus

161
Q

Bacterial Infection

of small intestine

A

Clostridium difficile colitis

Escherichia coli O157:H7 Infection

162
Q

Protozoal Infection

intestine

A

E. histolytica

163
Q

Ulcerative Colitis

A

ONLY THE COLON - nonspecific inflammatory condition of the colon

CONTINOUS INFLAMMATION

164
Q

Crohn Disease

A

A recurrent, granulomatous type of inflammatory response that can affect any area of the gastrointestinal tract from the mouth to the anus
SKIP LESSIONS
CAN AFFECT ANYWHERE IN THE GI TRACT

165
Q

Peritonitis

A 
- Perforated peptic ulcer
RUPTURED APPENDIX
- Perforated diverticulum
- Gangrenous bowel
- Pelvic inflammatory disease
- Gangrenous gallbladder
- Abdominal trauma and wounds
166
Q

Intestinal Malabsorption

A

Failure to transport dietary constituents from the lumen of the intestine to the extracellular fluid

167
Q

Types of Diarrhea

A

Large Volume
- osmotic = when you eat something your stomach cant absorb

  • secretory = when your body secretes electrolytes into your intestine
168
Q

Small Volume

diarrhea

A

Inflammatory bowel disease
Infectious disease
Irritable colon

169
Q

Common Causes of Constipation

A
  • Failure to respond to the urge to defecate
  • Inadequate fiber in the diet
  • Inadequate fluid intake
  • Weakness of the abdominal muscles
  • Inactivity and bed rest
  • Pregnancy
  • Hemorrhoids
170
Q

Fecal Impaction

A

large, hard mass of stool that gets stuck so badly in your colon or rectum

171
Q

characteristics of fecal impaction

A
  • Painful anorectal disease
  • Tumors
  • Neurogenic disease
  • Use of constipating antacids or bulk laxatives
  • A low-residue diet
  • Drug-induced colonic stasis
  • Prolonged bed rest and debility
172
Q

Intestinal Obstruction

A

Mechanical obstruction can result from post operative causes such as external hernia and postoperative adhesions.

  • IMPAIRMENT OF PERISTALSIS
173
Q

Functions of the Liver

A
  • Production of bile salts
  • Elimination of bilirubin
  • Metabolism of steroid hormones
  • Metabolism of drugs
174
Q

Cause of Jaundice

A
  • Excessive destruction of red blood cells
  • Impaired uptake of bilirubin by the liver cells
  • Decreased conjugation of bilirubin
  • Obstruction of bile flow in the canaliculi of the hepatic lobules or in the intrahepatic or extrahepatic bile ducts
175
Q

Prehepatic jaundice ( Unconjugated bilirubin )

A

Major cause is excessive hemolysis of red blood cells.

  • the unconjugated bilirubin that remains in the blood stream to cause the jaundice.
176
Q

Intrahepatic jaundice ( Conjugated bilirubin )

A

Caused by disorders that directly affect the ability of the liver to remove bilirubin from the blood or conjugate it so it can be eliminated in the bile

  • The liver loses the ability to conjugate bilirubin for it to be eliminated in the bile
177
Q

Posthepatic (Conjugated bilirubin)

A

Occurs when bile flow is obstructed between the liver and the intestine

178
Q

which categories of jaundice are conjugated

A

intrahepatic and post hepatic

179
Q

conditions that affect liver

A
  • injury from drugs and toxins
  • Infection, inflammation, and immune responses
  • Metabolic disorders
  • Neoplasms
180
Q

Phase 1 reaction Hepatic Detoxification and Metabolism

A

involve chemical modification or inactivation of a substance

181
Q

Phase 2 reactions Hepatic Detoxification and Metabolism

A

Involve conversion of lipid-soluble substances to water-soluble derivatives

182
Q

Causes of Hepatitis

A
  • Autoimmune disorders
  • Reactions to drugs and toxins
  • Infectious disorders
  • Hepatotropic viruses that primarily affect liver cells or hepatocytes
183
Q

Infectious disorders hepatitis

A

Malaria, infectious mononucleosis, salmonellosis, and amebiasis

184
Q

Hepatotropic viruses that primarily affect liver cells or hepatocytes

A

Direct cellular injury and induction of immune responses against the viral antigens

185
Q

Early symptoms Intrahepatic Biliary Disease

A
  • Unexplained pruritus or itching
  • Weight loss
  • Fatigue
186
Q

Later symptoms Intrahepatic Biliary Disease

A
  • Dark urine and pale stools

- Jaundice

187
Q

examples of Portal Hypertension

A
  • Ascites
  • Esophageal varices
  • Splenomegaly
188
Q

Manifestations of Liver Failure

A
  • Hematologic disorders
  • Endocrine disorders
  • Skin disorders
  • Hepatorenal syndrome
  • Hepatic encephalopathy
189
Q

Hepatic Encephalopathy

A

Complex neurological syndrome characterized by impaired behavioral, cognitive, and motor function

190
Q

Clinical manifestations of Hepatic Encephalopathy

A 
Personality changes
Confusion
Irritability
Lethargy
Sleep disturbances
Flapping tremor (asterixis)
Stupor, coma, death
191
Q

treatment of Hepatic Encephalopathy

A
  • Correct fluid and electrolyte imbalances.
  • Withdraw depressant drugs metabolized by the liver.
  • Restrict dietary protein intake.
  • Hypertonic saline, mannitol, hypothermia
    Eliminate intestinal bacteria.
192
Q

Hepatocellular carcinoma

A

Arises from the liver cells

193
Q

Cholangiocarcinoma

A

A primary cancer of bile duct cells

194
Q

Effects of Malnutrition and Starvation

A
  • Loss of muscle mass
  • Impaired wound healing
  • Impaired immunologic function
  • Decreased appetite
  • Loss of calcium and phosphate from bone
  • Anovulation and amenorrhea
    Decreased testicular function
195
Q

Kwashiorkor-like secondary protein–energy malnutrition

A

Hypermetabolic acute illnesses

- Trauma, burns, and sepsis

196
Q

Marasmus-like secondary protein–energy malnutrition

A

Chronic illnesses

  • Chronic obstructive pulmonary disease (COPD)
  • Congestive heart failure
  • Cancer and human immunodeficiency virus (HIV) infection
197
Q

Anorexia nervosa

A
  • Refusal to maintain normal body weight
  • Intense fear of gaining weight or becoming fat
  • Disturbance in the way body is perceived
  • Causes amenorrhea (ABSENCE OF MENSTRUATION) in girls
198
Q

Bulimia nervosa

A
  • Recurrent binge eating
  • Inappropriate compensatory behaviors (purging)
  • Self-evaluation unduly influenced by body shape and weight
  • Determination that eating disorder does not occur exclusively during episodes of anorexia nervosa
199
Q

Action of Vitamin D

A
  • Increases intestinal absorption of CALCIUM
  • Increases intestinal absorption of PHOSPHATE
    Increases renal excretion of phosphate
    Can increase bone resorption
    Can increase bone formation
200
Q

Causes of Musculoskeletal Injuries

A
  • Blunt tissue trauma
  • Disruption of tendons and ligaments
  • Fractures of bony structures
201
Q

Acute Athletic injuries

A
  • Caused by sudden trauma
  • Include injuries to soft tissues (contusion, strains, and sprains) and to bone (fractures)

FRACTURES=bones

202
Q

what are Overuse injuries

A
  • Chronic injuries
  • Include stress fractures that result from constant high levels of physiological stress without sufficient recovery time
203
Q

Contusion injury

A
  • An injury to soft tissue that results from direct trauma and is usually caused by striking a body part against a hard object

EXAMPLE = BRUISE

204
Q

Hematoma

injury

A

A large area of local hemorrhage

205
Q

Laceration injury

A

an injury in which the skin is torn or its continuity is disrupted

206
Q

strain joint injuries

A

A stretching injury to a muscle or a musculotendinous unit caused by mechanical overloading.

207
Q

Sprain joint injuries

A

Involves the ligamentous structures surrounding the joint, pain and swelling subside more slowly than in a strain
- Caused by abnormal or excessive movement of the joint

208
Q

Dislocation joint injuries

A

Displacement or separation of the bone ends of a joint with loss of articulation

209
Q

Loose bodies joint injuries

A

Small pieces of bone or cartilage within a joint space

210
Q

Hematogenous Osteomyelitis

A

Originates with infectious organisms that reach the bone through the blood stream

211
Q

Contiguous Spread Osteomyelitis

A
  • Secondary to a contiguous focus of infection

- Direct inoculation from an exogenous source or from an adjacent extraskeletal site

212
Q

chronic Osteomyelitis

A

Occur secondary to an open wound

213
Q

Chronic Osteomyelitis

A
  • Chronic osteomyelitis usually occurs in adults
  • It generally occur secondary to an open wound, most often to the bone or surrounding tissue
  • It includes all inflammatory processes of bone, excluding those in rheumatic diseases that are caused by microorganisms.
  • The hallmark feature of chronic osteomyelitis is the presence of infected dead bone, a sequestrum, that has separated from the living bone.
214
Q

what is Osteonecrosis

A

Osteonecrosis, or death of a segment of bone, is a condition caused by the interruption of blood supply to the marrow, medullary bone, or cortex in the absence of infection.

215
Q

Causes of osteonecrosis

A
  • Mechanical disruption of blood vessels
  • Thrombosis and embolism
  • Vessel injury
  • Increased intraosseous pressure
216
Q

functions of Gamma globulins

A

antibodies of the body, protects the body from infectious diseases

217
Q

function of alpha globulin

A

transport bilirubin and steroids

218
Q

functions of beta globulin

A

transport iron and copper

219
Q

components of plasma

A

albumin
globulins
fibrinogen

220
Q

fuction of albumin

A

maintanence of osmotic pressure and FLUID/BLOOD IMBALANCE

221
Q

The heme molecule is converted to

A

bilirubin and transported to the liver

222
Q

The red blood cell has a life span

A

approximately 120 days

It is broken down in the spleen.
The degradation products (iron and amino acids) are recycled.

223
Q

Eosinophils

A

increase in number during allergic reactions and parasitic infections
The agents associated with allergic reactions
In parasitic infections, the eosinophils use surface markers to attach themselves to the parasite and then release hydrolytic enzymes.

224
Q

Because DNA synthesis requires

A

vitamin b12

225
Q

Internal hemorrhage may cause pain that is localized or referred.

A

YES

226
Q

clinical manifestations of acute blood loss

A

The patient may have pain at the same time due to
Internal hemorrhage
Tissue distention, organ displacement, nerve compression
Retroperitoneal bleeding
Numbness
Pain in lower extremities
Shock is major complication

227
Q

major complication of acute blood loss

A

shock!

228
Q

When anemia exists after acute blood loss,……

A

dietary sources of iron will probably not be adequate to maintain iron stores

229
Q

Goals of Treatment for CML

A

A hematological response characterized by normalized blood counts

A cytogenetic response demonstrated by the reduction or elimination of the Ph chromosome from the bone marrow

A molecular response confirmed by the elimination of the BCR-ABL fusion protein

230
Q

Criteria for Remission of ALL and AML

A

Less than 5% blasts in the bone marrow

Normal peripheral blood counts

Absence of cytogenetic abnormalities

Return to preillness performance status

231
Q

Factors Affecting the Likelihood of Achieving Remission

A

Age (most significant prognostic variable)

Type of leukemia

Stage of the disease at time of presentation

232
Q

Leukemic Cells

A

Are immature and poorly differentiated
Proliferate rapidly and have a long life span
Do not function normally
Interfere with the maturation of normal blood cells
Circulate in the blood stem
Cross the blood–brain barrier
Infiltrate many body organs

233
Q

Requirements for Blood Clotting Process

A

Presence of platelets produced in the bone marrow

Von Willebrand factor generated by the vessel endothelium

Clotting factors synthesized in the liver using vitamin K

234
Q

Why Should Blood Clot?

A 
Hemostasis is designed to maintain the integrity of the vascular compartment.
Infection
Volume
Oxygen production
Tissue damage
Healing
235
Q

Characteristics of Malignant Bone Tumors

A

Tend to be ill defined

Lack sharp borders

Extend beyond the confines of the bone

236
Q

Types of Malignant Bone Tumors

A
  • Osteosarcoma = Aggressive and highly malignant
  • Ewing sarcoma = Peripheral primitive neuroectodermal tumor
  • Chondrosarcoma = Malignant tumor of cartilage
237
Q

tumors that frequently spread to skeletal system

A

breast, lung, prostate, kidney, and thyroid,

238
Q

Treatment Goals for Metastatic Bone Disease

A

Preventing pathologic fractures

Promoting survival with maximum functioning

Allowing the person to maintain as much mobility and pain control as possible

239
Q

treatment Methods for Metastatic Bone Disease

A

Chemotherapy

Irradiation

Surgical stabilization

240
Q

Mild limb deformities (relatively common)

A
  • Syndactyly = simple webbing of the fingers or toes
  • Polydactyly = the presence of an extra digit
  • Absence of a bone such as the phalanx, rib, or clavicle
241
Q

Congenital Deformities

A
  • Mild limb deformities

- Major limb malformations

242
Q

Major limb malformations (relatively rare)

A
  • Joint contractures and dislocations

- Absence of entire bones, joints, or limbs

243
Q

Osteogenesis imperfecta

A

Hereditary disease characterized by defective synthesis of type I collagen

244
Q

Developmental dysplasia of the hip (DDH)

A

Abnormality in hip development that leads to a wide spectrum of hip problems in infants and children

245
Q

Clubfoot or talipes

A

Congenital deformity of the foot that can affect one or both feet

246
Q

Juvenile Osteochondrosis

A

A group of children’s diseases in which one or more growth ossification centers undergoes a period of degeneration, necrosis, or inactivity that is followed by regeneration and usually deformity

247
Q

Scoliosis

A

Lateral deviation of the spinal column that may or may not include rotation or deformity of the vertebrae

248
Q

Postural scoliosis:

A

a small curve that corrects with bending

249
Q

Structural scoliosis:

A

fixed deformity that does not correct with bending.

250
Q

Idiopathic scoliosis

A

Structural spinal curvature for which no cause has been established

251
Q

Neuromuscular scoliosis

A

Develops from neuropathic or myopathic diseases

252
Q

Congenital scoliosis

A

Caused by disturbances in vertebral development during the 6th to 8th week of embryologic development

253
Q

Major Influences on Equilibrium of Bone Tissue

A

Mechanical stress

Calcium and phosphate levels in the extracellular fluid

Hormones and local growth factors

Cytokines

254
Q

Types of Bone Remodeling

A
  • Osteoblasts and osteoclasts in homeostatic balance in normal tissue
  • Structural remodeling
  • Internal remodeling
255
Q

what is Internal remodeling

A

Largely involves the replacement of trabecular bone

Continuous during adulthood

256
Q

what is structural remodelling

A

Involves deposition of new bone on the outer aspect of the shaft at the same time that bone is resorbed from the inner aspect of the shaft

257
Q

Osteopenia

A

Reduction in bone mass greater than expected for age, race, or sex

258
Q

causes of osteopenia

A
  • Decrease in bone formation
  • Inadequate bone mineralization
  • Excessive bone deossification
259
Q

Osteoporosis

A
  • Skeletal disorder characterized by the loss of bone mass and deterioration of the architecture of cancellous bone with a subsequent increase in bone fragility and susceptibility to fractures
  • Loss of mineralized bone mass causes increased porosity of the skeleton. = more holes in the bones. Most likely due to aging
260
Q

Causes of osteoporosis

A
  • Can occur as the result of an endocrine disorder or malignancy
  • Most often associated with the aging process
261
Q

treatment of osteoporosis

A
  • Regular exercise and adequate calcium intake are important factors in preventing osteoporosis
  • Weight-bearing exercises such as walking, jogging, rowing, and weight lifting are important in the maintenance of bone mass
262
Q

Osteomalacia softening of bone

A

A generalized bone condition in which inadequate mineralization of bone results from a calcium or phosphate deficiency, or both

263
Q

Rickets

A

A disorder of vitamin D deficiency, inadequate calcium absorption, and impaired mineralization of bone in children

264
Q

Primary arthritis

A
  • Those affecting body systems in addition to the musculoskeletal system
  • Resulting from an immune response
265
Q

Secondary arthritis

A
  • Rheumatoid conditions limited to a single or few diarthrodial joints
  • Resulting from a degenerative process and the resulting joint irregularities that occur as the bone attempts to remodel itself
266
Q

Systemic Autoimmune Rheumatic Diseases =

A

A group of chronic disorders characterized by diffuse inflammatory lesions and degenerative changes in connective tissue
These disorders share similar clinical features and may affect many of the same organs

Rheumatoid arthritis

Systemic lupus erythematosus

Systemic sclerosis/scleroderma

Polymyositis

Dermatomyositis

267
Q

Characteristics of Rheumatoid Arthritis

A

Associated with extra-articular as well as articular manifestations

Usually has an insidious onset marked by systemic manifestations such as fatigue, anorexia, weight loss, and generalized aching and stiffness.

Characterized by exacerbations and remissions

May involve only a few joints for brief durations, or it may become relentlessly progressive and debilitating

268
Q

Criteria for Rheumatoid Arthritis

A

Morning stiffness at least 1 hour for at least 6 weeks
Swelling of three or more joints for at least 6 weeks
Swelling of wrist, metacarpophalangeal or proximal interphalangeal joints for 6 or more weeks
Systemic joint swelling
Hand roentgenogram changes typical of RA
Rheumatoid nodules
Serum rheumatoid factor

269
Q

Rheumatoid Arthritis symptoms

A 
Fatigue
Weakness
Anorexia
Weight loss
Low-grade fever
Anemia
270
Q

Treatment Goals for a Person with RA

A

Reduce pain

Minimize stiffness and swelling

Maintain mobility

Become an informed health care consumer

271
Q

Systemic Sclerosis

A

Systemic sclerosis, sometimes called scleroderma, is an autoimmune disease of connective tissue characterized by excessive collagen deposition in the skin and internal organs
Diffuse or generalized form
Skin changes involve the trunk and proximal extremities.
Limited or CREST variant
Hardening of the skin (scleroderma) is limited to the hands and face.

272
Q

Osteoarthritis

A

Osteoarthritis, formerly called degenerative joint disease, is the most prevalent form of arthritis
It is a leading cause of disability and pain in older adults
Primary variants of OA occur as localized or generalized syndromes
Secondary OA has a known underlying cause such as
congenital or acquired defects of joint structures, trauma, metabolic disorders, or inflammatory diseases.

273
Q

Causes of Osteoarthritis- induced joint chnages

A 
Postinflammatory diseases
Posttraumatic disorders
Anatomic or bony disorders
Metabolic disorders
Neuropathic arthritis
Hereditary disorders of collagen
Idiopathic or primary variants
274
Q

Osteoarthritis-Induced Joint Changes PROGRESSIONS

A

A progressive loss of articular cartilage
Synovitis
Osteophytes=Bone spurs

275
Q

MANIFESTATIONS of Osteoarthritis-Induced Joint Changes

A 
Joint pain
Stiffness
Limitation of motion
Joint instability 
Deformity
276
Q

Metabolic and Endocrine Diseases Associated with Joint Symptoms

A 
Amyloidosis
Gout syndrome
Osteogenesis imperfecta
Diabetes mellitus
Hyperparathyroidism
Thyroid disease
AIDS
Hypermobility syndromes
277
Q

Gout Syndrome

A

Acute gouty arthritis with recurrent attacks of severe articular and periarticular inflammation

Tophi or the accumulation of crystalline deposits in articular surfaces, bones, soft tissue, and cartilage

Gouty nephropathy or renal impairment

Uric acid kidney stones

278
Q

Primary gout

A
  • Designate cases in which the cause of the disorder is unknown or an inborn error in metabolism
  • Characterized primarily by hyperuricemia and gout
279
Q

Secondary gout

A

The cause of the hyperuricemia is known but the gout is not the main disorder

280
Q

Objectives for Treatment of Gout

A

Termination and prevention of the acute attacks of gouty arthritis

Correction of hyperuricemia

Inhibition of further precipitation of sodium urate

Absorption of urate crystal deposits already in the tissues

281
Q

Juvenile Idiopathic Arthritis categories of diseases with three principle types of onset:

A

(1) Systemic onset disease
(2) Pauciarticular arthritis
(3) Polyarticular disease

282
Q

Symptoms of Juvenile Idiopathic Arthritis

A

Synovitis
Stunted growth also may occur
Influence epiphyseal growth by stimulating growth of

283
Q

Juvenile Rheumatoid Arthritis (JRA)

A

A chronic disease characterized by synovitis

284
Q

Manifestations

of juvinile rheumatoid arthritis

A

Can influence epiphyseal growth by stimulating growth of the affected side
Generalized stunted growth also may occur.

285
Q

paget disease

A

abnormal bone resorption. leading to osteoporosis

Definition
A progressive skeletal disorder that involves excessive bone destruction and repair
Etiology
Genetic and environmental influences.
People with Paget disease have been found to have a mutation of the SQSM1/p62 gene in their diseased bone and tumor samples.
Clinical Manifestations
Characterized by increasing structural changes of the long bones, spine, pelvis, and cranium
Diagnosis
Treatment

286
Q

pathophysiology of rheumatoid arthritis

A

aberrant immune response that leads to synovial inflammation and destruction of the joint architecture.

287
Q

medication does the nurse recognize is useful in treating inflammation, arthritis, and pleuritis?

A

NSAIDS

288
Q

Characteristics of Systemic Lupus Erythematosus (SLE) (AUTOANTIBODIES)

A

Systemic Lupus Erythematosus is a chronic inflammatory disease that can affect virtually any organ system, including the musculoskeletal system.
It is a major rheumatic disease, with approximately 1.5 million Americans and over 5 million people worldwide diagnosed with lupus.
Etiology
Formation of autoantibodies and immune complexes
B-cell hyperreactivity
Increased production of antibodies against self- (autoantibodies) and nonself antigens

289
Q

Auto-antibodies SLE

A 
The autoantibodies can directly damage tissues or combine with corresponding antigens to form tissue-damaging immune complexes.
Autoantibodies
Antinuclear antibodies
Other antibodies
Platelets
Coagulation factors
Red blood cell surface antigens
290
Q

dermatomyositis

A

long-term muscle, joint, and organ damage. Corticosteroids are the mainstay of treatment for this condition.

291
Q

Risk Factors for Development of Stress Ulcers

A 
Large surface area burns
Trauma
Sepsis
Acute respiratory distress syndrome
Severe liver failure
Major surgical procedures
Zollinger-Ellison syndrome
292
Q

prevention and treatment of diverticular disease

A

EATING MORE FIBER

293
Q

irritable bowel disease

A

Persistent or recurrent symptoms of abdominal pain
Altered bowel function
Varying complaints of flatulence, bloatedness
Nausea and anorexia
Constipation or diarrhea
Anxiety or depression

PATHO (6 decks)

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