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
2
Q
What action does filtration do in the kidneys?
A
Removes metabolic waste and removes drugs and other foreign materials
3
Q
What action does reabsorption do to the kidneys?
A
Regulate water and electrolytes and maintain acid-base balance
4
Q
What action does secretion do to the kidneys?
A
Secrete erythropoietin, activates Vitamin D, and secretes renin to regulate BP through RAAS
5
Q
Causes of prerenal dysfunction of the kidney?
A
Hypovolemia, decreased cardiac output, septic shock, embolism
6
Q
Causes of intrarenal dysfunction of the kidney?
A
Nephrotoxic medications, acute pyelonephritis, prolonged prerenal ischemia
7
Q
Causes of postrenal dysfunction of the kidney?
A
Prostate cancer, calculi formation
8
Q
What is normal excreted in urine?
A
Urea, nitrogen, creatinine, sodium, and potassium
9
Q
What are abnormal findings in urine?
A
Hematuria, proteinuria, casts, glucose and ketones, bilirubin, WBC
10
Q
What lab values are bad value when elevated (kidney)?
A
Serum creatinine and BUN
11
Q
What lab values are good when elevated (kidney)?
A
Urine clearance creatinine and GFR
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
13
Q
What occurs to urine frequency during renal dysfunction?
A
Olgiuria
14
Q
What occurs to the perfusion during renal dysfunction?
A
Poor perfusion which triggers the RAAS to raise BP
15
Q
What acid-base condition occurs during renal dysfunction?
A
Metabolic acidosis
16
Q
What occurs to potassium during renal dysfunction?
A
Hyperkalemia which can increase the risk of cardiac dysrhythmias
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
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)
19
Q
Symptoms of pyelonephritis.
A
Flank pain, high fever, chill, confusion, nausea and vomiting, and hematuria
20
Q
What shows on a UA of someone with pyelonephritis?
A
+ leukocytes, + nitrate, proteinuria, and + culture
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
22
Q
Symptoms of glomerulonephritis
A
Symptoms begin 7- 21 days after strep infection.
Edema (facial edema), oliguria, hypertension, hypoalbuminemia, dark “cola-colored” urine
23
Q
What shows on a UA of someone with glomerulonephritis?
A
Proteinuria, low GFR, and hematuria
24
Q
What is nephrotic syndrome?
A
Symptoms/findings that occur when the glomerulus is damaged.
25
What is the primary cause of nephrotic syndrome?
Diabetic nephropathy from DM
26
Symptoms of nephrotic syndrome
Edema (facial edema), oliguria, hypertension, hypoalbuminemia, dark "cola-colored" urine
27
What is polycystic kidney disease?
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
28
Symptoms of polycystic kidney disease
Abdominal and flank pain, renal calculi, and hematuria
29
What are risk factors for lower urinary tract infections (UTIs)?
Bacterial access to urinary tract
- poor perineal hygiene
- indwelling urinary catheters
Retention of urine
- benign prostatic hyperplasia
- indwelling urinary catheter not
draining properly
30
Symptoms of UTIs
Dysuria, frequency, and urgency
31
What is interstitial cystitis (IC)?
Also called painful bladder syndrome (PBS) can be nonulcerative or ulcerative
32
Symptoms of IC
Chronic pelvic and perineal pain, dysuria, full bladder, urgency, and frequency
33
What is urolithiasis?
The formation of stones, aka calculi, in the urinary system
Uro- meaning in the urinary system and -lithiasis meaning formation of stones
34
What are risk factors for urolithiasis?
Genetic susceptibility, dehydration, and diet high in animal protein, sodium, and calcium
35
Symptoms of urolithiasis
Flank pain that is severe and intermittent, nausea and vomiting, fever, hematuria, pyuria, painful urination
36
Is bladder cancer the most common type of urological cancer?
Yes
37
What is the environmental risk factor for bladder cancer?
Cigarettes
38
What is the occupational risk factor for bladder cancer?
Exposure to organic chemicals
39
Symptom of bladder cancer
Hematuria without pain is the primary symptoms
Others include:
- Frequent urination
- Incomplete bladder emptying
- Burning during urination
40
Leukocytosis
A WBC elevation above 11,000/mm3
41
Leukopenia
Decrease in WBC count below 4,000/mcL
42
What do blood cells arise from?
Pluripotent stem cells
43
Blast Cells
Immature precursor cells for each WBC cell line
44
Hematologic Neoplasms
Types of cancer that affect blood, bone marrow, lymph nodes, and lymphoid tissues
45
Which category of hematologic neoplasms is the most common?
Lymphomas
46
What is the etiology of hematologic neoplasms?
Any agent that damages the DNA of developing cells in the bone marrow that turns on oncogenes and turns off tumor suppressant genes
47
What are the risk factors for hematologic neoplasms?
Exposure to radiation, contact with benzene, some viruses, EPV, HIV, human T-lymphotropic virus, chronic gastric infection (H. pylori), congenital or acquired immunodeficiency disorders
48
Signs and symptoms of hematologic neoplasms?
Bone marrow suppression, low RBC count (anemia), leukopenia, thrombocytopenia, enlarged lymph nodes, splenomegaly
49
What is leukemia?
A cancer of developing WBC within the bone marrow
50
Acute Lymphoblastic Leukemia (ALL) and Acute Myelogenous Leukemia (AML)
ALL: An aggressive cancer that is more common in children and abrupt onset
51
What is the etiology of ALL/ AML?
Chromosomal and genetic alterations
52
What are the risk factors for ALL/ AML?
Previous chemotherapy/radiation therapy, white males older than 70, exposure to pesticides, EBV, HIV, and genetic disorders
53
Signs and symptoms of ALL/ AML and CLL/CML?
Frequent infection, opportunistic infections, anemia, fatigue, wt loss, bone pain, hemorrhage, lymphadenopathy, thrombocytopenia, and high WBC count.
54
Chronic Lymphocytic Leukemia (CLL) and Chronic Myelogenous Leukemia (CML)
Even high proportion of mature cells with reduced function; gradual onset with longer survival time
55
Multiple Myeloma
Involves the B-lymphocytes, malignant plasma cell increase and spread to other organs, bone becomes eroded
56
Symptoms of multiple myeloma
Infection, pain, fractures, anemia, bleeding, proteinuria, renal failure, pathologic bone fractures
57
What is Hodgkins Lymphoma?
A single node beginning that is large, non-tender, painless, and very localized
Reed Sternberg cell marker
58
What is Non-Hodgkins Lymphoma?
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
59
Normal WBC
5,000-10,000mm3
60
Normal Hgb in males
14-18g/dl
61
Normal Hgb in females
12-16g/dl
62
Normal Hct in males
42%-52%
63
Normal Hct in females
37%-47%
64
Normal platelet value
90,000-400,000 per microliter of blood
65
What causes Iron Deficiency Anemia?
Blood loss
66
Signs and symptoms of Iron Deficiency Anemia
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
What is the pathologic cause of Pernicious Anemia?
Lack of intrinsic factor since it is required for absorption of vitamin b12
68
What are the risk factors for pernicious anemia?
Chronic gastritis, heavy alcohol use, cigarette smoking, complete or partial gastrectomy, gastric bypass
69
Signs and symptoms of pernicious anemia?
Red/sore and shiny tongue, GI discomfort, numbness and tingling of the extremities, loss of coordination (ataxia), and fatigue
70
What causes Folate Anemia?
Lack of folate (folic acid) since it is required for RNA and DNA synthesis in erythrocyte
Occurs more often than vitamin b12 deficiency
71
Signs and symptoms of Folate Anemia
Red/sore and shiny tongue, GI discomfort, loss of coordination (ataxia), and fatigue
72
What are the risk factors of Folate Anemia?
Alcoholics and malnourished people
73
What causes Aplastic Anemia?
A failure of a tissue to produce normal daughter cells by mitosis; bone marrow failure; can be temporary or permanent
74
What are risk factors for Aplastic Anemia?
Chemical or radiation, viruses that damage the bone marrow
75
Signs and symptoms of Aplastic Anemia
Anemia, leukopenia, thrombocytopenia aka pancytopenia
76
What causes Sickle Cell Anemia?
Autosomal recessive genetics
77
What can alter the shape of RBCs in Sickle Cell Anemia?
Dehydration, Acidosis, Infection, Hypoxia
78
What occurs during Sickle Cell Anemia?
High blood viscosity and low circulation which causes pain and ischemia
79
Signs and symptoms of Sickle Cell Anemia
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
What is the process of hemostasis?
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
What is Thalassemia?
A genetic disorder of one or more genes for a Hgb; autosomal dominant
82
What causes Thalassemia?
Lack of Hgb production
83
Signs and symptoms of thalassemia
Hemolysis, stunted growth and development due to hypoxia, hyperactivity of bone marrow, impairing bone marrow, CHF
84
What is Polycythemia Vera?
An increase of RBS
85
What are the complications of Polycythemia Vera?
increase risk of thrombi and infarctions, bone marrow becomes fibrotic
86
Signs and symptoms of Polycythemia Vera?
increase blood viscosity, distention of blood vessels, HTN
87
What are the labs of Polycythemia Vera?
Increase in RBCs, granulocytes, and platelets
88
What is Thrombocytopenia?
Too few platelets
89
Signs and symptoms of thrombocytopenia
Petechiae, ecchymoses or purpura, hemorrhage
90
Thrombocytosis
Platelets above 400,000/mm3
91
Complications of Thrombocytosis
Ischemia and infarctions from emboli
92
Signs and symptoms of thrombocytosis
pain, numbness, burning, warmth, hemorrhage
93
What causes Hemophilia?
Lack of factor 8 in coagulation cascade
94
Signs and symptoms of hemophilia
hemorrhage with minor injuries, pain and swelling, joint bleeding
95
What is Von Willebrand Disease?
A genetic disorder due to a deficiency of Von Willibrand factor
96
Signs and symptoms of Von Willibrand Disease
Hemorrhage, epistaxis, rashes, easy bruising
97
What is Disseminated Intravascular Coagulation?
Massive clotting initially then causing multiple emboli and infarctions
Coagulation factors are used up
Hemorrhages follow
98
What line of defense is the innate immunity?
1st line
99
What line of defense is adaptive immunity?
2nd line
100
Which immunity will respond immediately without prior encounter of antigen?
Innate
101
What are the compensatory mechanisms of the innate immunity system?
Barriers like the skin and bacterial flora
Phagocytes like macrophages and dendrites
Natural killer cells
102
Which immunity has to be taught to respond?
Adaptive immunity
103
What two systems are part of adaptive immunity?
Cell-mediated and Humoral (antibody-mediated)
104
What cells are involved in the cell-mediated system?
T lymphocytes, helper T cells (CD4), cytotoxic T cells (CD8)
105
Where do T cells mature?
Thymus
106
What are antigen-presenting cells (APC)?
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
What do helper T cells do?
Stimulate B cells, stimulate other T cells, stimulate macrophages and natural killer cells
108
What do cytotoxic cells do?
Destroy specific antigens that have been processed by APCs
109
What cell is involved in the humoral (antibody-mediated) immunity system?
B-cells that later mature into plasma cells
110
How long is the maturation process of B-cells to plasma cells?
5-7 days
111
What do B-cells do?
Become a production factory for the antibodies and flag antigen for phagocytosis
112
What happens to the antigens when Igs attach to them?
The antigen cannot infect or reproduce
113
Which immune system (cell-mediated or antibody-mediated) will stimulate a quicker response when encountering an antigen a second time?
Humoral (antibody-mediated)
114
What is active acquired immunity?
When a person develops their own Igs
115
What is the immunity duration for active acquired immunity?
Long term
116
What are ways to get active acquired immunity?
Vaccines or illness
117
What is passive acquired immunity?
Igs that are passed on or given to the person
118
What is the immunity duration for passive acquired immunity?
Short term
119
What are ways to get passive acquired immunity?
Breastfeeding and injection of formed antibodies
120
What is type 1 hypersensitivity?
Also called "immediate"
IgE binds to the mast cell (containing histamie) and combines with antigen
Inflammation response is triggered
121
What is an example of type 1 hypersensitivity?
Allergies, rash, hives, asthma
122
What is type 2 hypersensitivity?
Also called "cytotoxic"
Cells (donor or own coated cells) attacked rapidly by own Igs
123
What is an example of type 2 hypersensitivity?
Patient being administered the wrong blood type or medicine coating cells
124
What is type 3 hypersensitivity?
Also called "immune complex"
Igs are combined with antigens and deposited into tissues
125
What are examples of type 3 hypersensitivity?
SLE and RA
126
What is type 4 hypersensitivity?
Also called "delayed"
T lymphocytes delay days before attacking antigen or donor cells
127
What is Systemic Lupus Erythematosus (SLE)?
An immune complex formed by autoantibodies embedded into connective tissue in organs and tissue triggering inflammation
128
What is an example of type 4 hypersensitivity?
Poison ivy and organ transplant rejection
129
Which organs does SLE affect?
KIDNEYS, lungs, skin, joints, synovial membranes, and heart
130
Signs and symptoms of SLE
-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
What is Rheumatoid Arthritis?
Symmetrical swollen joints in the hands, knees, and hips that causes permanent damage in the joints because of chronic inflammation
132
Signs and symptoms of RA
Morning stiffness that improves with movement, classic hand deformity: swan neck, Boutonniere deformity, ulnar deviation
133
What is Sarcoidosis?
A chronic, autoimmune multisystem disorder characterized by accumulation of T lymphocytes, macrophages, and epitheliod granulomas in various organs
134
What is the etiology of Sarcoidosis?
Unknown
135
Signs and symptoms of Sarcoidosis?
Can be asymptomatic with fever, fatigue, malaise, anorexia, cough, dyspnea, chest discomfort, skin rash (erythema nodosum), and wt loss
136
What is Sjogren's Syndrome?
Chronic, autoimmune disease that is characterized by dry eyes (keratoconjunctivitis) and dry mouth (xerostomia)
137
Signs and symptoms of Sjogren's Syndrome
Fatigue, fibromyalgia, blurred vision, burning and itching of eyes, and thickening secretions
138
What is Scleroderma?
Abnormal accumulation of fibrous tissue in the skin and various organs
139
Signs and symptoms of Scleroderma
Chronic fatigue, muscle aches, joint pain, swelling with limited ROM, shiny/smooth/stretched skin appearance on face and hands, dysphagia
140
What is Polyarthritis Nodosa?
Necrotizing inflammation of the blood vessel walls
141
Signs and symptoms of Polyarthritis Nodosa
fever, myalgia, skin lesions, HTN, abdominal pain, malaise
142
What is selective IgA deficiency?
Genetic defect; sIgAD cells that produce IgA are dysfunctional
143
What are the risk factors of IgA Deficiency?
Rubella, EBV, CMV, Toxoplasma gondii
144
Signs and symptoms of IgA Deficiency
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
What is Hypoglobulinemia?
Decreased number of Igs related to a defect in B-cell development and maturation
146
Signs and symptoms of hypoglobulinemia?
Sx begins 6 months of age, respiratory infections, diarrhea with malabsorption syndrome, gastritis with achlorhydria and pernicious
147
Whats is Wiskott-Aldrich Syndrom?
X-linked recessive disease caused by a mutation in gene that encodes Wiskott-Aldrich protein
148
Signs and symptoms of Wiskott-Aldrich Syndrome
Lack of platelets, bleeding, prolonged bleeding from circumcision, purpura, unusual bruising, blood in stool
149
What is DiGeorge Syndrome?
An isolated T-cell deficiency that results from maldevelopment of thymus gland
150
Signs and symptoms of DiGeorge Syndrome
Congenital cardiac abnormalities, parathyroid gland maldevelopment with hypocalcemic tetany, and absence of the thymus, eye wide apart, top lip disfigurement
151
What is Primary (Congenital) immunodeficiency?
It is genetic, mostly manifest in infants, and is an X-linked genetic disorders
152
What is secondary (acquired) immunodeficiency?
Disorders with immunosuppression effects like leukemia, chemotherapy, and HIV/AIDS
153
What are the three stages of HIV/AIDS infection?
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
