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Pathophysiology 201 > Exam 1 > Flashcards

Exam 1 Flashcards

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1
Q

tumor staging

A

Staging: clinical spread of cancer -> treatment and prognosis
- TNM: T - tumor size (1-4), N - lymph node involvement (0-3), M - metastasis (0-1)

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2
Q

tumor grading

A

examination of differentiation
Scale of 1-4 (4 is poorly differentiated) - tumor grade ¾ doesn’t respond well to treatment

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3
Q

What is the purpose of a pap smear,what does the clinician look for when examining the collected specimen

A

To catch cancer early, the clinician looks for dysplasia, anaplasia, and neoplasia
Look for differentiation of cells

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4
Q

Amiocentesis

A

at 16 weeks of gestation, a clinician inserts needle through abdominal cavity into amniotic sac and collects fluid. Puts the fluid in petri dich and replicates the cells. Thye stop the replication and look at the chromosomes. When babies are in amniotic fluid they shed skill cells.

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5
Q

Chorionic villi (extensions on the placenta)

A

with sampling, you go transabdominally or transvaginally and collect chorionic villi. Then you put them in a petri dish and have them grow, and then you do a carrier type and look at the chromosomes. Can be done at ten weeks.

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6
Q

cardiac dysrythmias

A

caused by hyper and hypo kalemia

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7
Q

Cell free DNA testing

A

some fetal cells enter maternal circulation, so do a blood test on mom and separate mom cells from fetal cells. Grow cells and do a carrier type. Can be done at 10 weeks. Non invasive procedure - but upon finding genetic abnormality, you are advised to perform one of the other two tests.

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8
Q

Resolution

A

cells were not damaged beyond recovery, they can recover and return to normal function (does not require mitosis)

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9
Q

Regeneration

A

replacement of lost or necrotic tissue with tissue that is structurally and functionally identical, healthy neighboring cells undergo mitosis and proliferate to replace the cells lost in the tissue

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10
Q

Scar formation

A

dead cells are replaced by a different cell type than the original. First granulation tissue forms (highly vascularized connective tissue) and then it matures into fibrous tissue. Area loses its function.

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11
Q

complication of scar formation

A

Conrtactures and obstructions - scar is smaller than wound but can limit function
Adhesions (can hold loops of intestines together)
Hypertrophic scar tissue (orignal wound size but raised) excessive deposition of connective tissue
Keloid: excessive scar formation / deposition and growth of connective tissue outside of margins

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12
Q

Dry gangrene

A

lack of arterial blood supply but venous flow carries fluid out of tissue. Dry, shrinks, skin wrinkles, dark brown / black. Spreads slowly and symotoms are not as marked as wet gangrene. Clear line of demarcation between gangrenous area and healthy tissue. Confined to extremities - external. (diabetes)

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13
Q

Wet gangrene

A

lack of venous flow lets fluid accumulate in tissue. Area is cold, swollen, pulseless, moist, black. Bulbs form on surface, liquefation occurs, foul odor from bacteria. No line of demarcation between normal and dead tissue. Spread of damage tissue is rapid, affects internal organs and extremities.

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14
Q

Gas gangrene

A

clostridum infection. Bacterial infection that produces gas in tissue. Deadly. Bubbles kill muscle cells. Massive spreading edema, hemolysis of RBCs, hemolytic anemia, hemoglobinemia and renal failure

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15
Q

Connective tissue repair

A

1) hemostasis, angiogenesis, and ingrowth of granulation tissue
2) emigration of fibroblasts and deposition of the extracellular matrix
3) maturation and reorganization or the fibrous tissue (remodeling) usually starting during first 24 hr of injury

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16
Q

Cutaneous healing stages

A

inflammatory phase, proliferative phase, remodeling phase

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17
Q

inflammatory phase

A

starts right after injury and preps the wound for healing
Hemostasis
Vascular phase - vasoconstriction followed by vasodilation
Cellular phase - migration of phagocytic cells that digest and remove invading organisms and cellular debris - cleaning up the site

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18
Q

proliferative phase

A

build up of new tissue to fill the wound space
Formation of granulation tissue
Wounds that heal by secondary intention have more necrotic debris and exudate that must be removed and requires a larger amount of granulation tissue
Epithelialization (no loss of function)
migration , proliferation, and differentiation of epithelia cells at the wound edges

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19
Q

remodeling phase

A

increases the strength of the wound

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20
Q

Liquefaction necrosis

A

brain tissue dies or bacterial infection (leaves a hole)

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21
Q

Coagulative necrosis

A

hypoxic injury leading to infarctions → myocardial infarction (tissue architecture/cell outlines are preserved despite dead cells) (leaves discolored area of regular shaped organ)

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22
Q

Caseous necrosis

A

dead cell persis indefintely as soft, cheese like debris -> found in TB patient’s lungs

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23
Q

promote wound healing

A

Youth, good nutrition, adequate hemoglobin, effective circulation, clean undisturbed wound, no complications or chronic conditions

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24
Q

delay wound healing

A

advanced age (reduced mitosis), poor nutrition, anemia, circulatory problems, irritation, bleeding, infection.

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25
Downs
3 chromosomes for 21
26
Edwards
3 chromosomes for 18
27
Klinefelters
extra x chromosome in male XXY
28
Turners syndrome
single x chromosome XO
29
stage 1 TNM
T1 – 2 cm or less, No – no lymph node involvement, Mo - no metastasis
30
stage 2 tnm
between 2 - 5 cm, N1 – lymph node involvement (1-3 under arm), Mo - no metastasis
31
stage 3 tnm
t3 larger then 5 cm, N1 to N2 – lymph node involvement (3-9 under arm), Mo - no metastasis
32
stage 4 tnm
T4 – tumor any size but fixed to chest wall, N3 – greater than 10 lymph nodes are involved or has spread to clavicular node involvement (spread), M1 – metastasis to distant organ
33
Atrophy
cells get smaller (esp when not used)
34
Hypertrophy
cells get larger - think working out: not more cells, just bigger
35
Hyperplasia
muscle gets bigger because there are more cells in the tissue
36
Metaplasia
cell under stressful condition changes to a cell type that can deal with the stress (acid reflux)
37
Dysplasia
precancerous state, cells being to vary in shape in size, develop large nuclei, increased rate of mitosis.
38
Anaplasia
associated with malignancy or cancer. Cells are undifferentiated, have variable nuclei, cell structure, and mitotic figures.
39
Neoplasm
tumor or new growth, benign or malignant.
40
local and systemic signs/symptoms of inflammation
swelling , redness, pain, heat/warmth, loss of function
41
vascular stage of acute inflammation
vasodilation and capillaries become more permeable
42
vasodilation
Increasing blood flow to the injured area Mediators include histamine and nitric oxide Redness and warmth results
43
increased capillary permeability
Allowing exudate to escpate into the tissues Mediators include histamine, bradykinin, and leukotrienes Swelling, pain, and impaired function result
44
Cellular stage of acute inflammation
White blood cells enter the injured tissue: Chemotaxis Destroying infective organisms Removing damaged cells Releasing more inflammatory mediators to control further inflammation and healing Diapedesis - WBCs move from blood vessels to harmed tissue
45
Increase body temp (fever)
Vasoconstriction Shivering Increased BMR Curl up body Decreased rate of replication of invading organism, sequesters iron
46
Decrease body temp
Vasodilation Sweating Lethargy Extend body
47
granulation tissue
Highly vascularized connective tissue
48
Benign
well differentiated. Cells look and act like the cells in the normal tissue. Non cancerous - cells that make up tumor contain well differentiated cells.
49
Malignant
less differentiated. Cells look less like cells in the normal tissue Cancerous, undifferentiated cells. Do not look or act like normal cells in the tissue. Cells often do not mature (differentiate) to do the job the tissue is supposed to do.
50
hereditary cancer
Retinoblastoma (rb) Brca 1 and brca 2
51
paraneoplastic syndromes
hormones or factors secreted by tumor cells, symptoms are caused by substacnes that the tumor releases. (ADH ACTH PTH related protein Promote or inhibit blood clot formation )
52
Tumor markers
enzymes, antigens, hormones used for screening, for diagnosis, establishing prognosis, monitoring treatment and for detecting relapse
53
AFP
oncofetal antigens - liver cancer
54
CEA
carcinoembryonic antigen - colorectal cancer
55
hCG
human chorionic gonadotropin - gestationsion tumors or testicular cancer
56
PSA
prostate specific antigen - prostate cancer
57
CA 125
ovarian cancer
58
complications of chemotherapy
Affects both neoplastic cells and rapidly proliferating normal cells Bone marrow depression: limiting factor with chemotherpay. Blood cell count must be taken before each treatment. Bone marrow is depressed, wbc level is low, pt is now susceptible to infection nausea/vomitting: due to stimulation of the emetic center of the brain or damage to the mucosal lining of the digestive tract Anorexia Hair loss Breakdown of skin and mucosa linings mutagenic /carcinogenic (cause other mutations) Teratogenic (cause birth defects) Azoospermia or oligospermia (decreased sperm count, change in menstrual cycle, destory ovaries) Changes in menstrual cycle → amenorrhea Cellular resistance - adapt to chemo
59
SIADH
Excess production of ADH causes Hyponatremia and its s/s
60
hypoaldosteronism
Hyponatremia, hyperkalemia
61
Hyperaldosteronism
Hypokalemia
62
dystrophic calcification
calcium on dead and dying tissue, visible to nake eye Normal calcium levels Microscopic deposits of calcium colts into injured tissue Often visible to naked eye Gritty sand like grains to firm hard rock like material Calcium phosphate Components of the calcium deposits come from dead or dying cells Ie advanced atherosclerosis, damaged heart valves, TB lesions
63
Metastatic calcification: high calcium levels, deposited in any soft tissue (not dead tissue)
Occurs in normal tissue and is caused by increased serum calcium levels (lung, kidney, blood vessles) → abnormality in calcium metabolism Hyperparathyroidism, hyperparathyroidism in renal failure, bone destruction Ie immobilized patients, paget disease, cancer with metastatic bone lesions
64
potassium sparing
aldactone/spironolactone Causes hyperkalemia
65
potassium wasting
Lasix and hydrochlorothiazide hypokalemia
66
Intermittent fever
fever returns to normal at least once every 24 hours
67
Remittent fever
fever does not go down and varies a few degrees in either direction
68
Sustained fever
the temperature remains above normal with minimal variations
69
Recurrent or relapsed fever
there is one or more episodes of fever. Each as long as several days with one or more days of normal temperature in between episodes
70
Initiation stage of carcinogenesis
initial mutation occurs
71
Promotion stage of carcinogenesis
mutatued cells are stimulated to divide in an unregulated manner
72
progression stage of carcingogenesis
cells acquire malignant appearances. Tumor cells compete with one another and develop more mutations, which make them more aggressive → appearance of tumor/you have a tumor
73
causes of edema
Increased capillary pressure (transudative) Decrease osmotic/oncotic pressure (transudative) Lymphatic obstruction (transudative) Increased capillary permeability (exudative)
74
electrolyte imbalance in a patient with diabetes insipidus
Comes from lack of ADH Hypernatremia
75
leukopenia
Bone marrow breakdown from chemo prevents the production of WBCs (neutrophils), leading the patients to be at risk for infection
75
A patient is given an IV infusion of albumin, a plasma protein, what will happen to the levels of bound, ionized and total calcium in this patient and what are some signs and symptoms
More albumin means more calcium binding - more bound ca and less ionized ca. More total ca.
76
41)What happened to the physiological active form of calcium during acidosis
more ionized calcium (more h+ binding to oxygen, leaving less room for calcium to bind)
77
Alkalosis
less ionized calcium - more bound calcium because the calcium can bind to the oxygen
78
Proto-oncogenes
code for normal cell division proteins Growth factors, growth factor receptors, transcription factors, cell cycle proteins, apoptosis inhibitors
79
Oncogene
proto oncogenes mutate to these Increased activated or they are activated
80
Tumor suppressor gene
inhibit cell division Mutations inhibit or decrease
81
electrolyte imbalances you would expect to see in a patient suffering from kidney failure
Sodium decreases Potassium increases Calcium decreases Phosphate increases Magnesium increases H+ increases * blood volume increases (but this is not an electrolyte)
82
How can you tell if patient is retaining fluid
By weighing them same time of day and in same apparel - a few pounds gained within a day is most likely not due to eating.
83
What happens to potassium in acidosis and alkalosis
Acidosis: k leaks out of cells and enters the blood (hyperkalemia) increases Alkalosis: k levels in the blood decrease (hypokalemia)
84
different types of exudate
Serous: mostly water Fibrinous: thick and sticky with a lot of fibrin and cell content Purulent: thick, yellow-gree → designating an infection (pus) - white heads bloody /hemorrhagic → if blood vessels are damaged (if you popped a blister and it bled) Membranous, pseudomembranous: necrotic cells with fibropurulent exudate (mucous membranes)
85
naming benign tumors
tissue name + oma Lipoma, osteoma, chondroma Benign tumor of liver: hepatoma Benign tumor of fat: lipoma
86
naming malignant tumors
Epithelial tissue: tissue name + carcinoma malignant tumor of liver - hepatocarcinoma Glandular tissue: tissue name + adenocarcinoma meschymal/connective tissue: tissue name + sarcoma Malignant tumor of fat - liposarcoma
87
Transudative edema
Increased hydrostatic pressure / low oncotic pressur: high in fluid, low in protein (heart failure, nephrotic syndrome, cirrhosis
88
Exudative edema
inflammation - high in fluid and protein
89
aldosterone
tells kidneys to secrete potassium and hold onto sodium

Pathophysiology 201 (23 decks)

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