Pathophysiology Exam 3

Front 1

What are the three goals of cancer?

Back 1

1. Curative

2. Controlling
(prevent metastasis)

3. Palliative
(reduce severity)

Front 2

Surgery

Back 2

Removal of the tumor

Try to clear margins of research
(want them to be negative)

Front 3

Radiation Therapy

Back 3

zap tumor with ionizing radiation to try to kill it

it produces free radicals that hopefully kill cancer cells

* FOCAL - directed beam

Front 4

What is brachy therapy?

Back 4

implanted radioactive seeds that release
radiation at the tumor site

Front 5

Chemotherapy

Back 5

- Toxic chemical substances target all rapidly diving cells

- Has serious side effects for the patient

- Tends to loose effect with time

- SYSTEMIC

Front 6

When do we use chemo?

Back 6

After the cancer has metastasized

Front 7

What does chemo also target in addition to CA cells?

Back 7

Hair
Skin
Mucus Membranes
Bone Marrow Cells

Front 8

Immunotherapy

Back 8

- Attempts to use immune system to fight tumor

- Disappoint results

Front 9

Examples of immunotherapy

Back 9

- Interferon or IL-2
(hyperactivates killer T cells)

- Monoclonal antibodies

- Vaccines

- Prophalactive Vaccines
(preventative)

Front 10

bone marrow & stem cell transplants

Back 10

use other people's marrow and/or
stem cells to help cure certain diseases

Front 11

Gene Therapy

Back 11

- Alteration of one's genetic material to
fight or prevent disease

- Fix mutations or trigger apoptosis

* Virus incorporates DNA into cells
(viral vectors)

Front 12

Antiangiogenesis Therapy

Back 12

target VEGF pathway

Front 13

Combination Therapy

Back 13

use two or more of the therapies

surgery and/or radiation first-followed by chemo

Front 14

Anterior Lobe of the Prostate

Back 14

fibrous and normally non-pathological in mature

stromal tissue

Front 15

Median Lobe of the Prostate

Back 15

- is famous for Bening Prostatic Hyperplasia

- lobe may undergo hyperplasia, resulting of obstruction
of the urethra and the visceral neck of the urinary bladder

Front 16

Bening Prostatic Hyperplasia
(BPH)

Back 16

NOT CANCER

doesn't turn into prostate cancer

Front 17

What are the signs and symptoms of BPH?

Back 17

urinary frequency

dysuria
(difficult urination)

infection due to retention

Front 18

What age does BPH start at?

Back 18

About 45 years old

Occurs in 80% of all men by
80-years-old

Front 19

How do we treat BPH?

Back 19

Use medications to shrink it

<10% of BPH require TURP

Front 20

Posterior Lobe of the Prostate Gland

Back 20

most predisposed to malignant transformation

highly mitotic tissue

carcinoma of the prostate

Front 21

Stats of Prostate Cancer

Back 21

- Most common in males
(besides skin cancer)

- Most cases in older males

- African Americans are affected more and its more aggressive

Front 22

Etiology of Prostate CA

Back 22

- genetics and testosterone play a role

- BRACA 1 & BRACA 2 are mutated in prostate cancer

Front 23

Risk factors of prostate ca

Back 23

Age
Race
Heredity

(avg. diagnosis in the 70's)

Front 24

Pathology of prostate CA?

Back 24

- 85% originates in the posterior lobe

- metastasizes through lymphatic vessels into adjacent structures:
rectum, bladder, pelvic structures,
vertebral column, liver, etc

Front 25

Where does prostate cancer usually metastasize to?

Back 25

Bones

Front 26

Diagnosis

Back 26

- Medical history

- Digital Rectal Exam (DRE)

- Confirmed by biopsy

- PSA (prostatic specific antigen) Test:
positive test for it

> 10 ng = abnormal
an elevated PSA is only cancerous 1/3 of the time

Front 27

Treatment of prostate CA

Back 27

- Depending on age of patient and characteristic of the tumor

- Watchful waiting is sometimes warranted

- Usually treated with a combination of radiation and hormone therapy
with some type of surgery to remove the cancerous tissue

(chemo isnt very effective)

Front 28

Staging of Prostate Cancer

Back 28

T1 = not palpable, detected by biopsy

T2 = tumor palpable
10 year survival rate as high as 80%

T3 = invasion outside capsule

T4 = indications of metastasis
10 yr survival rates from 50% - 0%
depending on specific case

Front 29

Screening

Back 29

- Need to offer men 50 or older a yearly digital exam and PSA test

- Medical community doesn't agree if we should screen or not

- older than 75, do NOT need prostate screening

Front 30

Cervical Cancer

Back 30

- Accounts for 20% of all malignant tumors in female reproductive tract

- 8th major cancer-related cause of death

- Incidence is declining due to early detection and prevention

Front 31

Etiology of Cervical CA

Back 31

- Considered an STD

- VIrtually all are caused by Human Papilloma Virus

- Passed through skin to skin contact

Front 32

Which strains cause 70% of all cervical cancers?

Back 32

Types 16 and 18

* most high risk do not lead to cancer

Front 33

What are the low risk strains of HPV?

Back 33

Types 6 and 11

cause genital warts in both sexes

Front 34

Risk Factors of Cervical CA?

Back 34

- Sexual intercourse at an early age

- multiple partners

- smoking
(2x the risk of cervical cancer)

- other STDs

Front 35

Signs and Symptoms

Back 35

Vaginal bleeding
Pain during sex
Depends on site

Front 36

What kind of carcinoma is it?

Back 36

Squamous cell

Front 37

Exocervix

Back 37

Projects into superior vagina and is covered with squamous epithelium

is more exposed to environment

Front 38

Endocervix

Back 38

Portion towards uterine body and is lined with columnar epithelium

Front 39

Transformation Zone

Back 39

* SITE OF MOST CERVICAL CANCER

- were 2 epithelia meet
- undegoing metaplasia

Front 40

Stages of Cervical Intraepithelial Neoplasia (CIN)

Back 40

CIN I:
mild dysplasia
low-grade lesion

CIN II:
moderate dysplasia
high-grade lesion

CIN III:
severe dysplasia in >2/3 of cells
carcinoma in situ (CIS)

Front 41

Stages of Cervical Carcinoma and Prognosis

Back 41

-

Front 42

Stage 0

Back 42

Same as CIS (CIN III)

- 5 year survival rate up to 100%

Front 43

Stage I

Back 43

- tumor confined to cervix
- 5 yr survival rate of 85%

Front 44

Stage II

Back 44

- invasion of adjacent structures
- not reaching pelvic wall of middle third of vagina

- 5 year survival rate of 75%

Front 45

Stage III

Back 45

- invasion to lower 1/3 of vagina or wall of pelvis

- 5 year survival of 35%

Front 46

Stage IV

Back 46

- Extension to bladder or rectum or structure beyond pelvis

- 5 year survival of 10%

Front 47

Diagnosis of Cervical CA

Back 47

Pap smear detects dysplatic cells in exo- and enocervix

Front 48

Treatment

Back 48

1. Cone biopsy/ LEEP procedure
- used to examine or remove a portion of both exo- and endocervical tissue

2. Hysterectomy
- removal of uterus is used in cases of advanced cancer
- sometimes take ovaries too

3. Pelvic Exenteration
- removal of all pelvic viscera is the last resort to reduce tumor burden
- can include radiation along with surgery

Front 49

Prevention

Back 49

Gardisil injections prevent 70% of known HPV cancers

1. Avoid HPV
- Gardasil
- Lifestyle
(monogomy, condoms, abstinence)

2. Prevent precancerous from becoming cancerous

Front 50

How effective is Gardasil?

Back 50

Protects 90% against low risk and 70% against high

Front 51

Hemostasis

Back 51

Normal hemostatic mechanism to maintain the fluidity of the blood in
the vascular system and yet allow the rapid formation
of a solid plug to close a vessel defect

Front 52

What are the two reasons it occurs?

Back 52

1. To prevent blood loss

2. After death

Front 53

What is a thrombus?

Back 53

- A solid mass of platelets, cells, and fibrin formed within an intact vessel

- can only occur during LIFE

Front 54

Morphology

Back 54

- Granular and friable mass
- Grainy and crumbly

- Lines of Zahn
dark red striations of red blood cells with
alternating lighter bands of platelets and fibrin

Front 55

Embolus

Back 55

Abnormal mass moving in the bloodstream

Front 56

Embolism

Back 56

sudden occlusion of an embolus

may be solid, liquid, or gas

Front 57

Factors that predispose thrombosis

Back 57

Virchow's Triad

1. Endothelial damage

2. Stasis or turbulence of flow/disturbance of flow

3. Hypercoagulation

Front 58

Endothelial Damage

Back 58

Disruption in the endothelial leads to exposure of subendothelial collage

- more common in arteries than veins
(because of the higher pressure)

- collagen starts clotting cascade

Front 59

Hemodynamic Stress

Back 59

Wear and tear

ex. hypertension

Front 60

Atherosclerosis

Back 60

deposition of fatty plaque in the arterial walls

Front 61

Trauma

Back 61

physical injury and damage to endothelium

ex. car accident crushes vertebrae and can occlude vertebral artery

Front 62

What causes endothelial damage in the veins?

Back 62

Inflammation
Iatrogenic
(caused by venous IV)
Trauma

Front 63

What are the characteristics of a post mortem clot?

Back 63

When blood slows, it activates clotting cascade
and becomes a gel-like mass

blood flow stops after death and activates coagulation sequence

Front 64

What is normal flow called

Back 64

Axial/Laminar

Front 65

What is abnormal blood flow?

Back 65

Turbulent

Front 66

Disruption of normal flow

Back 66

- allows for clotting factors to accumulate and
increases blood contact with endothelium

Front 67

Stasis of flow

Back 67

sluggish flow

leads to aterial and venous thrombosis

Front 68

Turbulent flow

Back 68

loss of normal, laminar flow

Front 69

Arterial Thrombosis

Back 69

Can occur in areas with atherosclerotic lesions
and over an infarcted region of ventricular wall

ex. heart attack
mural thrombosis
(occurs in wall over infarcted area)

Front 70

Venous Thrombosis
Thrombophelia
Deep Vein Thrombosis

Back 70

Favored by Virchow's Triad

Caused by:
- post op recovery
- bed rest
- congestive heart failure
- trauma
- surgery

Front 71

Large venous thrombosis can lead to?

Back 71

Edema, pain, cyanosis, and iscehmia

Front 72

Complications of DVT?

Back 72

Pulmonary Embolism

- massive PE can cause CV and or pulmonary collapse
- a significant cause of mortality

Front 73

Where do most DVTs arise from?

Back 73

Ileofemoral Vein

Front 74

What can cause turbulent flow?

Back 74

- plaque
(fatty deposition in wall)

- aneurysm

- bifurcations
(where vessel splits)

Front 75

Hypercoagulability States

Back 75

Imbalance between coagulation and anticoagulation states

a. older women
b. birth control pills
c. pregnancy
d. cancer
d. liver disease

Front 76

Thrombi in arteries tend to form because of what?
And thrombi in veins from due to what?

Back 76

Arteries - injury and turbulent flow

Veins - stasis

Front 77

Sequela of Thrombosis

Back 77

1. Resolution / Dissolution
2. Infarction
3. Embolus
4. Aneurysm

Front 78

1. Resolution / Dissolution

Back 78

* Best outcome

Via fibinolytic system

Rapid shrinkage or complete lysis

Front 79

2. Infarction

Back 79

Region of necrosis caused by ischemia

A thrombus can either narrow or occlude the lumen of a vessel
leading to ischemia/infarction

Front 80

Infarctions

Back 80

Occlusion of the coronary arteries = myocardial infarction

Occlusion of the cerebral arteries = cerebrovascular accident

Renal artery = renal infarction

Mesentary artery = mesentary infarction

Front 81

Infarction outcome depends on:

Back 81

1. Tolerance to hypoxia
2. Tissue vascularization
3. Rate of occlusion
4. Occlusion duration

Front 82

1. Tolerance to hypoxia

Back 82

- depends on how metabolically active it is
* brain lasts 3-4 mins
* heart lasts 30 mins - 1 hr
* smooth muscle can go days without blood

Front 83

2. Tissue vasculature

Back 83

- Anastomoses allow for an alternate route

Ex. circle of willis

Front 84

3. Rate of occlusion

Back 84

Slow occlusion allows for collateral circulation to develop
(develop by way of VEGF)

Atherosclerosis and thrombus are slow and have better outcomes

Front 85

4. Occlusion duration

Back 85

Length of ischemia

D2B (door to balloon): balloon angioplasty to open up vessel
* quicker is best!

Front 86

What is the D2B goal?

Back 86

Under 90 minutes

Front 87

Embolism

Back 87

The sudden occlusion of a traveling mass (embolus)

Usually a piece of thrombus or plaque

Front 88

Systemic Embolus

Back 88

- aortic valve thrombus could wedge in areas of high blood flow
ex. brain, kidneys, spleen

- bifurcation of carotid likely to lodge in brain

- just depends on chance where it will end up

Front 89

Venous Embolus

Back 89

- most likely to lodge in lungs
(b/c veins get bigger till heart, then lungs)

- vein draining GI tract likely to lodge in liver b/c of hepatic portal system

Front 90

What are the two ways we treat thromboemboli?

Back 90

1. Anticoagulants

2. Fibrinolytic Agents
(Thrombolytic)

Front 91

Anticoagulants

Back 91

"Blood Thinners"

- make blood less likely to clot

Ex. aspirin (makes platelets slippery)
cumadin

Front 92

Fibrinolytic Agents

Back 92

"Clot Busters"

- dissolve the clot

Ex. t-PA (Tissue Plasminogen Activator) dissolves fibrin
streptokinase

Front 93

Aneurysm

Back 93

- localized dilation of a blood vessel

Front 94

Where is the most common aneurysm?

Back 94

In the aorta

(has a lot of stress and high blood flow)

Front 95

Types of aneurysms

Back 95

1. Berry
- small, spherical dilation usually found in circle of willis

2. Fusiform
- entire circumference of vessel dilates

3. Dissecting
- layers of the vessel wall separate and fill with blood
- common in aorta because of high pressure
- chips away at tunica interna and separates it from interna media

Front 96

Pathogenesis / Etiology of Aneurysm

Back 96

- Congenital defect
- Trauma
- Infection
(monocytes and leukocytes damage normal tissue when cleaning up)
- Atherosclerosis
(most common)
- Hypertension

Front 97

Signs & Symptoms

Back 97

Asymptomatic

- sometimes can see a pulsating mass
- most are found by accident

Front 98

Sequela and Hemodynamic Effects

Back 98

T.C.R.

1. Thrombus formation
(due to turbulent blood flow)
2. Compression
(necrosis on tissue edges)
3. Rupture
(especially aorta)

Front 99

Treatment of Aneurysms

Back 99

- surgery (put in a graft)
- endovascular coiling
- clipping
- meds to prevent enlargement
(blood thinners, BP medicine for HTN)

Front 100

Systolic Blood Pressure

Back 100

The maximal aortic pressure following ejection

ventricles contracting

Front 101

Diastolic Blood Pressure

Back 101

the lowest pressure in the aorta just before ejection

ventricles relaxing

Front 102

Blood pressure is determined by what three things

Back 102

1. Cardiac Output
2. Total Peripheral Resistance
3. Blood Volume

Front 103

Cardiac Output

Back 103

CO = SV * HR

in mL/min

average 5 L/min at rest

Front 104

Cardiac output during exercise

Back 104

Increases during exercise

can increase up to 25 mL/min

Front 105

What is heart rate?

Back 105

How many times the heart beats in a minute

Front 106

What is stroke volume?

Back 106

The volume ejected each stroke (mL)

Front 107

How is cardiac output controlled?

Back 107

By the autonomic nervous system

- Cardiac center inputs to SA node

- sympathetic nervous system = increases HR

- parasympathetic nervous system = decreases HR

Front 108

Total Peripheral Resistance

Back 108

Factors that oppose blood

* Vasoconstriction:
decrease diameter = increase resistance = move blood to bigger arteries = increase blood pressue

* Vasodilation:
increase diameter = decreases resistance = decreases BP

* Viscosity:
thickness of blood

Front 109

How is TPR controlled?

Back 109

Autonomic Nervous System

Vasomotor Center:
sympathetic innervation of tunica media

Front 110

How does increased sympathetic stimulation affect TPR?

Back 110

vasocontricts

Front 111

How does decreased sympathetic stimulation affect TPR?

Back 111

Vasodilation of smooth muscle

Front 112

How does local control affect TPR?

Back 112

Release of vasoactive mediators

Ex. nitric oxide (vasodilator)

Front 113

Dehydration does what to the blood?

Back 113

Lowers the water (plasma) level in it and makes it more viscous

Front 114

what is blood volume?

Back 114

sum of blood in the cardiovascular system

* kidneys play a main role

* atrial natriuretic factor (ANF):
hormone produced in heart and released in response to increased stretch
- increases Na* secretion
(so therefore water loss)

blood volume decreases so blood pressure does too

Front 115

What is blood pressure controlled by?

Back 115

ANS : symp and para

Front 116

Sympathetic NS controls it by what kind of receptors?

Back 116

Postganglionic Receptors

(adrenergic NE)

* alpha and beta

Front 117

A1 receptors

Back 117

Found in tunica media

* Excitatory = vasoconstriction of GI vessels

Front 118

A2 receptors

Back 118

Found in GI tract of smooth muscle

* Inhibitory

Front 119

B1 receptors

Back 119

Found in heart

Binding of NE results in:
1. Increase in HR
2. Increased contractability of myocardium
3. Increase conductivity through conduction system

Front 120

B2 receptors

Back 120

Found in smooth muscle of bronchioles and
tunica media of some (coronary) vessels

* inhibitory = vasodilation and bronchodilation

Front 121

Baroreceptors

Back 121

Pressure sensitive receptors found in aortic arch and carotid arteries

Give input to the vasomotor and cardiac centers

Front 122

When we stand up...

Back 122

Activates baroreceptor reflex

Front 123

Chronotropic

Ionotrophic

Dromotrophic

Back 123

Chrono: HR

Iono: Contractability

Dromo: Conduction

Front 124

RAAS System

Back 124

BB

Front 125

What blood pressure designates HTN?

Back 125

greater than or equal to 140/90

Front 126

Classification

Back 126

Table

Front 127

Two types of hypertension

Back 127

1. Essential / Primary
2. Secondary

Front 128

Essential Hypertension

Back 128

Is present without evidence of other disease

No known cause

90% - 95% of HTN

Front 129

Secondary Hypertension

Back 129

Occurs with some other disorder such as heart or kidney disease

5% - 10% of HTN

Ex. Adrenal Gland Tumor:
too much epinephrine puts them in a false increase
in sympathetic NS

Front 130

Diagnosing Hypertension

Back 130

1. Systolic ≥ 140

2. Diastolic ≥ 90

3. At least two measurements averaged on separate occasions

4. Make sure patient has rested 5 minutes before taking it

5. No cigarette or caffeine within 30 minutes

6. Proper cuff size

Front 131

Risk Factors

Back 131

....

Front 132

Family History

Back 132

- Approximately doubles the risk of HTN

- Risk is more dependent on closeness of relative
(1st degree at an increased risk)

Front 133

Age

Back 133

Increases with age

Front 134

Race

Back 134

- more prevalent among african americans than whites
- tends to be more severe too
- tends to occur at an earlier age in African Americans
- it increases their risk of other CV diseases

Front 135

High Salt Intake

Back 135

- does not cause HTN in all individuals
- salt restriction doesn't lower HTN in all people

- mechanism is still being researched. heories include:
1. increased blood volume
2. increased sympathetic sensitivity

Front 136

Obesity

Back 136

1. Incidence of HTN in obese 20-30 year olds is 2x that of normotensive

2. Fat distribution may be an indicator of HTN
- waist hip ratio
- waist circumference
* men >40 in women > 35 in

3. Poor dietary habits
- high Na+, cholesterol

Front 137

Excess Alcohol Consumption

Back 137

> two drink per day leads to an increased risk

- reasons remain unclear

Front 138

Intake of K, Ca, and Mg

Back 138

still being researched

Front 139

Diabetes Mellitus

Back 139

increased insulin resistance

Front 140

Emotional Stress

Back 140

1. Increase sympathetic outflow
2. Increase epinephrine release
3. Ateriole smooth muscle hypertophy

Front 141

Use of oral contraceptives

Back 141

1. Cause mild BP increase in many women, overt HTN in 5%

2. HTN disappears when discontinue use (in about 6 months)

3. Smoking increases risk of CV complications

Front 142

Signs and Symptoms of HTN

Back 142

Most frequently asymptomatic

Also:
headache
nocturia (urinating @ night)
epistaxis (nose bleeds)
tinnitus (ringing in the ears)
vertigo

Front 143

Effects / Sequela

Back 143

TARGET ORGAN DAMAGE

1. Weakens/damages heart and blood vessels

2. Increases myocardial oxygen requirement

3. Initiates/accelerates rate of atherosclerosis

4. Increases risk of aneurysms

5. Kidney failure

6. Retinal damage

7. CNS damage

Front 144

What is the treatment goal?

Back 144

BP <140/90

In those with diabetes we want it under 130/80

Front 145

Nonpharmacological Treatments

Back 145

1. Decrease weight
2. Decrease sodium intake
3. Exercise
4. Decrease alcohol intake
5. Stop smoking
6. DASH diet
(dietary approach to stop hypertension)
- increase fruits/veggies
- low fat diet

Front 146

Pharmacologic Treatments

Back 146

...

Front 147

Diuretics

Back 147

Increase urine volume

- decrease blood volume
- decrease CO
- decrease TPR

Front 148

Beta Blockers

Back 148

decrease catecholamine stimulation to decrease cardiac
rate and kidney filtration and release of renin

Block B1 receptors
Negative Chronotrope

Front 149

Alpha Blockers

Back 149

Reduce sympathetic input to smooth muscle

Blocks A1 receptors
Vasodilates vessels

Front 150

Vasodilator Drugs

Back 150

decrease TPR and afterload

Front 151

ACE Inhibitors

Back 151

Prevent conversion of AG I to AG II

Relaxes blood vessels and lowers BP

Less AG II means less aldosterone release, which means less Na+ reabsorbed
ultimately leading to a decrease in extracellular fluid volume

Front 152

What a side effect of ACE Inhibitors

Back 152

Coughing

Front 153

Calcium Channel Blocker

Back 153

Decreases Ca++ entry into vascular smooth muscle causing arterioles to
dilate and reduce peripheral resistance

(negative ionotrope)

Front 154

A II Receptor Blocker

Back 154

no cough!

Front 155

Or a combination of the two above

Back 155

--

Front 156

Treatments of Cancer

Back 156

...