Path test 2 Flashcards
what does chromic mean?
hemoglobin
what does cytic mean?
cell (RBC)
What are the clinical manifestations of anemia related to?
tissue hypoxia
What is a normocytic normochromic type of anemia and is associated with a problem with stem cell production?
Aplastic anemia
Which types of anemia are not normocytic normochromic?
Pernicious anemia(macrocytic normochromic) Iron-deficiency(microcytic hypochromic)
What is abnormal in sickle cell disease?
Abnormal Hgb S
Also VALINE is present which is an amino acid that is not normally present
What triggers a sickle cell crisis?
decreased oxygenation
dehydration
What are the sickle cell manifestations related to?
RBCs become non-flexed and stiff
(sickled)
Occluded blood vessels and decreased perfusion and oxygenation
Hemophilia is seen more often in males because
it is X-linked recessive
People with hemophilia are at risk for bleeding, so they need
to be given clotting factors so we need to educate friends and family to donate blood.
In acute leukemias cells are
immature while in chronic leukemias cells are mature
Pedritiatic Respiratory-who is at risk for apriration?
- Impaired swallowing
- Impaired gag reflex
- tubes
- weak
- unconscious
Which type of croup is the most life-threatening?
Acute Epiglottis
The development of Respiratory Distress Syndrome in infants is related to what two things?
- Decreased surfactant production
- Immature lung tissue because the infants are immature
In Bronchopulmonary Dysplasia, mechanical ventilation with oxygen leads to what things :
inflammation
scarring and stiffness of lung tissue
eventually mucus and plugging of alveoli
What are the three main components of asthma?
mucus, edema, bronchospasm
The etiology of Cystic Fibrosis is
autosomal recessive
Cystic Fibrosis involves which two organs:
Lungs and Pancreas
In anaphylactic reaction, what specific step leads to the mast cell degranulation and release of large amounts of histamine?
The IgE on the mast cell connecting with the alleged
what manifestations in anaphylaxis are life-threatening
bronchial constriction
shock which causes increased vascular permeability and vasodilation
Why can people with Lupus have anemia?
IgG attacks RBCs
As lupus progresses:
AG and AB complexes form and deposit in vessel walls and destroy cells of vessel walls, and destroy cells of vessel walls, leading to poor perfusion of tissues and organs
What two things aid in the binding of the HIV viral particle to a CD4receptor?
- gp120 a surface glycoprotein
- chemokine(a co-receptor)
What three enzymes aid in converting the viral RNA to DNA?
reverse transcriptase, integrase, protease
What is the main etiology in DIC?
septicemia(sepsis)
In DIC what is the first part of the pathophys:
procoagulants overstimulate the coagulation system
What causes the hemorrhaging in DIC?
increased consumption of platelets and clotting factors
What lab test is the most indicative of DIC?
increased D-Dimer
In multiple myeloma, abnormal plasma B lymphocytes produce what that is found in the bloodstream?
Myeloma (M) protein
The Reed-Sternberg cell is found in lymph nodes in which type of lymphoma?
Hodgkins
If your level is high, your doctor should recheck it. If two or more levels are high, you may have kidney disease. The normal serum creatinine range is 0.6–1.1 mg/dL in women and 0.7–1.3 mg/dL in men. This test compares creatinine in your blood and urine.
A high BUN usually means that kidney function is less than normal, but other factors may affect the BUN level. … The normal BUN level for healthy individuals is 7-20 mg/dL in adults, and 5-18 mg/dL in children. Patients on dialysis have higher BUN levels, usually 40-60 mg/dL.
autoimmunity:
breakdowns of the “code of recognition” Body immune system begins to recognize self antigens as being foreign
autoimmunity hypersensitivity type 1:
IgE mediated allergic reactions (allergy/anaphylaxis)
autoimmunity hypersensitivity type2:
Tissue specific
Blood transfusion reaction
autoimmunity hypersensitivity type3:
Immune-complex mediated reactions
AG-AB complexes form and deposit into tissues
autoimmunity hypersensitivity type4:
cell-mediated reactions
involves T-cells, macrophages
allergy/anaphylaxis
a rapid/immediate hypersensitivity reaction upon re-exposure to an antigen
allergy/anaphylaxis:
produces IGE antibody specific, IGE goes to mast cell receptors sites there.
clinical manifestations of gallery/anaphylaxis
is related to the release of histamine/leukotrienes
with localized allergy/anaphylaxis there is
local inflammation
systemic clinical manifestations of allergy/anaphylaxis is related to histamine receptors include
-bronchial constriction, laryngeal edema, itching(pruritus/erythema)
GI includes abdominal cramps, vomiting, diarrhea, mucous membranes-increased secretions
-vasculature-increased permeability/vasodilation(can go into shock)
The steps that occur during allergy/anyphylaxis include:
1) B-cell is exposed to allergen and produces antibody-IgE(takes time) IgE is specific to particular antigen
2) IgE antibody goes to receptors on the mast cell and sits on those receptors and waits for the next time allergen is reintroduced.
3) next time the body is exposed to allergen-the IgE antibody recognizes it and induces mast cell degranulation
4) During mast cell degranulation: release of large amounts of histamine and leukotrienes cause clinical manifestations.
SLE is:
Systemic Lupus Erythematous:a chronic autoimmune , multisystem inflammatory disease, common in females ages 20-40. Something triggers it and then it stays with the person forever
What type of hypersensitivity is Lupus:
Type 3, which means AG/AB complexes form and deposit in vessel walls(never good)
Five steps of Lupus pathophysiology:
1) B cell produces IgG (Immunoglobulin), attacks what it thinks is foreign DNA. It attacks cells of vessel walls
2)T-helper cells further stimulate B-cell
production of IgG
3)Macrophages are recruited to further attack “foreign” DNA
4) IgG also attacks RBCs because it thinks they are foreign
5)T-suppressors are supposed to slow down immune reaction, but aren’t really effective in Lupus.
Rheumatoid arthritis or RA is an autoimmune inflammatory disease characterized by:
destruction of the synovial membrane. It is a type 3 and 4 hypersensitivity. *Normal antibodies become autoantibodies-and attack antigens on cell membranes.
Pathophysiology of RA:
Normal Antibodies(IgM/IgG) are transformed into Rheumatoid Factor and attacks the DNA that is in the synovial membrane and surrounding vasculature. It causes vasodilation and increased permeability in the vasculature surrounding the synovial membrane which allows WBCs to enter and further attack…it also allows more fluid in which causes clogging, congestion, and pressure..fibrin, collagen, and scar tissue(three things that should not be in the synovial fluid space make the joints stiff, and difficult to move.
HIV is:
a retrovirus that carries its genetic coding in its RNA.
Steps of the infection of a CD4(T-helper) cell with the HIV virus.
1)The HIV surface glycoprotein(gP120) attaches to the CD4
2) chemokine aids in the binding of gp120 (its a coreceptor)
3) viral RNA is converted into DNA with the help from 3 enzymes:
reverse transcriptase, integrase, protease
4)DNA inserted and integrated into the T-helper cell DNA and takes over the cell
serologically negative test results:
does not necessarily mean the patient doesn’t have HIV, it is just not yet detected.-person must make antibodies before the virus is detected.
serologically positive test results:
is when the antibodies are detected, but the patient is asymptomatic(no symptoms)
Early stages of HIV disease:
OLD CARTS, they have many different symptoms, but is not AIDS
AIDS
serios clinical symptoms and or malignancies and often the T-helper cell number is less than 200
The lack of what substance in the alveoli leads to respiratory distress syndrome?
surfactant
What etiological factors can lead to Bronchopulmonary dysplasia?
premature birth, respiratory distress Syndrome, prolonged mechanical ventilation, or O2 toxicity
Which type of croup leads to airway obstruction?
Acute Laryngotracho bronchitis
What occurs pathophysiologically with cystic fibrosis?
production and stasis of thick, tanacious mucous causing obstuctive pulmonary disease. Pancreatic exocrine deficiency of trypsin, amylase, and lipase leads to malabsorption
clinical manifestations of Lupus:
chronic Lupus has periods of exacerbations and of remissions
- arthritis of peripheral joints(very prevalent/ related to inflammation)
- vasculitis(skin rash)
- photosensitivity(sensitive to ultraviolet light)
- renal disease caused by damage from vasculitis(usually the first thing to see
- Hematologic abnormality caused by anemia because of destruction
- Cardiovascular disease(pericarditis)
Clinical Manifestations of Rheumatoid arthritis:
Early: synovitis (inflammation of synovial membrane)
systemic manifestations of inflammation
minor stiffness and achyness
Then: start to get tenderness and stiff joints
Late: PAin, deformity, loss of function
-Rheumatoid nodules(inflammatory cells congregate in pockets) not painful
-ulnar drift(on wrist-wrist deviates to pinky side out)
Why are erythrocytes or RBCs so efficient in carrying O2?
they are doughnut shaped discs, their shape increases there surface area so that they can carry more O2, also they are very flexible and can flatten to squeeze through capillaries.
Thrombocyopenia is a platelet count of less than 100,000, and is caused by:
autoimmune disorder, complications of heparin therapy, or blood loss.
clinical manifestations of thrombocytopenia include:
hemorrhage, epistaxis, petechia, and hematuria
Clinical manifestations of DIC varies between only having an abnormal D-Dimer to having massive hemorrhage and clotting:
microvascular (capillaries) clotting -
hemorrhage
Pathophysiology of Multiple Myeloma:
Excess number of abnormal plasma cells(B lymphocytes) infiltrate the bone marrow, develop into tumors, destroy the bone, and invade lymph nodes, liver, spleen, and kidneys
produce the abnormal plasma cell: myeloma protein
Clinical manifestations of Multiple Myeloma include:
frequent infections, anemia/bleeding, bone pain/pathological fractures, renal insufficiency/failure
Hodgkins lymphoma:
Reed-sternbergs cells in lymph node
enlarged painless lymph nodes, night sweats, fever, weight loss
complete remission if treated in early stages(1 and 2)
Non-Hodgkins lymphoma has the same symptoms as Hodgkins, but:
can be more fatal because bone marrow involvement occurs more often than in Hodgkins, but it varies: can be slowly developing or aggresive
Hodgkins lymphoma is diagnosed microscpically by:
biopsying lymph tissue
What are the changes seen in macrocytic-normochromic anemia?
Decreased gastric secretion of instrinsic factor (basically absent) leads to malabsorption of vitamin B-12, which leads to decreased RBC production
RBCs are abnormal and large, they die and this causes anemia-
Is usually seen in late adult life, but there is also a congenital form developing before two years of age
Example: Pernicious Anemia
Hemophilia:
Genetic disease caused by deficiency of blood clotting factors essential for froming a clot.
LAb tests used to detect Kidney failure(measure GFR):
BUN: waste product of cell metabolism
NL= 10-20
Creatinine(produced by muscle) need only one blood sample
NL=.7-1.5
*more accurate than BUN in indicating renal function
24-hour urine sample is called a creatinine clearance test
Type A Hepatitis:
acute, sudden, caused by contaminated food/water or poor sanitation, fecal/oral route
No chronic state/self-limiting
diagnose by HAV antigen and antibodies
Manifestations include: fever, malaise, anorexia, nausea, jaundice,
*there is a vaccine available
Type B Hepatitis:
Insidious, gradual,
blood, needles, syringes, semen, bodily fluids
chronic if manifestations occur for more than 6 months
dignosed by HBV antigens and antibodies
manifestations are: anorexia, malaise, joint aching, abdominal discomfort, jaundice, may lead to liver failure
*Hep B vaccine/interferon
*can live outside the body for 7-10 days
Hepatitis C:
4 million Americans have hep C, fatigue can progress to permanent liver damage, Those at risk are those with a history of snorting/injecting drugs, and recieving blood transfusions before 1992
Only mode of transmission is blood
Most of the manifestations of Leukemia are related to:
bone marrow suppression: anemia(decreased RBC)
bleeding-decreased platelets
fever-decreased WBC
Sickle cell anemia does not usually appear before 6 months of age because:
of a decrease of Hg F at that time
An example of microcytic hypochromic anemia is:
iron-deficiency
aplastic anemia, post hemorrhagic anemia, hemolytic anemia, anemia with chronic conditions, and sickle cell anemia are all:
normocytic-normochromic anemias
when Red blood cells become sickled it causes them to:
become nonflexable and stiff, causes occluded blood vessels, increased viscosity of blood, and further sickling of cells leading to increased deoxygenation of tissue and infarctions and pain.
*pallor, fatigue, jaundice, irritability.
Pathophysiology of Respiratory Distress Syndrome(lower :
Premature infants lungs are not mature-alveoli unable to be inflated or opened to exchange O2 and Co2 (causing atelectasis)
decreased surfactant, alveoli have difficulty expanding, need for increased respiratory effort to inhale air and prevent collapse of alveoli during expiration, increased PCO2, and decreased pO2-co2 and o2 cant cross alveolar-capillary membrane hypoxemia leads to respiratory acidosis
there may be development of fibrin clots or film(hyaline membrane) which decreased gas diffusion in alveolar.
Pathophysiology of Bronchopulmonary dysplasia:
Mechanical ventilation with oxygen acts as an irritant to lung tissue, this leads to continuous inflammation, there is scarring and stiffening of the lung tissue, alveoli fail to multiply
chronic inflammation result in increased mucus and plugging of the alveoli and shunt unit
Pathophys of Asthma:
both the large and small airways are affected
- allergens trigger released of IgE which causes mast cell degranulation resulting in edema of bronchial mucosa, bronchospasm, and increased mucous productions
- Air is trapped in lungs resulting in inadequate ventilation, hypoxemia, hypercapnia, respiratory acidosis, and respiratory failure.
Clinical Manifestations of:
wheezing-mostly on expiration cough-sometimes causes vomiting irritability, restlessness dyspnea- chest tightness tachypnea, nasal flaring, anxious facial expressions, diaphoresis
Pathophysiology of cystic fibrosis:
production and stasis of thick, tenacious mucous-causing obstructive pulmonary disease
pancreatic exocrine deficiency of trypsin, amylase, and lipase-leading to malabsorption
chronic respiratory disease
elevated sodium chloride in the sweat due to ineffective chloride movement out of the cell and high reabsorption of sodium into the cells
complications of CF affect all organ systems
Clinical manifestations of cystic fibrosis:
thick mucus blocks airways, causes air trapping, and atelectasis
causes frequent respiratory infections and inflammatory response
chronic cough/sputum production
barrell chest
chronic rhinitis
clubbing of fingers-chronic hypoxia
Acute Laryngotracheo-bronchitis (1st type of croup)
as a gradual onset, rhinitis/fever/inspiratory stridor, and harsh, high crowing noise
Viral Croup:2nd type of croup
sudden onset at night/afrebrile/high pitch stridor, muffled voice
Acute Epiglottis (3rd type of croup)
sudden onset(life-threatening) fever inspiratory wheezing restlessness drooling difficulty swallowing
