Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

patho test 2 > Path test 2 > Flashcards

Path test 2 Flashcards

1
Q

what does chromic mean?

A

hemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what does cytic mean?

A

cell (RBC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the clinical manifestations of anemia related to?

A

tissue hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a normocytic normochromic type of anemia and is associated with a problem with stem cell production?

A

Aplastic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which types of anemia are not normocytic normochromic?

A 
Pernicious anemia(macrocytic normochromic)
Iron-deficiency(microcytic hypochromic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is abnormal in sickle cell disease?

A

Abnormal Hgb S

Also VALINE is present which is an amino acid that is not normally present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What triggers a sickle cell crisis?

A

decreased oxygenation

dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the sickle cell manifestations related to?

A

RBCs become non-flexed and stiff
(sickled)
Occluded blood vessels and decreased perfusion and oxygenation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hemophilia is seen more often in males because

A

it is X-linked recessive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

People with hemophilia are at risk for bleeding, so they need

A

to be given clotting factors so we need to educate friends and family to donate blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

In acute leukemias cells are

A

immature while in chronic leukemias cells are mature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pedritiatic Respiratory-who is at risk for apriration?

A
  • Impaired swallowing
  • Impaired gag reflex
  • tubes
  • weak
  • unconscious
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which type of croup is the most life-threatening?

A

Acute Epiglottis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

The development of Respiratory Distress Syndrome in infants is related to what two things?

A
  • Decreased surfactant production

- Immature lung tissue because the infants are immature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

In Bronchopulmonary Dysplasia, mechanical ventilation with oxygen leads to what things :

A

inflammation
scarring and stiffness of lung tissue
eventually mucus and plugging of alveoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the three main components of asthma?

A

mucus, edema, bronchospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

The etiology of Cystic Fibrosis is

A

autosomal recessive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cystic Fibrosis involves which two organs:

A

Lungs and Pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

In anaphylactic reaction, what specific step leads to the mast cell degranulation and release of large amounts of histamine?

A

The IgE on the mast cell connecting with the alleged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what manifestations in anaphylaxis are life-threatening

A

bronchial constriction

shock which causes increased vascular permeability and vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why can people with Lupus have anemia?

A

IgG attacks RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

As lupus progresses:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What two things aid in the binding of the HIV viral particle to a CD4receptor?

A
  • gp120 a surface glycoprotein

- chemokine(a co-receptor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What three enzymes aid in converting the viral RNA to DNA?

A

reverse transcriptase, integrase, protease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the main etiology in DIC?

A

septicemia(sepsis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

In DIC what is the first part of the pathophys:

A

procoagulants overstimulate the coagulation system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What causes the hemorrhaging in DIC?

A

increased consumption of platelets and clotting factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What lab test is the most indicative of DIC?

A

increased D-Dimer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

In multiple myeloma, abnormal plasma B lymphocytes produce what that is found in the bloodstream?

A

Myeloma (M) protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

The Reed-Sternberg cell is found in lymph nodes in which type of lymphoma?

A

Hodgkins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

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

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

autoimmunity:

A

breakdowns of the “code of recognition” Body immune system begins to recognize self antigens as being foreign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

autoimmunity hypersensitivity type 1:

A

IgE mediated allergic reactions (allergy/anaphylaxis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

autoimmunity hypersensitivity type2:

A

Tissue specific

Blood transfusion reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

autoimmunity hypersensitivity type3:

A

Immune-complex mediated reactions

AG-AB complexes form and deposit into tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

autoimmunity hypersensitivity type4:

A

cell-mediated reactions

involves T-cells, macrophages

37
Q

allergy/anaphylaxis

A

a rapid/immediate hypersensitivity reaction upon re-exposure to an antigen

38
Q

allergy/anaphylaxis:

A

produces IGE antibody specific, IGE goes to mast cell receptors sites there.

39
Q

clinical manifestations of gallery/anaphylaxis

A

is related to the release of histamine/leukotrienes

40
Q

with localized allergy/anaphylaxis there is

A

local inflammation

41
Q

systemic clinical manifestations of allergy/anaphylaxis is related to histamine receptors include

A

-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)

42
Q

The steps that occur during allergy/anyphylaxis include:

A

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.

43
Q

SLE is:

A

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

44
Q

What type of hypersensitivity is Lupus:

A

Type 3, which means AG/AB complexes form and deposit in vessel walls(never good)

45
Q

Five steps of Lupus pathophysiology:

A

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.

46
Q

Rheumatoid arthritis or RA is an autoimmune inflammatory disease characterized by:

A

destruction of the synovial membrane. It is a type 3 and 4 hypersensitivity. *Normal antibodies become autoantibodies-and attack antigens on cell membranes.

47
Q

Pathophysiology of RA:

A

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.

48
Q

HIV is:

A

a retrovirus that carries its genetic coding in its RNA.

49
Q

Steps of the infection of a CD4(T-helper) cell with the HIV virus.

A

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

50
Q

serologically negative test results:

A

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.

51
Q

serologically positive test results:

A

is when the antibodies are detected, but the patient is asymptomatic(no symptoms)

52
Q

Early stages of HIV disease:

A

OLD CARTS, they have many different symptoms, but is not AIDS

53
Q

AIDS

A

serios clinical symptoms and or malignancies and often the T-helper cell number is less than 200

54
Q

The lack of what substance in the alveoli leads to respiratory distress syndrome?

A

surfactant

55
Q

What etiological factors can lead to Bronchopulmonary dysplasia?

A

premature birth, respiratory distress Syndrome, prolonged mechanical ventilation, or O2 toxicity

56
Q

Which type of croup leads to airway obstruction?

A

Acute Laryngotracho bronchitis

57
Q

What occurs pathophysiologically with cystic fibrosis?

A

production and stasis of thick, tanacious mucous causing obstuctive pulmonary disease. Pancreatic exocrine deficiency of trypsin, amylase, and lipase leads to malabsorption

58
Q

clinical manifestations of Lupus:

A

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)
59
Q

Clinical Manifestations of Rheumatoid arthritis:

A

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)

60
Q

Why are erythrocytes or RBCs so efficient in carrying O2?

A

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.

61
Q

Thrombocyopenia is a platelet count of less than 100,000, and is caused by:

A

autoimmune disorder, complications of heparin therapy, or blood loss.

62
Q

clinical manifestations of thrombocytopenia include:

A

hemorrhage, epistaxis, petechia, and hematuria

63
Q

Clinical manifestations of DIC varies between only having an abnormal D-Dimer to having massive hemorrhage and clotting:

A

microvascular (capillaries) clotting -

hemorrhage

64
Q

Pathophysiology of Multiple Myeloma:

A

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

65
Q

Clinical manifestations of Multiple Myeloma include:

A

frequent infections, anemia/bleeding, bone pain/pathological fractures, renal insufficiency/failure

66
Q

Hodgkins lymphoma:

A

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)

67
Q

Non-Hodgkins lymphoma has the same symptoms as Hodgkins, but:

A

can be more fatal because bone marrow involvement occurs more often than in Hodgkins, but it varies: can be slowly developing or aggresive

68
Q

Hodgkins lymphoma is diagnosed microscpically by:

A

biopsying lymph tissue

69
Q

What are the changes seen in macrocytic-normochromic anemia?

A

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

70
Q

Hemophilia:

A

Genetic disease caused by deficiency of blood clotting factors essential for froming a clot.

71
Q

LAb tests used to detect Kidney failure(measure GFR):

A

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

72
Q

Type A Hepatitis:

A

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

73
Q

Type B Hepatitis:

A

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

74
Q

Hepatitis C:

A

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

75
Q

Most of the manifestations of Leukemia are related to:

A

bone marrow suppression: anemia(decreased RBC)
bleeding-decreased platelets
fever-decreased WBC

76
Q

Sickle cell anemia does not usually appear before 6 months of age because:

A

of a decrease of Hg F at that time

77
Q

An example of microcytic hypochromic anemia is:

A

iron-deficiency

78
Q

aplastic anemia, post hemorrhagic anemia, hemolytic anemia, anemia with chronic conditions, and sickle cell anemia are all:

A

normocytic-normochromic anemias

79
Q

when Red blood cells become sickled it causes them to:

A

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.

80
Q

Pathophysiology of Respiratory Distress Syndrome(lower :

A

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.

81
Q

Pathophysiology of Bronchopulmonary dysplasia:

A

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

82
Q

Pathophys of Asthma:

A

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.
83
Q

Clinical Manifestations of:

A 
wheezing-mostly on expiration
cough-sometimes causes vomiting
irritability, restlessness
dyspnea- chest tightness
tachypnea, nasal flaring, anxious facial expressions, diaphoresis
84
Q

Pathophysiology of cystic fibrosis:

A

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

85
Q

Clinical manifestations of cystic fibrosis:

A

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

86
Q

Acute Laryngotracheo-bronchitis (1st type of croup)

A

as a gradual onset, rhinitis/fever/inspiratory stridor, and harsh, high crowing noise

87
Q

Viral Croup:2nd type of croup

A

sudden onset at night/afrebrile/high pitch stridor, muffled voice

88
Q

Acute Epiglottis (3rd type of croup)

A 
sudden onset(life-threatening) 
fever
inspiratory wheezing 
restlessness
drooling 
difficulty swallowing

patho test 2 (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions