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Pathophysiology > Exam 2 > Flashcards

Exam 2 Flashcards

Disorders of WBC; Disorders of RBC; Disorders of Platelets, Hemostasis, and Coagulation; Disorders of the Immune System; Cancer; Renal Disorders; Urological Disorders

1
Q

What are the three actions of the kidney?

A

Filtration, Reabsorption, and Secretion

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2
Q

What action does filtration do in the kidneys?

A

Removes metabolic waste and removes drugs and other foreign materials

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3
Q

What action does reabsorption do to the kidneys?

A

Regulate water and electrolytes and maintain acid-base balance

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4
Q

What action does secretion do to the kidneys?

A

Secrete erythropoietin, activates Vitamin D, and secretes renin to regulate BP through RAAS

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5
Q

Causes of prerenal dysfunction of the kidney?

A

Hypovolemia, decreased cardiac output, septic shock, embolism

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6
Q

Causes of intrarenal dysfunction of the kidney?

A

Nephrotoxic medications, acute pyelonephritis, prolonged prerenal ischemia

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7
Q

Causes of postrenal dysfunction of the kidney?

A

Prostate cancer, calculi formation

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8
Q

What is normal excreted in urine?

A

Urea, nitrogen, creatinine, sodium, and potassium

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9
Q

What are abnormal findings in urine?

A

Hematuria, proteinuria, casts, glucose and ketones, bilirubin, WBC

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10
Q

What lab values are bad value when elevated (kidney)?

A

Serum creatinine and BUN

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11
Q

What lab values are good when elevated (kidney)?

A

Urine clearance creatinine and GFR

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12
Q

What occurs to the filtration during renal dysfunction?

A

Poor filtration can cause nitrogen buildup, RBC, and platelets lysis which leads to thrombocytopenia, anemia, and confusion

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13
Q

What occurs to urine frequency during renal dysfunction?

A

Olgiuria

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14
Q

What occurs to the perfusion during renal dysfunction?

A

Poor perfusion which triggers the RAAS to raise BP

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15
Q

What acid-base condition occurs during renal dysfunction?

A

Metabolic acidosis

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16
Q

What occurs to potassium during renal dysfunction?

A

Hyperkalemia which can increase the risk of cardiac dysrhythmias

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17
Q

What occurs to the synthesis of Vitamin D during renal dysfunction?

A

Vitamin D is not synthesized which decreases calcium absorption and results in hypocalcemia

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18
Q

What is pyelonephritis?

A

Bacterial infection of one or both kidneys that starts in the lower urinary tract and travels up (E. coli is common cause)

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19
Q

Symptoms of pyelonephritis.

A

Flank pain, high fever, chill, confusion, nausea and vomiting, and hematuria

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20
Q

What shows on a UA of someone with pyelonephritis?

A

+ leukocytes, + nitrate, proteinuria, and + culture

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21
Q

What is acute glomerulonephritis?

A

First occurs from a streptococcal infection then due to an antigen-antibody reaction there is damage to the glomerulus

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22
Q

Symptoms of glomerulonephritis

A

Symptoms begin 7- 21 days after strep infection.
Edema (facial edema), oliguria, hypertension, hypoalbuminemia, dark “cola-colored” urine

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23
Q

What shows on a UA of someone with glomerulonephritis?

A

Proteinuria, low GFR, and hematuria

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24
Q

What is nephrotic syndrome?

A

Symptoms/findings that occur when the glomerulus is damaged.

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25
Q

What is the primary cause of nephrotic syndrome?

A

Diabetic nephropathy from DM

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26
Q

Symptoms of nephrotic syndrome

A

Edema (facial edema), oliguria, hypertension, hypoalbuminemia, dark “cola-colored” urine

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27
Q

What is polycystic kidney disease?

A

A genetic disorder that affects the kidneys and other organs like the liver due to the development of cysts in the renal tissue. Function is impaired due to the pressure of the cysts which triggers the RAAS

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28
Q

Symptoms of polycystic kidney disease

A

Abdominal and flank pain, renal calculi, and hematuria

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29
Q

What are risk factors for lower urinary tract infections (UTIs)?

A

Bacterial access to urinary tract
- poor perineal hygiene
- indwelling urinary catheters
Retention of urine
- benign prostatic hyperplasia
- indwelling urinary catheter not
draining properly

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30
Q

Symptoms of UTIs

A

Dysuria, frequency, and urgency

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31
Q

What is interstitial cystitis (IC)?

A

Also called painful bladder syndrome (PBS) can be nonulcerative or ulcerative

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32
Q

Symptoms of IC

A

Chronic pelvic and perineal pain, dysuria, full bladder, urgency, and frequency

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33
Q

What is urolithiasis?

A

The formation of stones, aka calculi, in the urinary system
Uro- meaning in the urinary system and -lithiasis meaning formation of stones

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34
Q

What are risk factors for urolithiasis?

A

Genetic susceptibility, dehydration, and diet high in animal protein, sodium, and calcium

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35
Q

Symptoms of urolithiasis

A

Flank pain that is severe and intermittent, nausea and vomiting, fever, hematuria, pyuria, painful urination

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36
Q

Is bladder cancer the most common type of urological cancer?

A

Yes

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37
Q

What is the environmental risk factor for bladder cancer?

A

Cigarettes

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38
Q

What is the occupational risk factor for bladder cancer?

A

Exposure to organic chemicals

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39
Q

Symptom of bladder cancer

A

Hematuria without pain is the primary symptoms

Others include:
- Frequent urination
- Incomplete bladder emptying
- Burning during urination

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40
Q

Leukocytosis

A

A WBC elevation above 11,000/mm3

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41
Q

Leukopenia

A

Decrease in WBC count below 4,000/mcL

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42
Q

What do blood cells arise from?

A

Pluripotent stem cells

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43
Q

Blast Cells

A

Immature precursor cells for each WBC cell line

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44
Q

Hematologic Neoplasms

A

Types of cancer that affect blood, bone marrow, lymph nodes, and lymphoid tissues

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45
Q

Which category of hematologic neoplasms is the most common?

A

Lymphomas

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46
Q

What is the etiology of hematologic neoplasms?

A

Any agent that damages the DNA of developing cells in the bone marrow that turns on oncogenes and turns off tumor suppressant genes

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47
Q

What are the risk factors for hematologic neoplasms?

A

Exposure to radiation, contact with benzene, some viruses, EPV, HIV, human T-lymphotropic virus, chronic gastric infection (H. pylori), congenital or acquired immunodeficiency disorders

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48
Q

Signs and symptoms of hematologic neoplasms?

A

Bone marrow suppression, low RBC count (anemia), leukopenia, thrombocytopenia, enlarged lymph nodes, splenomegaly

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49
Q

What is leukemia?

A

A cancer of developing WBC within the bone marrow

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50
Q

Acute Lymphoblastic Leukemia (ALL) and Acute Myelogenous Leukemia (AML)

A

ALL: An aggressive cancer that is more common in children and abrupt onset

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51
Q

What is the etiology of ALL/ AML?

A

Chromosomal and genetic alterations

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52
Q

What are the risk factors for ALL/ AML?

A

Previous chemotherapy/radiation therapy, white males older than 70, exposure to pesticides, EBV, HIV, and genetic disorders

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53
Q

Signs and symptoms of ALL/ AML and CLL/CML?

A

Frequent infection, opportunistic infections, anemia, fatigue, wt loss, bone pain, hemorrhage, lymphadenopathy, thrombocytopenia, and high WBC count.

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54
Q

Chronic Lymphocytic Leukemia (CLL) and Chronic Myelogenous Leukemia (CML)

A

Even high proportion of mature cells with reduced function; gradual onset with longer survival time

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55
Q

Multiple Myeloma

A

Involves the B-lymphocytes, malignant plasma cell increase and spread to other organs, bone becomes eroded

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56
Q

Symptoms of multiple myeloma

A

Infection, pain, fractures, anemia, bleeding, proteinuria, renal failure, pathologic bone fractures

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57
Q

What is Hodgkins Lymphoma?

A

A single node beginning that is large, non-tender, painless, and very localized
Reed Sternberg cell marker

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58
Q

What is Non-Hodgkins Lymphoma?

A

Multiple nodes throughout the body that are large, non-tender, and painless
They are harder to treat with poorer prognosis
No Reed Sternberg cell marker

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59
Q

Normal WBC

A

5,000-10,000mm3

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60
Q

Normal Hgb in males

A

14-18g/dl

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61
Q

Normal Hgb in females

A

12-16g/dl

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62
Q

Normal Hct in males

A

42%-52%

63
Q

Normal Hct in females

A

37%-47%

64
Q

Normal platelet value

A

90,000-400,000 per microliter of blood

65
Q

What causes Iron Deficiency Anemia?

A

Blood loss

66
Q

Signs and symptoms of Iron Deficiency Anemia

A

Gradual onset, fatigue, mild SOB, gastritis, sore and red tongue, sores at the corners of the mouth, spoon-shaped brittle nails, numbness and tingling of the extremities

67
Q

What is the pathologic cause of Pernicious Anemia?

A

Lack of intrinsic factor since it is required for absorption of vitamin b12

68
Q

What are the risk factors for pernicious anemia?

A

Chronic gastritis, heavy alcohol use, cigarette smoking, complete or partial gastrectomy, gastric bypass

69
Q

Signs and symptoms of pernicious anemia?

A

Red/sore and shiny tongue, GI discomfort, numbness and tingling of the extremities, loss of coordination (ataxia), and fatigue

70
Q

What causes Folate Anemia?

A

Lack of folate (folic acid) since it is required for RNA and DNA synthesis in erythrocyte
Occurs more often than vitamin b12 deficiency

71
Q

Signs and symptoms of Folate Anemia

A

Red/sore and shiny tongue, GI discomfort, loss of coordination (ataxia), and fatigue

72
Q

What are the risk factors of Folate Anemia?

A

Alcoholics and malnourished people

73
Q

What causes Aplastic Anemia?

A

A failure of a tissue to produce normal daughter cells by mitosis; bone marrow failure; can be temporary or permanent

74
Q

What are risk factors for Aplastic Anemia?

A

Chemical or radiation, viruses that damage the bone marrow

75
Q

Signs and symptoms of Aplastic Anemia

A

Anemia, leukopenia, thrombocytopenia aka pancytopenia

76
Q

What causes Sickle Cell Anemia?

A

Autosomal recessive genetics

77
Q

What can alter the shape of RBCs in Sickle Cell Anemia?

A

Dehydration, Acidosis, Infection, Hypoxia

78
Q

What occurs during Sickle Cell Anemia?

A

High blood viscosity and low circulation which causes pain and ischemia

79
Q

Signs and symptoms of Sickle Cell Anemia

A

Severe anemia which causes pallor/weakness/tachycardia, jaundice from hemolysis, splenomegaly, vascular occlusion that causes pain/permanent damage to organs and tissues/infarcts/ periodic “crisis” events, increased risk of infections

80
Q

What is the process of hemostasis?

A
  1. Endothelial damage (blood vessel)
  2. Platelet adhesion/plug form
  3. Activation of coagulation cascade
    • prothrombin converts into thrombin
    • fibrinogen converts into fibrin
  4. Formation of clot
  5. Clot retraction (scab)
  6. Clot dissolution (lysis)
81
Q

What is Thalassemia?

A

A genetic disorder of one or more genes for a Hgb; autosomal dominant

82
Q

What causes Thalassemia?

A

Lack of Hgb production

83
Q

Signs and symptoms of thalassemia

A

Hemolysis, stunted growth and development due to hypoxia, hyperactivity of bone marrow, impairing bone marrow, CHF

84
Q

What is Polycythemia Vera?

A

An increase of RBS

85
Q

What are the complications of Polycythemia Vera?

A

increase risk of thrombi and infarctions, bone marrow becomes fibrotic

86
Q

Signs and symptoms of Polycythemia Vera?

A

increase blood viscosity, distention of blood vessels, HTN

87
Q

What are the labs of Polycythemia Vera?

A

Increase in RBCs, granulocytes, and platelets

88
Q

What is Thrombocytopenia?

A

Too few platelets

89
Q

Signs and symptoms of thrombocytopenia

A

Petechiae, ecchymoses or purpura, hemorrhage

90
Q

Thrombocytosis

A

Platelets above 400,000/mm3

91
Q

Complications of Thrombocytosis

A

Ischemia and infarctions from emboli

92
Q

Signs and symptoms of thrombocytosis

A

pain, numbness, burning, warmth, hemorrhage

93
Q

What causes Hemophilia?

A

Lack of factor 8 in coagulation cascade

94
Q

Signs and symptoms of hemophilia

A

hemorrhage with minor injuries, pain and swelling, joint bleeding

95
Q

What is Von Willebrand Disease?

A

A genetic disorder due to a deficiency of Von Willibrand factor

96
Q

Signs and symptoms of Von Willibrand Disease

A

Hemorrhage, epistaxis, rashes, easy bruising

97
Q

What is Disseminated Intravascular Coagulation?

A

Massive clotting initially then causing multiple emboli and infarctions
Coagulation factors are used up
Hemorrhages follow

98
Q

What line of defense is the innate immunity?

A

1st line

99
Q

What line of defense is adaptive immunity?

A

2nd line

100
Q

Which immunity will respond immediately without prior encounter of antigen?

A

Innate

101
Q

What are the compensatory mechanisms of the innate immunity system?

A

Barriers like the skin and bacterial flora
Phagocytes like macrophages and dendrites
Natural killer cells

102
Q

Which immunity has to be taught to respond?

A

Adaptive immunity

103
Q

What two systems are part of adaptive immunity?

A

Cell-mediated and Humoral (antibody-mediated)

104
Q

What cells are involved in the cell-mediated system?

A

T lymphocytes, helper T cells (CD4), cytotoxic T cells (CD8)

105
Q

Where do T cells mature?

A

Thymus

106
Q

What are antigen-presenting cells (APC)?

A

Cells that act as teachers in the cell-mediated immunity system that engulf antigens and present components on the cell surface to teach the cytotoxic cells what to attack

107
Q

What do helper T cells do?

A

Stimulate B cells, stimulate other T cells, stimulate macrophages and natural killer cells

108
Q

What do cytotoxic cells do?

A

Destroy specific antigens that have been processed by APCs

109
Q

What cell is involved in the humoral (antibody-mediated) immunity system?

A

B-cells that later mature into plasma cells

110
Q

How long is the maturation process of B-cells to plasma cells?

A

5-7 days

111
Q

What do B-cells do?

A

Become a production factory for the antibodies and flag antigen for phagocytosis

112
Q

What happens to the antigens when Igs attach to them?

A

The antigen cannot infect or reproduce

113
Q

Which immune system (cell-mediated or antibody-mediated) will stimulate a quicker response when encountering an antigen a second time?

A

Humoral (antibody-mediated)

114
Q

What is active acquired immunity?

A

When a person develops their own Igs

115
Q

What is the immunity duration for active acquired immunity?

A

Long term

116
Q

What are ways to get active acquired immunity?

A

Vaccines or illness

117
Q

What is passive acquired immunity?

A

Igs that are passed on or given to the person

118
Q

What is the immunity duration for passive acquired immunity?

A

Short term

119
Q

What are ways to get passive acquired immunity?

A

Breastfeeding and injection of formed antibodies

120
Q

What is type 1 hypersensitivity?

A

Also called “immediate”
IgE binds to the mast cell (containing histamie) and combines with antigen
Inflammation response is triggered

121
Q

What is an example of type 1 hypersensitivity?

A

Allergies, rash, hives, asthma

122
Q

What is type 2 hypersensitivity?

A

Also called “cytotoxic”
Cells (donor or own coated cells) attacked rapidly by own Igs

123
Q

What is an example of type 2 hypersensitivity?

A

Patient being administered the wrong blood type or medicine coating cells

124
Q

What is type 3 hypersensitivity?

A

Also called “immune complex”
Igs are combined with antigens and deposited into tissues

125
Q

What are examples of type 3 hypersensitivity?

A

SLE and RA

126
Q

What is type 4 hypersensitivity?

A

Also called “delayed”
T lymphocytes delay days before attacking antigen or donor cells

127
Q

What is Systemic Lupus Erythematosus (SLE)?

A

An immune complex formed by autoantibodies embedded into connective tissue in organs and tissue triggering inflammation

128
Q

What is an example of type 4 hypersensitivity?

A

Poison ivy and organ transplant rejection

129
Q

Which organs does SLE affect?

A

KIDNEYS, lungs, skin, joints, synovial membranes, and heart

130
Q

Signs and symptoms of SLE

A

-Kidney: nephrotic syndrome, hematuria, edema, HTN
-Lungs: pleuritis and pleural effusion
-Vasculitis on Skin: butterfly rash, Raynaud’s
-Joint Synovial Membranes: arthralgias
-Blood Cells: leukopenia, anemia, thrombocytopenia
-Heart: ischemic coronary artery disease and pericarditis
-Other: enlarged spleen, headache, fever, fatigue

131
Q

What is Rheumatoid Arthritis?

A

Symmetrical swollen joints in the hands, knees, and hips that causes permanent damage in the joints because of chronic inflammation

132
Q

Signs and symptoms of RA

A

Morning stiffness that improves with movement, classic hand deformity: swan neck, Boutonniere deformity, ulnar deviation

133
Q

What is Sarcoidosis?

A

A chronic, autoimmune multisystem disorder characterized by accumulation of T lymphocytes, macrophages, and epitheliod granulomas in various organs

134
Q

What is the etiology of Sarcoidosis?

A

Unknown

135
Q

Signs and symptoms of Sarcoidosis?

A

Can be asymptomatic with fever, fatigue, malaise, anorexia, cough, dyspnea, chest discomfort, skin rash (erythema nodosum), and wt loss

136
Q

What is Sjogren’s Syndrome?

A

Chronic, autoimmune disease that is characterized by dry eyes (keratoconjunctivitis) and dry mouth (xerostomia)

137
Q

Signs and symptoms of Sjogren’s Syndrome

A

Fatigue, fibromyalgia, blurred vision, burning and itching of eyes, and thickening secretions

138
Q

What is Scleroderma?

A

Abnormal accumulation of fibrous tissue in the skin and various organs

139
Q

Signs and symptoms of Scleroderma

A

Chronic fatigue, muscle aches, joint pain, swelling with limited ROM, shiny/smooth/stretched skin appearance on face and hands, dysphagia

140
Q

What is Polyarthritis Nodosa?

A

Necrotizing inflammation of the blood vessel walls

141
Q

Signs and symptoms of Polyarthritis Nodosa

A

fever, myalgia, skin lesions, HTN, abdominal pain, malaise

142
Q

What is selective IgA deficiency?

A

Genetic defect; sIgAD cells that produce IgA are dysfunctional

143
Q

What are the risk factors of IgA Deficiency?

A

Rubella, EBV, CMV, Toxoplasma gondii

144
Q

Signs and symptoms of IgA Deficiency

A

Most are asymptomatic, sinus and pulmonary infections, swelling/pain/tenderness of maxillary and frontal sinuses, chronic otorrhea, decreased auditory acuity or deafness, chronic nasal discharge, fever, non-productive or productive cough, dyspnea

145
Q

What is Hypoglobulinemia?

A

Decreased number of Igs related to a defect in B-cell development and maturation

146
Q

Signs and symptoms of hypoglobulinemia?

A

Sx begins 6 months of age, respiratory infections, diarrhea with malabsorption syndrome, gastritis with achlorhydria and pernicious

147
Q

Whats is Wiskott-Aldrich Syndrom?

A

X-linked recessive disease caused by a mutation in gene that encodes Wiskott-Aldrich protein

148
Q

Signs and symptoms of Wiskott-Aldrich Syndrome

A

Lack of platelets, bleeding, prolonged bleeding from circumcision, purpura, unusual bruising, blood in stool

149
Q

What is DiGeorge Syndrome?

A

An isolated T-cell deficiency that results from maldevelopment of thymus gland

150
Q

Signs and symptoms of DiGeorge Syndrome

A

Congenital cardiac abnormalities, parathyroid gland maldevelopment with hypocalcemic tetany, and absence of the thymus, eye wide apart, top lip disfigurement

151
Q

What is Primary (Congenital) immunodeficiency?

A

It is genetic, mostly manifest in infants, and is an X-linked genetic disorders

152
Q

What is secondary (acquired) immunodeficiency?

A

Disorders with immunosuppression effects like leukemia, chemotherapy, and HIV/AIDS

153
Q

What are the three stages of HIV/AIDS infection?

A
  1. Acute Stage: occurs within 28 days of contracting the virus, pt presents with flu-like sx, the virus becomes dormant, but pt is still contagious
  2. Chronic Stage: latent stage, if untreated then virus replicates and CD4 cells decrease, lasts 6 months to 10 years
  3. AID Stage: CD4 count is less than 200, active opportunistic infection, fatal if left untreated
154
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Pathophysiology (8 decks)

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