SumExam3 Flashcards
1
Q
What is a neoplasm?
A
New growth or tumor
2
Q
What are the characteristics of a benign tumor?
A
Slow growing and in a local area/not invasive
Necrosis is rare, prognosis is good and rare regrowth if treated.
3
Q
What are the characteristics of a malignant tumor?
A
Rapid growth and invades other tissue and metastasizes.
Noticeably not normal tissue, more common necrosis and regrowth after treatment
4
Q
What are the 6 characteristics of cancer cells?
A
RAISEE Resisting cell death Activating invasion and metastasizing Inducing angiogenesis Sustaining proliferative signals Evading growth suppressors Enabling immortality
5
Q
What are some lifestyle factors that can impact the growth of cancer?
A
Tobacco use Nutrition Obesity Sun exposure (skin cancer) Sexual exposure to HPV (cervical cancer)
6
Q
What two things to carcinogens do?
A
Promote tumor growth
Initiate tumor growth
7
Q
What are carcinogens and what can they do?
A
potential cancer-causing agent
Gain of function mutations- genes to be overactive or loss of function.
8
Q
What is a proto-oncogene?
A
The name of genes that have been altered by carcinogen.
Gain of function: become overactive
9
Q
What is an Oncogene?
A
Proto-oncogene in its mutant overactive form
10
Q
What is a tumor suppressor gene?
A
Gene that Inhibits cell proliferation
11
Q
When a tumor suppressor gene is altered by a carcinogen, what type of gain of function happens?
A
Underactive mutation
12
Q
How to proto-oncogenes get activated into an oncogene?
A
The are impacted by a carcinogen which causes mutations and growth, it is then a oncogene once it is full cancer
13
Q
What is an example of an inherited defective copy of tumor suppressor gene
A
BRCA1- breast cancer gene
14
Q
What does Epigenetic process mean?
A
“Silences” the gene
Does not require a mutation
Changes how the gene is read.
15
Q
What are the three stages of carcinogenesis?
A
Initiation
Promotion
Progression
16
Q
During the Initiation stage of carcinogenesis, what happens?
A
event for genetic mutation- multiple mutations needed and certain amounts need to happen in order to be malignant- proliferation starts**
17
Q
During the Promotion stage of carcinogenesis, what happens?
A
Cancer cells become immortal by producing telomerase- repairs the ends of the chromosomes in replication
18
Q
What types of environmental factors can encourage proliferation?
A
environment of body- hormonal, infection, nutrition can encourage proliferation.
19
Q
During the Progression stage of carcinogenesis, what happens?
A
mutant proliferative cells are becoming tumors, invading
20
Q
What are the two ways cancer cells move within the body to start metastasizing?
A
blood stream or to lymph system
21
Q
What is staging of cancer?
A
Staging-describes how big or if it has metastasized
22
Q
What is grading of cancer?
A
grading- how malignant- higher number the worse it is
23
Q
What are the clinical manifestations or warning signs of cancer?
A
Change in bowel or bladder habits A sore that does not heal Unusual bleeding or discharge Thickening or lump in breast or elsewhere Indigestion or difficulty swallowing Obvious change in wart or mole Nagging cough or hoarseness Other:Pain Cachexia Immune system deficits Bone marrow suppression
24
Q
Besides early detection, What are treatments for cancer?
A
Surgery
Radiation therapy
Drug therapy/chemotherapy
25
```
Lung Cancer:
Etiology
Clinical Manifestations
Tests
Treatment
```
Smoking
Hoarse, cough, sputum
X-ray, CAT scan, biopsy
Chemo, radiation, surgery
26
```
Breast Cancer:
Etiology
Clinical manifestations
Tests
Treatment
```
Hormonal, later in life menopause, no pregnancies, possible diet, family history, older age
Lump, tumor, discharge, skin changes
Mammogram, biopsy
Surgery, radiation, chemo
27
In terms of the growth fraction, when can chemo be the most damaging?
Higher the growth fraction
28
What are the three ways Alkylating Agents work?
1- attachment- DNA fragmenting
2- Cross-bridge = can’t be separated= no copying
3- miss-pair= mutation= no continuing
29
Cyclophosphamide (Cytoxan)
Alkylating Drug
Backbone of many chemo agents
**Prodrug**---is their liver working?
Not harmful to tissue
30
Cyclophosphamide Toxicity
Dose-limiting toxicity: Bone marrow suppression
Hemorrhagic cystitis: hydration**-protective agent called Mesna
Other: Nausea, Vomiting, Alopecia
Decresed RBC, WBC, platelets – can affect the dose pt can get
31
How does Cisplatin work, how is it administered?
Cross-linking
| IV
32
What are some AV/ signs of toxicity of Cisplatin?
Highly emetogenic: N/V begin about 1 HR- several days *N/V pre-treatment
Toxicity:
Peripheral neuropathy, mild-moderate bone marrow suppression, kidney damage, ototoxicity
33
What can you give with Methotrexate to assist?
Leucovorin
34
Methotrexate (MTX)
Folic acid pathway- interrupts the Dihyfrofolate Reductase
We need folic acid for DNA/RNA
Methotrexate – ectopic pregnancies, autoimmune
Bigger doses of methotrexate because some cancer cells do not want the drug in them= higher toxicity
Can be given PO, IM, IV, intrathecally
Renally eliminated
35
Methotrexate (MTX) toxicity
```
Dose limiting
Bone marrow suppression**
Pulmonary infiltrates & fibrosis**
Oral and GI ulcers**: intestinal perforation & hemorrhagic enteritis
Kidney damage with high doses
N/V shortly after administration
```
36
Fluorouracil (5FU)
```
Inhibits thymidylate synthetase – blocks production of thymidylate
Shows some S-phase specificity
Administered IV as continuous infusion
Enters CNS well**
Rapidly metabolized by liver
```
37
Fluorouracil (5FU) toxicity
Dose limiting: bone marrow suppression (neutropenia) oral & GI ulceration
Other: alopecia, hyperpigmentation, neurologic defecits
Hand-and-foot syndrome****
Tingling, burning, redness, flaking, swelling, blistering of palms and soles
38
Doxorubicin
Distorts structure and it can’t be used
Causes Apoptosis
IV infusion, no crossing blood brain barrier
Metabolized by liver
39
Doxorubicin toxicity
Acute: nausea & vomiting; red color to urine and sweat (harmless)**
Dose limiting = bone marrow suppression**
Alopecia, stomatitis, anorexia, conjunctivitis, pigmentation in extremeties
40
Doxorubicin Cardiotoxicity
Acute: Dysrhythmia, ECG changes, within minutes of dosing, Usually transient (lasting no more than 2 weeks)
Delayed: Months to years after therapy
Manifests as heart failure secondary to diffuse cardiomyopathy (myofibril degeneration)
Usually unresponsive to treatment
41
Why is dosing so important with Doxorubicin?
To prevent the cardiotoxicity, it is the CUMULATIVE lifetime amount
* normal treatment for heart failure will not work
* will probably need transplant
42
Vincristine
```
Blocks mitosis during metaphase: disrupts assembly of the microtubules
IV only
Poor penetration into CNS
Hepatic metabolism
Bone marrow sparing**
```
43
What is the biggest concern of toxicity with vincristine?
Peripheral neuropathy: major dose limiting effect
44
Paclitaxel
inhibits cell division and produces apoptosis
Used in combination
IV infusion
45
What are the two formulations of Paclitaxel?
Older: Taxol: contains solvent (Cremaphor & alcohol) that can trigger severe hypersensitivity reactions
Newer: Abraxane: bound to nanoparticles of albumin – no solvent used
46
Paclitaxel Toxicity
Severe hypersensitivity reaction: older formulation
Bone marrow suppression (neuropenia); peripheral neuropathy with repeated infusions, bradycardia
Muscle and joint pain
Alopecia, mild GI reactions (nausea, vomiting, diarrhea and mucositis)
47
Tamoxifen
SERM: Blocks estrogen receptors in some soft tissues and activates in other tissues
Blocks in breast cells
Activation in other areas: increased bone mineral density, reduction of LDL, elevation of hDL
Readily absorbed orally
Drug interactions (watch SSRIs)
48
Adverse effects of Tomoxifen
Hot flashes, fluid retention, vaginal discharge, nausea, vomiting, menstrual irregularities
Increased risk of thromboembolic events
Endometrial cancer: estrogen agonist at receptors in uterus causing proliferation of endometrial tissue
49
What are the 7 functions of the kidneys? (AWETBED)
```
A cid base balance
W ater balance
E lectrolye balance
T oxin removal
B lood pressure control
E rythropoietin making
D vitamin metabolism
```
50
What are some defense mechanisms that the kidneys have for infection?
Urination, mucous, prostate, acidic environment, anatomy, inflammatory response
51
What are some risk factors for UTI?
Anatomic alteration- born or surgery, declining immune function, comorbidity (diabetes), Women more at risk- shorter urethra, hormonal- pregnancy-reflux more likely, or retention
52
What is pyelonephritis//how does it happen?
| Tests//labs?
Inflammation of the kidney- Result of an ascending UTI- moving up- (can move through blood )
Bacteria gets to kidneys and bacteria binds to eoithelial cells- inflammation, bacteria toxins and inflammatory mediators cause kidney damage
Testing: symptoms and uranalysis , elevated WBC
Treatment is antibiotics
53
What is AKI and what are some risk factors?
Sudden reduction in renal function.
| Risk: preexisting kidney problems, cardiovascular disease (comorbidities),hypertension, diabetes, heart failure, cancer
54
What can happen a a result of AKI?
As a result- disruptions in fluids and electrolytes, acid base balance, serum creatinine increase**, decreased glomular filtration rate
55
What is the RIFLE classification of AKI?
```
Risk
Injury
Function
Loss
End-stage kidney disease
```
56
What is the best lab test that indicates kidney failure?
Creatinine levels
57
What are the normal creatinine levels?
0.5-1.2
58
What are the three types of acute kidney injury?
prerenal
intrarenal
postrenal
59
Prerenal kidney injury
something else is affecting the kidney- such as cardiovascular- circulation problem
Most common: hypoperfusion
60
Intrarenal kidney injury
Disorders involving kidneys themselves
| Acute tubular necrosis (ATN) caused by ischemia: Most common cause
61
Postrenal kidney injury
Normally causes by an obstruction
benign prostatic hypertrophy (BPH), retention or backflow
*rare
62
What are the 3 phases of AKI?
Initiation/ prodromal
Maintenance/ oligurea
Recovery/ postoligurea
63
Initiation/Prodromal Phase
Injury to kidneys
Creatinine & BUN increasing
Urine output decreasing
Variable duration
64
Maintenance/Oliguric Phase
Kidneys are not functioning very well
Creatinine & BUN increased - metabolic acidosis can occur
Urine output low or none
Will last anywhere from 2 weeks to 8 weeks
65
Recovery/postoliguric phase
Kidneys are starting to function better- full recovery not always possible
Electrolyte imbalances may happen due to diuresis
Can last as long as a year for recovery
66
What are some treatment options for AKI?
```
Correct fluid and electrolyte disturbances.
Manage blood pressure.
Prevent and treat infections.
Maintain nutrition.
Remember certain drugs can be toxic
```
67
CKD- Chronic kidney disease
Greater than 3 months- irreversible loss of functional nephrons – death of cells
Progressive
75% of nephrons being damaged is irreversible – remaining nephrons will try to compensate- enlargement and working harder- which causes more damage through overworking
Shrinking
End story is dialysis, transplant or death
68
CKD risk factors?
```
Diabetes
Hypertension
Recurrent pyelonephritis
Glomerulonephritis
Polycystic kidney disease
Family history of CKD
History of exposure to toxins
Age over 65
Ethnicity
```
69
What are the 3 stages of CKD and amount of nephron loss?
Decreased renal reserve- 75%
Renal insufficiency- 75%-90%
End-Stage renal disease- over 90%
70
During decreased renal reserve, what types of signs and symptoms will you see?
Many times you will not see any S&S
71
During renal insufficiency, What signs and symptoms will you see?
Urination- increased but not concentrated
| Lab value changes- BUN creatinine- diet & medications
72
During end-stage renal failure, what signs ans symptoms will you see?
Dialysis –not cleaning of blood- increased nitrogen products in blood(BUN, Cr) Azotemia. Uremia (symptomatic azotemia)
73
What is azotemia?
an increase in blood creatinine and BUN
74
What are clinical manifestations of CKD?
```
Uremic Syndrome-azotemia
Calcium, phosphate & bone
Acid base- Protein, carbohydrate and fats metabolism
Cardiovascular//Pulmonary
Hematological
Immune
Neurological
Gastrointestinal
Endocrine
Integumentary
```
75
What are some treatments for CKD?
Vit D levels supp
Not too much protein but need the calories
Bowel routine
76
What are the three levels of immunosuppression and a transplant?
Induction- knocking everything out so that body won’t reject
Maintenance – prolong life of new organ
Rescue- treat rejection – immunosuppression
77
What drugs are the backbone to anit-rejection therapy?
Calcineurin Inhibitors
78
Cyclosporine
IV//PO- monitor through blood serum levels
3 trand names- NOT interchangeable
Must first bind to cyclophilin in order to act
Can also be used for other autoimmune: Rheumatological diseases, psoriasis
**drug interactions- grapefruit juice
79
AE of cyclosporine
```
Nephrotoxicity – generally dose dependent
Avoid using with NSAIDS
Hypertension
Hyperlipidemia
Gingival hyperplasia
Facial hair growth
Infection
Tremor
Hepatotoxicity
Lymphomas
```
80
Tacrolimus (FK506)
IV//Oral//topical- must first bind to an intracellular protein (FKBP-12) to inhibit calcineurin
**drug interactions AND avoid NSAIDS
81
AE of tacrolimus
```
Nephrotoxicity
Neurotoxicity: headache, tremor, insomnia, demylinating polyneuropathy
GI: diarrhea, nausea, vomiting
Hyperglycemia
Hypertension
Infection
Lymphoma
```
82
Mycophenolate
IV/Oral- metabolized in liver- rapidly converted in body to mycophenolic acid (MPA)
*Cell cycle specific *
83
AE of mycophenolate
GI symptoms: diarrhea, vomiting, abdominal pain
***Bone marrow suppression: leukopenia, thrombocytopenia, anemia
Infection
Lymphomas
Teratogenic
84
When giving myocophenolate, what interactions would you want to be aware of?
Decreased absorption when given with magnesium and aluminum products
Decreased absorption when given with cholestyramine
85
What are Glucocorticoids responsible for?
CHO, protein, fat metabolism
Effects on CV system, skeletal muscles
Stress response
86
What are Mineralocorticoids responsible for?
Controls electrolyte and water balances
| Aldosterone
87
How do Glucocorticoid Interrupt inflammatory process ?
Inhibit synthesis of mediators: prostaglandins, leukotrienes, histamine
Suppress infiltration of phagocytes
Suppress proliferation of lymphocytes
88
What are the AE of glucocorticoids?
```
Adrenal insufficiency
****Osteoporosis: suppresses bone formation by osteoclasts- clacium supplements
Infection
Glucose intolerance
Myopathy
Fluid & electrolyte abnormalities
Growth retardation
Psychologic disturbances
Cataracts and glaucoma
Peptic ulcer disease
```
89
What drug interactions and precautions do you need to take for Prednisone and Methylprednisolone?
NSAIDs
| Anticoagulations
90
What type of teaching points would you want to emphasize to a patient taking Prednisone or Methylprednisolone?
```
How to taper
Calcium supp
Diabetes and glucose
Watch tongue- rinse
WITH FOOD
Morning- insomnia
DO NOT stop abruptly
```
91
What are signs and symptoms of pulmonary disease?
Dyspnea, Cough
Altered breathing patterns, Hyper//Hypoventilation
Abnormal sputum (incl hemoptysis)
Cyanosis. Chest pain, Clubbing
92
What is Obstructive Pulmonary Disorders described as?
Resistance to breathing
| can be inside airway or outside
93
What are the two types of COPD?
Chronic bronchitis
| Emphysema
94
Why can it be hard to tell the difference between Chronic bronchitis and Emphysema?
Can have features of both. Many times symptoms are similar
95
How is COPD different for women?
May be more severe for women- anatomical- smaller lungs
Dose related- women have more concentration while smoking than a man because of the smaller lungs
Hormonal differences may have a role in how COPD is manifested in women
96
If someone is called the blue bloater, what form of COPD would they have?
Chronic bronchitis
97
What is chronic bronchitis classified by?
Chronic inflammation and swelling of the bronchial mucosa resulting in scarring
Hyperplasia of bronchial mucous gland/goblet cells
Increased bronchial wall thickness
Pulmonary hypertension
Destruction of bronchial walls
98
What kinds of clinical manifestations would you see with someone who has chronic bronchitis?
```
Productive cough lasting more than 3 months, often in the morning
Often times overweight and round
SOB on exertion
Edema- late sign
Cyanosis- late sign
```
99
What are the diagnostic tools used for chronic bronchitis?
Chest x-ray- abnormalities
Pulmonary function tests
Arterial blood gas (ABG)
ECG
CBC- elevated RBC- trying to provide more sources for oxygen to be carried
Potential evidence of right ventricular hypertrophy- & higher right for arrhythmias – a fib
100
What are the treatments for chronic bronchitis?
Block or slow down progression
Want them to be able to be active in their ADLs
Meds- beta agonist inhaled- albuterol- bronchodilators – anticholinergics- cough suppressants for sleep aide- antibiotics for infections – inhaled steroids
O2- low dose –expected levels are going to be lower
Encourage them to stop smoking- irritants
Rest- hydration, nutrition, preventing infections
101
What is Emphysema characterized by?
Destruction and enlargement of alveoli
Loss of surface area for gas exchange- air trapping & bullae formation
Release of proteolytic enzymes- alveolar damage
Loss of alveolar walls leads to reduction in pulmonary capillary bed
Loss of elastic tissue in lung
102
If someone is called the pink puffer, what type of COPD would they have?
Emphysema-type A
103
What is something about the progression of emphysema that is important?
Damage is irreversible – majority of people will often have chronic bronchitis
104
What type of clinical manifestations would you see in someone who has emphysema?
- Progressive dyspnea with exertion
- Thin- excess calories burned trying to breath or eat
- Use of accessory muscles- pursed lip breathing – not often coughing or a very low amount, lean forward to breathe
- Clubbing
- Barrel chest- changes in posterior to lateral diameter
105
What type of diagnostic tools are used for emphysema?
```
Pulmonary function tests (PFTs)*
Chest x-ray
ECG
ABG
Patient history
Common physical findings
```
106
What are the treatments for emphysema?
Block or slow down progression
Want them to be able to be active in their ADLs
Meds- beta agonist inhaled- albuterol- bronchodilators – anticholinergics- cough suppressants for sleep aide- antibiotics for infections – inhaled steroids
O2- low dose –expected levels are going to be lower
Encourage them to stop smoking- irritants
Rest- hydration, nutrition, preventing infections
107
What are Restrictive Pulmonary Disorders a result of?
Decreased Lung Expansion
| Alterations in lung parenchyma, pleura, chest wall, or neuromuscular function
108
What is a pneumothorax?
Accumulation of air in the pleural space
109
What are the 4types of pneumothorax?
1-Primary- spontaneous – tends to happen in tall thin men age 20-40 yrs with no underlying disease
2-Secondary- next to another preexisting pulmonary disease
3-Catamenial- associated with mensuration and endometriosis
4-Tension- trauma, penetration or not- acute 911 very dangerous
110
How is a primary pneumothorax caused?
Bleb- air between lung and plura -If one ruptures you get collapse typically in apex of lung
111
How is a secondary pneumothorax caused?
bleb, cyst – rupture
112
How is a tension pneumothorax caused?
build up of air under pressure- air continues to go in and it builds- collapse – can cause tracheal deviation
113
What is an open pneumothroax and how is it caused?
air in from outside – displacing lung tissue
114
What types of clinical manifestations would you see with pneumothorax?
Small ones may not be noticeable
Tachycardia, Diminished or absent breath sounds
Chest pain
Dyspnea
Large/ tension= 911
Tachycardia, low BP, tracheal shift, neck vein distention, subQ emphysema
115
What is subcutaneous emphysema?
air under skin, many times on face-crepitation on palpation
116
How do you diagnose a pneumothorax?
ABG
ECG
Chest x-ray
Acute respiratory alkalosis decreased PO2
117
What are the treatments for pneumothroax?
Monitor if it’s small
Larger- chest tube- O2
Decompression
Chemical pleurodesis- makes pleura adhere – recurrent spontaneous
Thoracotomy- laser or stable to adhere or obliterate blebs
118
What is a pleural effusion and what are the 5 types?
Collection of fluid or puss in cavity
Transudates- heart failure- edematous states
Exudates- malignant cancer- infections, pancreatic disease
Emopyema- infection
Hemothorax- blood- chest trauma, or hemmorrahge
Chylothorax- lymph fluid
119
Why does fluid accumulate so much with Pleural Effusion?
there is either too much formation, or there is no removal
120
What are the clinical manifestations of pleural effusion?
Cause and size
May not have symptoms- less than 300 mLs
Dyspnea, chest pain- sharp with inspiration
Cough, Absence of breath sounds, deviation is large
121
What diagnostic tools are used for pleural effusion?
Chest x-ray
Thoracentesis
CT or ultrasonographic tests
122
What is the treatment for pleural effusion?
Directed at underlying cause
| Alleviate symptoms
123
what is Pneumonia and how is it caused?
Definition: Inflammatory reaction in the alveoli and interstitium caused by an infectious agent
Causes: aspiration, inhalation, contamination
124
What are the classifications of Pneumonia?
```
Community acquired
Hospital acquired
Bacterial
Atypical
Viral
```
125
What populations are at risk for pneumonia?
```
Elderly
Those with a diminished gag reflex
Seriously ill
Hospitalized patients
Hypoxic patients
Immune-compromised patients
```
126
What happens inside the body during pneumonia?
Normal defense mechanisms compromised
Organisms enter, multiply, trigger inflammation
Alveolar spaces fill with exudate
127
What are the clinical manifestations of pneumonia?
Fever, chills, cough with sputum, malaise – breath sounds
| Viral symptoms may be more subtle
128
What diagnostic tools are used for pneumonia?
Chest x-ray
Sputum C&S
Labs
129
What are our 2 short acting pulmonary drugs?
Albuterol and Ipratroprium
130
What are our 2 long acting pulmonary drugs?
Salmeterol and Tiotropium
131
Which two drugs are Muscarinic Antagonists//anticholinergic ?
Ipratroprium and tiotropium
132
What two drugs are beta agonists?
Albuterol and salmeterol
133
What do Corticosteroids do to inflammatory cells?
Decrease apotosis, cytokines, machrophages and dendritic cells
134
What do Corticosteroids do to structural cells?
decreases cytokines and mediators, leaks, mucous secreations but increases beta 2 receptors
135
What Inhaled Corticosteroids is the mainstay for asthma? and why?
Fluticasone
Minimal systemic absorption
Available as MDI and nebulization
136
What are the most common AE of fluticasone?
Oropharyngeal candidiasis
Dysphonia
Can promote bone loss
137
What is albuterol used for?
Immediate: short-acting
| Used for relieving acute bronchospasm & prevention of exercise induced bronchospasm (EIB)
138
What are the AE of albuterol?
tachycardia, tremor, hypokalemia
139
How long do the effects of albuterol last?
lasts about 30 – 60 minutes
140
What is Ipratropium used for? What is the onset and how long does it last?
Used to relieve bronchospasm
| 30 seconds and may last for 6 hours
141
What are the AE of Ipratropium?
minimal systemic effects
| Dry mouth, pharyngeal irritation
142
Mnemonic for COPD
```
Lack of energy
Unable to do activity- SOB
Nutrition poor- breathing//calories
Gases abnormal
Dry productive cough
Accessory muscles use- abnormal lung sounds
Modification of skin color
Anteriorposterior diameter increase
Gets in tripod position for easier breathing
Extreme dyspnea
```
