Patho Exam 3 Flashcards

1
Q

Normal values for HR

Increase/decrease with activity?

A

60-100

INCREASES with activity (b/c increasing work load)

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2
Q

Normal values for BP

Increase/decrease with activity?

A

<90/60 for low BP)

BP should go UP with increased work load

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3
Q

Normal values for RR

Increase/decrease with activity?

A

12-20 (some say 12-18)

Should INCREASE with activity (generally, you take deeper breaths first, then increase RR)

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4
Q

Normal values for SpO2

Increase/decrease with activity?

A

98-100
*O2 drops as you age. By 90+ you might see a “normal” value <90
INCREASES with activity (if it has room to do so; otherwise if normal, will stay normal unless you have a respiratory disorder)

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5
Q

Cardiac output = __ x ___. Normal cardiac output = ___

A
CO = SV x HR
Normal = 4-8 L/min
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6
Q

___ is the amount of blood coming out to the [right/left] ventricle every time it contracts.

This is the difference between the end [diastolic/systolic] minus the end [systolic/diastolic] volume. This is about what percentage of the blood in that ventricle? What percentage remains after each contraction?

A

STROKE VOLUME = amt of blood coming from LEFT ventricle each contraction.

Difference between the end DIASTOLIC (bigger) and end SYSTOLIC volume (smaller). 55-70% of blood is pumped out each time, so 30-40% sticks around in LV!

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7
Q

What factors contribute to Stroke Volume?

A

Contractility
Preload
Afterload

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8
Q

Describe contractility. When might it be weird?

A

Contractility = how well/the amount the LV can contract

  • Abnormal arrhythmia can cause the ventricle to depolarize at a different rate and contract abnormally
  • Frank Sterling relationship comes into play here
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9
Q

Describe preload. Why might it be low?

A

Preload = how much blood volume RETURNS to the LV before it contracts. Think of it as venous return (how much blood is getting back from the periphery during diastole right before systole). End diastolic volume

Might be low:

  • Dysfunctional valves in peripheral veins –> blood pooling
  • Low blood volume (b/c dehydrated, excess blood loss, etc)
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10
Q

Describe afterload.

A

Afterload = pressure in the aorta that the LV has to overcome to get blood out of the LV, into the aorta, and to the periphery.

Harder to get blood out if you have aortic stenosis (stiff and narrowed), or if aortic valve is a little broken/small

RESISTANCE TO FLOW

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11
Q

What factors regulate heart rate?

A

Intrinsic rate (from different nodes in heart, generally SA node)

Autonomic Regulation

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12
Q

__ is the inability for heart rate to increase in response to increased activity and/or inability to achieve 85% of HR max.

A

CHRONOTROPIC INCOMPETENCE

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13
Q

Chronotropic incompetence is associated with [right/left] [ventricle/atrium] dysfunction, ___, and increased ___. Other potential associations include… (8)

A

Chronotropic incompetence is associated with LEFT VENTRICLE dysfunction, myocardial ischemia, and increased mortality

OTHERS:

  • Older age
  • Presence of CAD
  • Smoking
  • Exercise intolerance
  • LV dilation
  • Ischemia
  • SA or AV node dysfunction
  • Issue with modulating autonomic tone
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14
Q

___ describes a sustained HR increase of greater than or equal to 30 bmp within 10 minutes of standing or head-up tilt without orthostatic hypotension. Who do we see this in? Symptoms include __ and ___. Etiology is unknown, but it’s associated with ___, __, __, and/or limited/restricted ___.

A

POTS: POSTURAL TACHYCARDIA SYNDROME describes a sustained HR increase of greater than or equal to 30 bmp within 10 minutes of standing or head-up tilt without orthostatic hypotension.

COMMON IN TEENAGERS (in adolescents 12-19yo, >40bpm required). MORE COMMON IN WOMEN

Symptoms include LIGHTHEADEDNESS and VISUAL BLURRING. Etiology is unknown, but it’s associated with DECONDITIONING, RECENT VIRAL ILLNESS, CHRONIC FATIGUE, LIMITED/RESTRICTED AUTONOMIC NEUROPATHY

*A general aerobic conditioning program helps!

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15
Q

HR Recovery describes a [rapid/delayed] decrease in HR (</= __bpm) during the first minute post activity.

A

HR recovery = DELAYED decrease in HR ( increased mortality. </=12bpm

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16
Q

Abnormal HR responses may be associated with…(5)

A
  • Medications
    Eg. beta blockers (HR increase with workload is MUCH Smaller % than without beta blocker)
    Eg. Ca2+ channel blocker (reduces resting HR, but HR increases at normal proportion with activity)
  • Heart transplant
    Vagus n is severed so you lack parasympathetic inhibition of HR, so resting HR is higher. These pts need longer to respond to exercise b/c they rely on hormonal response to increase HR and let body respond, rather than normal sympathetic response

-Autonomic dysfunction
Eg diabetics

  • Ischemia
    E.g blockage to R coronary artery that supplies AV or SA node –> abnormal HR
  • Mechanical support
    Devices takeover heart workload –>abnormal HR response)
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17
Q

A [ventricular/atrial] arrhythmia is predictive of mortality or diagnostic for CAD

A

VENTRICULAR

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18
Q

Ventricular arrhythmias:
- Increased ventricular ectopy [implies/does not necessarily mean] ischemic dz.

  • Increased ventricular ectopy during [activity/ recovery] predicts mortality.
  • Runs of ventricular [bradycardia/ tachycardia] are associated with CAD/ischemia
A
  • Increased ventricular ectopy DOES NOT NECESSARILY MEAN ischemic dz.
  • Increased ventricular ectopy during RECOVERY predicts mortality.
  • Runs of ventricular TACHYCARDIA are associated with CAD/ischemia
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19
Q

What is the Frank-Starling Relationship?

A

Describes the relationship and “sweet spot” between ventricular end diastolic volume (think optimal sarcomere length) and stroke volume (y axis)

  • With a way stretched or way contracted ventricle, it’s very hard to get a contraction. Sweet spot gives an optimum length-tension relationship and ventricle can contract.
  • Stroke volume can change based on extra volume (eg heart failure) or not enough volume (e.g dehydration, bleeding post trauma) and can affect length-tension relationship in heart contractions
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20
Q

In a normal BP response to activity, systolic should [go up/go down/ stay same/ depends]. If changes, how much?

Diastolic should [go up/go down/ stay same/ depends]

A

Systolic should GO UP ~10 mmHg per MET (metabolic equivalent) of exercise.
(Walking 2mph = ~2 METS)

Diastolic can stay same, go up or go down - all normal!

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21
Q

If you increase workload, what would be an ABNORMAL BP response to activity? Why is this bad?

A

Abnormal = increase workload and see a DROP in systolic

Bad because you’re not maintaining cardiac output. The workload is too great for that pt for somer reason.

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22
Q

Drop in systolic BP is associated with ___ and __. It identifies those at risk for __

A

Drop in systolic BP associated with severe CAD and ischemic LV dysfunction. It identifies those at risk for VENTRICULAR FIBRILLATION

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23
Q

Describe the normal response to standing

A

1) 500-1000 mL blood pooling in legs
2) DECREASED venous return to <3
3) Decreased CO and BP
4) Decreased arterial baroreceptor response and INCREASED sympathetic activity
5) Increased venous return, PVR, CO
6) Limits fall in BP (~5-10 mmHG SBP, 5-10 mmHG SBP), and INCREASEs in HR (10-25 bpm)

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24
Q

Orthostasis defines a change in BP from __ to ___. Systolic BP drops __ mmHg, and Diasotlic BP drops __ mmHg.

A

Orthostasis: change in BP with postion change from SUPINE to STANDING

Systolic drops >= 20mmHg
Diastolic drops >= 10mmHg
Within 3 mins of standing or at last 60 on tilt table

Confounded by:

  • food inestion
  • time of day
  • state of hydration
  • ambient temperature
  • recent recumbency
  • postural deconditioning
  • hypertension
  • medications
  • gender
  • age
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25
Q

What might cause orthosasis?

  • [incr/decr] intravascular volume
  • _____
  • Alcohol consumption (impairs ___)
  • [incr/decr] age
  • Medications, including…(6)
A
DECREASED intravascular volume
Autonomic Insufficiency
Alcohol consumption (impairs VASOCONSTRICTION)
AGING
Medications:
- Antidepressants
-Beta and alpha blockers
- ACE inhibitors
- Vasodilators/nitrates
- Ca2+ channel blockers
- Opiates
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26
Q

How do you treat orthostasis?

A
  • Meds (midodrine, florinef)
  • Increased salt in diet
  • Compression:
  • –LE compression therapy: 40-60 mmHg
  • — Abdominal binder
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27
Q

Renal problems may mimic…

A

LOW BACK PAIN

If it’s there all of the time and isn’t reproducable or aggravated by movement/test, then it’s likely not something we can treat

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28
Q

The kidneys deal with fluid and chemical balance. Metabolic waste is excreted through the urine and includes…

A
  • Urea nitrogen (from protein metabolism)
  • Creatinine (from muscle)
  • Normal cellular environment ion regulation (Na+, k+, Ca2+, Mg2+, PO4)
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29
Q

What labs do we look at for renal function?

A

BUN, Creatinine, Na+, K+, GFR (Glomerular Filtration Rate)

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30
Q

___ increases with dehydration, high protein diet, blood in GI tract, catabolic states, injury, infection, fever and steroids.

A

BUN

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31
Q

___ is a more accurate determination of renal fxn because it is liberated from muscle tissue at a constant rate and excreted at the same rate. Women have less because of lower muscle mass.

A

CREATININE

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32
Q

Changes in __ levels can result in changes in mental status because of its involvement in the CNS and PNS.

A

Na+

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33
Q

With changes in K+ levels, what is most susceptible? What might we see clinically?

A

K+ = heart most susceptible. May see arrhythmias, cardiac arrest, weakness, irritability, difficulty with muscle contraction, pain or spasm.

High OR low K+ can cause sudden cardiac death

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34
Q

We want to see glomerular filtration rates (GFRs) >___. Under that, we suspect some kidney damage.

A

GFR <90 = kidney damage

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35
Q

What renal test would we use to look at pH levels, protein levels, specific gravity, glucose detection, ketones, blood cells, and infection?

A

Urinalysis. Also looks at color (dark = blood)

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36
Q

If you get an abnormal urinalysis and suspect infection, what might you test next?

A

Culture and sensitivity. Determines what exactly is causing the infection (microorganism)

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37
Q

What can we see with a plain film KUB (means: ___)

A

KUB = Kidney-ureters-bladder

XR of abdominal area, lets you see huge obstructions, large stones, etc. Not a ton of detail

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38
Q

___ uses a fiberoptic scope to look at bladder and urethra. It [can/cannot] visualize kidneys

A

Cystocopy looks at bladder and urethra. CANNOT visualize kidneys

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39
Q

What might indicate a renal issue? (11)

A

a. Aneuria or oliguria
b. Dysuria
c. Nocturia
d. Hematuria or pyuria
e. Increased frequency
f. Increased urgency
g. Intermittency/post-void dribbling
h. Chronic retention or voiding issues
i. Pain: shoulder back, flank, pelvis, lower abdomen (generally at costovertebral angle)
j. Costovertebral tenderness
k. Fever and/or chills

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40
Q

Urinary tract infections are called __ or ___ in the lower tract, and ___ in the upper tract.

A
Lower = cystitis, urethritis
Upper = pyelonephritis (kidney inflammation)
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41
Q

Risk factors for UTIs include…

A
  • Women
  • Pregnancy
  • Older adults
  • Catheterization
  • Instrumentation
  • Sexual intercourse
  • Obstruction
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42
Q

Kidney stones occur more in [men/women]. Onset is generally in __-__s (age range), but [increases/decreases] with age. Accompanied with [gradual/sudden] pain onset

A

Kidney stones occur in MEN > women

  • Onset in 30-40s but INCREASES with age
  • SUDDEN pain
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43
Q

Acute kidney failure has a [sudden/gradual] onset. Labs show [increased/decreased] Cr and BUN. It may be due to… (5)

A

Acute kidney failure = SUDDEN onset. INCREASED BUN & Cr. Due to:

  • Shock
  • Trauma
  • Obstruction
  • Toxicity
  • Infection
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44
Q

Chronic kidney failure is due to prolonged injury to ___ (potentially due to what diseases?) We see changes in multiple body systems. Discuss what systems and what we might see.

A

Chronic kidney failure = prolonged injury to nephron (incl glomerulus, renal tubules, or collecting duct), potentially secondary to DM or HTN.

  • Hematologic: anemia, toxins interfere with platelet aggregation
  • Cardiovascular: CAD, HTN, heart failure, pulm edema, DOE, pericarditis - heart failure stresses kidneys, but so do the meds you’re on!
  • GI (n/v, anorexia)
  • Musculoskeletal (Decrased Ca2+ absorption, joint calcifications)
  • Integumentary (itching, hyperpigmentation, bruising)
  • Eyes (blurring, dry/red eyes)
  • CNS: seizure, coma, lethargy, sleep problems, inability to concentrate
  • PNS: uremic toxins –> loss of vibratory sensation, decreased DTRs, paresthesia, muscle cramps/twitching, foot drop
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45
Q

How does hemodialysis work?

A
  • Blood travels to dialyzer in plastic tube with semi-permiable membrane
  • Dialyzing fluid contains electrolytes to facilitate osmosis (waste goes into dialysate)
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46
Q

Why would a patient use CVVH (____) or CRRT (___)?

A
CVVH = Continuous Venovenous hemofiltration
CRRT = Continuous Renal Replacement Therapy
  • These are for pretty severe patients that can’t handle the large fluid shifts (1-2 lbs!) that come with normal dialysis (esp if they have a <3 problem). Distributes the same fluid loss over a 24h period
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47
Q

How often do patients do dialysis? How long each time?

A

3-4 days/week, 3-4 hours a session

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48
Q

What is used to access blood for a dialysis?

A

Arteriovenous fistula - anastamose arterial and venous systems

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49
Q

Describe the different types of peritoneal dialysis.

A

CAPD = continuous ambulatory peritoneal dialysis. Osmosis faciltates waste removal -drains into a bag by gravity via a small catheter in abdomen.

CCPD = continuous cycling peritoneal dialysis. Uses machine to fill and empthy diasylate. Usually overnight

IPD = intermittent periotneal dialysis. Extended CCPD with multiple exchanges a day. Lets you spread dialysis out through the day and easier to do at home (easier than going to center for dialysis)
*Usually for 36-42 hours/week

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50
Q

PT concerns with dialysis patient

A
  • Treatment timing
  • Access location (no BP over a fistula!)
  • Complications: graft infection, peritonitis
  • Dialysis dementia (aluminum accumulation –> acute mental status changes)
  • Diet restrictions (low protein, Na, K, fluid restriction)
  • Dialysis disequilibrium (antibiotics –> vestibular problem b/c odotoxicity, osmotic pressure can increase in brain)
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51
Q

Differentiate between the following types of incontinence:

  • Functional
  • Overflow
  • Stress
  • Urge
A
  • Functional: can’t make it to restroom in time, but know need to urinate
  • Overflow: leakage from overfull bladder b/c not properly/adequately emptying bladder. Too much volume!
  • Stress: cough, laugh, sneeze, valsalva
  • Urge: strong, sudden need to urinate (more of a neurogenic cause b/c bladder spasms/contractions)
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52
Q

A [primary/secondary] tumor arises from cells that are normally local to the given structure. A [primary/secondary] tumor arises from cells that have metastasized from another part of the body.

A

A PRIMARY tumor arises from cells that are normally local to the given structure. A SECONDARY tumor arises from cells that have metastasized from another part of the body.

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53
Q

Differentiate between benign and malignant neoplams

A

Benign = usually harmless, doesn’t spread

Malignant = usually harmful, tends to spread

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54
Q

What is the name of the theory that says that neoplasm (tumor) originates from a single cell with a genetic change? This goes on to say that a ____ aberration creates tumor cell proliferation due to addition, delation, translocation, or inversions of part or entire chromosome.

A

SOMATIC MUTATION THEORY

chromosomal aberration

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55
Q

Why do we bother staging tumors?

A
  • Helps with prognosis

- Gives info about potential for metastasis

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56
Q

What are early warning signs of CA? Think CAUTIONS

A

C: Changes in bowel or bladder habits (often neuro-related)
A: A sore that doesn’t heal in 6 wks
U: Unusual bleeding or discharge
T: Thickening or lump in breast, elsewhere
I: Indigestion or difficulty in swallowing
O: Obvious change in wart or mole
N: Nagging cough or hoarseness
S: Supplemental signs and symptoms (rapid unintentional weight loss, changes in vital signs, frequent infections, night pain, pathologic fracture, proximal muscle weakness, change in DTRs)

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57
Q

What are early warning signs of cancer that we might see as PTs?

A
  • NIGHT PAIN that can’t be reproduced with testing
  • PROX. MUSCLE WEAKNESS (also might be b/c steroids or immunosuppressant meds)
  • Changes in VITAL SIGNS
  • Changes in DTRs
  • Pathologic FRACTURE (fx without trauma b/c tumor weakening bone)
  • Rapid, unintentional WEIGHT LOSS
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58
Q

Early signs of melanoma - ABCDE!

A
  • Asymmetry: uneven edges, unlike halves
  • Border: irregular, poorly defined
  • Color: black, shades of brown, red, white
  • Diameter: larger than a pencil eraser
  • Elevation/Evolving: raised, uneven
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59
Q

Systemic effects of CA (5)

“VAN For Days!”

A
Nausea
Vomiting
Anorexia
Fever without infection
Depression and/or anxiety
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60
Q

Pain occurs in __-__% of early stage and __-__% of late stage CA patients.

A

Pain occurs in 50-70% of early stage and 60-90% of late stage CA patients.

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61
Q

What causes pain in cancer? (5)

A
  • Nerve infiltration/compression (sharp stabbing)
  • Ischemic pain (throbbing, may have compression from tumor)
  • From diagnostic or therapeutic procedures
  • Bone destruction
  • Visceral compression
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62
Q

___% of patients with new CA have clinically detectable metastases, and __-__% have hidden metastases. Mets are usually seen within __-__ years of initial diagnosis. How does a tumor metastasize?

A

30% have clinically detectable mets
30-40% have hidden mets
Usually seen within 3-5 yrs of initial dx
- Tumors shed tumor cells into the blood stream. 99% of those cells are killed within 24h.
- This is more likely to occur via veins because arterial walls are stronger
SO tumor development depends heavily on blood supply from adjacent tissue (usually found in areas with HIGH blood flow)

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63
Q

Common locations of bone metastases?

A
Vertebrae (60% thoracic, 30% lumbar)
Pelvis
Ribs (posterior)
Skull
Femur (proximal)
Humerus (proximal)
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64
Q

What are common sites of mets in the body?

A
  • Pulmonary (venous drainage from body comes in SVC and IVC)
  • Hepatic systems (filters blood from stomach, colorectum, and pancreas)
  • Bone (poor prognosis)
  • CNS
  • Lymphatic system
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65
Q

With surgical resection, the primary PT concern is __. The three types of tumor resection are __, __, and __. Describe each.

A

PAIN.

PRIMARY TUMOR RESECTION
- takes out tumor. May therapeutically or prophylactically remove lymph nodes too

CYTOREDUCTIVE RESECTION (Debulking)
- Common for highly vascularized tumors and in brain

PALLIATIVE RESECTION
- MDs know they can’t treat it, but this reduces pain, corrects obstructions, and can alleviate pressure

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66
Q

What are side effects of surgical resection?

A
Fatigue
Disfigurement/deformity
Loss of function
Infection
Increased pain
Bleeding
Scar Tissue
Fibrosis
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67
Q

____ change or modify the relationship between the tumor and the host by strengthening the host’s biological response to the tumor. This is a type of ___

A

BIOLOGIC RESPONSE MODIFIER

Type of BIOTHERAPY

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68
Q

A bone marrow or stem cell transplantation from YOUR OWN body is called ___ and from a donor is called __. Patients are generally first treated with ___ chemo with the goal being to ___. Then, the patient undergoes the ___. The lowest point post-transplant is called the __ and occurs _-__ days post transplant. Finally, the body undergoes ___ __-__ days post transplant.

A

AUTOGENIC - your own marrow/stem cell
ALLOGENIC - donor marrow/stem cell

Patients are generally first treated with CONDITIONING chemo with the goal being to WIPE OUT THE PT’S IMMUNE SYS. Then, the patient undergoes the TRANSPLANT. The lowest point post-transplant is called the NADIR and occurs 5-7 DAYS post transplant. Finally, the body undergoes ENGRAFTMENT 10-21 days post transplant.

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69
Q

The mortality rate in graft vs host disease (GVHD) is [high/low].

A

HIGH mortality rate

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70
Q

Radiation therapy is ideal for [diffuse/localized] lesions. Maximum radiation is delivered usually [daily/weekly/monthly] for at least ____ (how long?). Goal is to ____.

A

Radiation therapy (XRT) is good for LOCALIZED lesions. Radiation is delivered DAILY for at least a MONTH. Goal: shrink tumor, then surgically excise it.

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71
Q

Describe external vs internal delivery of radiation therapy.

A

EXTERNAL DELIVERY (Traditional method)

  • Goal: deliver max dosage for max tumor control, minimize sequelae in normal tissue
  • Set the patient up Stereotactically.
  • DO NOT wash off XRT markings
  • Uses an IONIZING BEAM via a linear accelerator
  • Frequency: 5 equal fractions weekly x 3-6 weeks

INTERNAL DELIVERY
- Intracavity and interstitial implants

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72
Q

A major side effect of XRT is ___. Describe the pathology of this as it gets more severe (3 phases)

A

FIBROSIS

1) LOSS of tissue ELASTICITY with induration
2) Significant INDURATION with rigidity of surface layers and retraction of surface contours in dermis, subcutaneous tissue
3) ULCERATION AND NECROSIS from extravasation of fibrinous exudate and/or vascular compromise –> nerve entrapment and stenosis, obliteration, obstruction of parenchymal or hollow structures

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73
Q

The goal of chemotherapy is to deliver maximal dosage to maximize ___. Most chemotherapeutic agents affect what kind of cells?

A

Chemotherapy goal: deliver max dosage to maximize CELL DEATH (limited by toxicity)
- Most chemotherapeutic agents affect DIVIDING cells

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74
Q

What are methods of chemo delivery?

A
IV
Arterial infusion
Intrathecal
Intramuscularly
Orally
Interstitially
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75
Q

Side effects of chemo:

  • [incr/decr] blood counts (AKA ___)
  • [Hyper/hypo] coagubility
  • [High energy/fatigue]
A

REDUCED blood counts (leukopenia, NADIR, Absolute Neutrophil Count)

HYPERcoagubility

FATIGUE

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76
Q

Describe WBC ranges for minimal, moderate, and severe risk of infection.

A

Low WBCs (Leukopenia) –> infection risk:
Minimal: 1,000-5,000
Moderate: 500-1,000
Severe: <500

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77
Q

Patients with cancer tend to clot [more/less] because of the cancer itself. Why? Patients with impaired __ function are more at risk for this.

A

CA pts clot MORE because of the cancer. The tumor disrupts clotting sequence and its natural inhibitors by mechanical and/or by cellular products. Pts with impaired BONE MARROW function are at increased risk. DVT is associated

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78
Q

What factors could contribute to fatigue in cancer patients?

A

Treatment-related myelosuppression
Sleep deprivation
Pain emotional distress
Advanced dz

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79
Q

Two chemo-drug-related side effects PTs should monitor

A

Cardiac Toxicity

Peripheral neuropathy

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80
Q

A “cure” means that ___. Complete remission = __ years

Complete remission means ___.
Partial remission means ___

A

Cure = disease is GONE. Remission = 5 years

Complete remission = all signs of dz are gone. Not “cured” until 5 year mark
Partial remission = primary tumor 1/2 of original size

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81
Q

Survival rate is expressed as the chances of ___

A

Chances of being alive at 1, 5, and 10-yr mark

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82
Q

Greatest PT considerations for CA patients involve __, __, and ___

A

Orthopaedic (pathologic fx, bone tumors)

Neuro (Sp cord, brain tumors/mets)

Immobility syndromes/other

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83
Q

What 3 questions are essential to ask about a lump or nodule?

A

1) Is this new/how long has it been there?
2) Has the size changed
3) Does your MD know?

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84
Q

What two areas tend to be the focus of interventions with pts with CA?

A
  • Energy conservation

- Functional retraining

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85
Q

Factors affecting aging include (4)

A

Genetics
Diet
Social conditions
Occurrence of age-related dzs

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86
Q

Cellular aging is/can be a combination of ___ shortening leading to ___, ___ insults that crete free radicals, DNA repair defects that lead to the accumulation of ___, and abnormal ___ signaling

A

Cellular aging is/can be a combination of TELOMERE shortening (leading to REPLICATIVE SENESCENCE), ENVIRONMENTAL insults that crete free radicals, DNA repair defects that lead to the accumulation of MUTATIONS, and abnormal GROWTH FACTOR signaling

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87
Q

With aging, we see:

  • [incr/decr] thickness of distal vessel walls
  • [incr/decr] size of proximal vessels
  • [incr/decr] connective tissue & lipids
  • Atrophy of ___ fibers
  • [incr/decr] elastic fiber content
  • [Epithelial/endothelial] thickening
  • Smooth muscle ___
  • [Incr/decr] collagen content
  • Loss of ____ integrity
A
  • INCREASED thickness of distal vessel walls
  • INCREASED size of proximal vessels
  • INCREASED connective tissue & lipids (subendothelial layer)
  • Atrophy of ELASTIC fibers (medial layer)
  • DECREASED elastic fiber content
  • ENDOTHELIAL thickening
  • Smooth muscle CALCIFICATION
  • INCREASED collagen content
  • Loss of VENOUS VALVE integrity
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88
Q

Vascular tissue changes with aging lead to increased ___ within vessel walls, increased ___, and subsequently increased ___

A

Increased STIFFNESS in vessel walls –>
Increased VASCULAR RESISTANCE –>
Increased BP

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89
Q

The potential for venous pooling with vascular changes in aging leads to what clinically?

A

LE edema

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90
Q

Why might less O2 be available for delivery to tissues in an older adult?

A

There’s potential for impaired diffusion of O2 across vessel walls because they’re no longer elastic/compliant like before

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91
Q

Clotting risk goes [up/down] in older adults. Give 3 contributing factors to this

A

Clotting risk goes UP

  • Increased fibrinogen
  • Increased platelet adhesiveness
  • Early activation of coagulation system
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92
Q

In older adults, oxygen carrying capacity and oxygen delivery to tissues go [up/down]. Give reasons related to blood composition and peripheral blood changes as to why.

A

O2 carrying capacity goes DOWN
Blood compositon
- DECREASED space in bone marrow occupied by hematopoietic tissue
- Increased RED CELL rigidity

Peripheral blood

  • Decreased HCT
  • Decreased Hgb with levels remaining normal
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93
Q

In cardiac tissue in older adults, what changes do we see in the…

  • Myocardium
  • Endocardium
  • Conduction System
  • Valves
A

MYOCARDIUM

  • INCR wall thickness
  • Accumulates lipofuscin
  • INCR elastin, fat, and collagen

ENDOCARDIUM

  • Thickened areas composed of elastic, collagen, and muscle fibers
  • Fragmentation/disorganized elastic, collagen, and muscle fibers

CONDUCTION SYSTEM

  • Atrophy and fibrosis of Left bundle branches
  • DECR number of SA node pacemaker cells (~10% left at age 75!)

VALVES
- Thickening/calcification of valves (esp aortic and mitral)

94
Q

Older adults have an [incr/decr] cardiac output. This is because there is a decrease in [early/late] [systolic/diastolic] filling, increased dependency on ___ contraction, and increased ___ time.

A

DECREASED Cardiac Output

  • DECR in early DIASTOLIC filling
  • INCR dependency on ATRIAL contraction
  • INCR contraction-relaxation time
95
Q

We see an increased systolic and diastolic BP with aging. Talk about changes in:

  • Vascular tone
  • Afterload
  • Left ventricular end diastolic pressure
  • LV size
A
  • INCR Vascular tone
  • INCR Afterload
  • INCR Left ventricular end diastolic pressure
  • LV HYPERTROPHY
96
Q

With aging, we see decreased ventilation and decreased gas exchange. Changes in…

  • Mucus layer
  • Alveolar wall thickness
  • Functional respiratory surface area
  • Alveolar diameter
  • Alveolar-capillary interface size
  • Lung compliance
  • Lung parenchymal weight
  • Vascular walls stiffness
  • Amount of surfactant-producing cells
A
  • THICKENING mucus layer
  • THINNING Alveolar walls
  • DECREASED Functional respiratory surface area
  • INCREASED Alveolar diameter (with a decreased in alveolar surface area)
  • DECR Alveolar-capillary interface size
  • INCREASED Lung compliance
  • DECR Lung parenchymal weight
  • STIFFENING Vascular walls
  • DECREASE in surfactant-producing cells
97
Q

In older adults, there are changes in respiratory muscles that lead to increased work of breathing. We see a [decr/incr] in contractile proteins and a [decr/incr] in non-contractile protein. We see [incr/decr] connective tissue and [incr/decr[ capillary # relative to muscle fibers. Finally we see [incr/decr] contraction-relaxation times

A
DECREASE in contractile protein
INCR non-contractile protein
INCR connective tissue
DECR capillary #s relative to muscle fibers
INCR contraction-relax times

–> STIFFNESS within CT and muscle

98
Q

Skeletal changes with aging

  • Bone mineralization
  • Disc space
  • Costal movements
  • A-P thorax diameter
  • Kyphosis
A
  • DECR Bone mineralization
  • DECR Disc space
  • DECR Costal movements (stiffness at joints)
  • INCR A-P thorax diameter
  • INCR Kyphosis b/c decrease in thoracic length
99
Q

How does collagen change with aging?

  • Collagen diameter
  • Tensile strength
  • Crosslinking of collagen and fibers
  • Hyaluronic acid production
  • Secretion and organization of contractile proteins
  • Exudation of fibrin
A
  • INCR Collagen diameter
  • INCR Tensile strength
  • INCR Crosslinking of collagen and fibers
  • INCR Hyaluronic acid production –> decreased ease of movement, increased tissue degradation
  • DECREASED Secretion and organization of contractile proteins
  • INCREASED Exudation of fibrin
100
Q

3 components of pulmonary pathology

A

Ventilatory pump
Gas exchange
Airway clearance
(Respiratory failure - combo of problems with the other 3)

101
Q

2 Components of vascular pathology

A

Cardiovascular pump dysfunction
Deconditioning
(Cardiovascular pump failure)

102
Q

___ is characterized as an abnormal reduction in pulmonary ventilation, meaning that the volume of gas/air moving in & out is decreased. This happens because of [incr/decr] compliance in the [lungs/thorax]

A

RESTRICTIVE LUNG DZ is characterized as an abnormal reduction in pulmonary ventilation, meaning that the volume of gas/air moving in & out is decreased. This happens because of DECREASED compliance in the THORAX. The lung tissue itself increases compliance and gets floppy, but the thorax stiffens.

103
Q

Compliance is the measure of ___ of a material.

Compliance = change in __ / change in ___

A

Compliance is the measure of DISTENSIBILITY of a material.

Compliance = change in VOLUME / change in PRESSURE

104
Q

When we talk about compliance, we think about 2 different types: __ compliance and __ compliance.

A

CHEST WALL compliance

LUNG compliance

105
Q

Changes in the elasticity (compliance) of thoracic wall structures may be due to what 5 things?

A
  • Skeletal muscle
  • Bone
  • Skin
  • Metabolic (e.g mitochondrial disorder can’t maintain activity of muscles)
  • Neurologic innervations of abs or respiratory muscles (e.g. myasthenia gravis)
106
Q

Changes in the compliance of the lungs (either high or low compliance) results in [more/less] work to breathe. With low compliance, more [inspiratory/expiratory] lung forces are required to [pull the lungs open/ expel air]. What about high compliance? Eg. of a lung dz has high compliance?

A

Changes in compliance –> MORE work to breathe.
With low compliance, more INSPIRATORY lung forces are required to PULL LUNGS OPEN. Severe hyperinflation can result in HIGH compliance, and it’s like trying to blow up an already inflated balloon. (e.g. COPD)

107
Q

In breathing, we maximize minute ventilation (which is _____) by optimizing __ and __.

A

In breathing, we maximize minute ventilation (which is AMT BREATHING IN 1 MIN) by optimizing RESPIRATORY RATE and TIDAL VOLUME.

108
Q

Tidal volume is ___

A

VT = how much you’re breathing at rest

109
Q

With increased compliance, to breath the same amount of air, you have to generate [greater/lesser] ___ [during activity/at rest]. So clinically, greater ___ are required to maintain ___ with restrictive lung dz. This decreases [VT/ RR] so [VT/RR] must increase to compensate. This increase causes an overall increase in the work of breathing and energy expenditure.

A

With increased compliance, to breath the same amount of air, you have to generate GREATER PRESSURES AT REST. So clinically, greater PRESSURES are required to maintain VT with restrictive lung dz. This decreases VT so RR must increase to compensate.
This increase causes an overall increase in the work of breathing and energy expenditure.

110
Q

5 signs that your patient has a ventilatory pump problem…

think tests, pressure changes, muscles, breathing patterns, imaging

A

(1) Pulmonary function tests (PFTs): measure different volumes and flows with a big breath and blow it out. Determines obstructive or restrictive
(2) Significantly decreased MIP/MEP (max pressures you can inspire or expire…indicates strength of ventilatory muscles)
(3) Accessory muscle use at rest
(4) Abnormal/uncoordinated or paradoxical breathing pattern at rest or in response to position change or activity (Normal: upper chest and diaphragm go out and in together. Paradoxical: diaphragm may go in while wall is going out, or happen at different times)
(5) Increased AP diameter to a 1:1 ratio, flat sub-costal angle on exam or chest film (“barrel chested” tells that air is trapped, diaphragm is flattened, and lungs are hyper inflated)

111
Q

Gas exchange dysfunction involves the exchange of __ and __. What 3 values indicate a gas exchange impairment (think pressures…)

A

Gas exchange dysfunction involves the exchange of O2 and CO2. Changes in these values in a pt indicate a gas exchange impairment:

(1) SpO2 <=97% (depending on age)
(2) PaO2: abnormal for age at rest or in response to activities (measured in ARTERIES)
(3) PaCO2: abnormal at rest or in response to activity

(You may also see PAO2…the capital A indicates ALVEOLAR oxygen pressure, rather than PaO2 which is measured in the arteries!)

112
Q

The oxyhemoglobin dissociation curve describes ___ affinity for ___, meaning how readily ___ acquires and releases __ molecules. This depends on the pressure of __ in the blood: higher ___ pressure = [more/less] dissociation.

A

The oxyhemoglobin dissociation curve describes HEMOGLOBIN affinity for OXYGEN, meaning how readily HEMOGLOBIN acquires and releases O2 molecules. This depends on the pressure of O2 in the blood: higher O2 pressure = LESS dissociation.

113
Q

Normally, our O2 sat is around ___. As PO2 reaches ___, O2 begins to dissociate QUICKLY, meaning that small changes in ___ result in [larger/smaller] changes in % ___ saturation. This is affected by… (4)

A

Normally, our O2 sat is around 100%. As PO2 reaches 60, O2 begins to dissociate QUICKLY, meaning that small changes in PO2 result in LARGER changes in % O2 saturation.

This is affected by…

(1) Temperature
(2) CO2
(3) pH
(4) 2,3-DPG (may promote release of O2 bound to Hg)

114
Q

Give the pressures of O2 when it is…

(1) Inhaled: ___ mmHg (__%)
(2) Alveoli: ___ mmHg (__%)
(3) Capillary (venous): ___ mmHg

Gas diffuses from [high/low] to [high/low] pressure, making it move from the __ into the ___.

A

Give the pressures of O2 when it is…

(1) Inhaled: 160 mmHg (21%)
(2) Alveoli: 100 mmHg (13%)
(3) Capillary (venous): 40 mmHg

Gas diffuses from HIGH to LOW pressure, making it move from the ALVEOLI into the CAPILLARIES.

115
Q

What happens to the diffusion of oxygen (ie gas exchange) in the presence of chronic infection/scarring or secretions?

A

These clinical changes INCREASE the distance between alveoli and capillaries, so it takes LONGER for O2 to diffuse across. These pts will be okay at rest, but if they exercise, they’ll have trouble with gas exchange because they need more time for O2 to diffuse across.

116
Q

[O2/CO2] needs a much higher pressure to diffuse from alveoli to capillaries compared to the other gas. This is a problem when people have less __ available or when they’re getting less into their system.

A

O2 needs a much higher pressure to diffuse from alveoli to capillaries compared to the other gas. This is a problem when people have less O2 available or when they’re getting less into their system.

117
Q

Give the pressures of CO2 when it is…

(1) Inhaled: ___ mmHg (__%)
(2) Alveoli: ___ mmHg (__%)
(3) Capillary (venous): ___ mmHg

Gas diffuses from [high/low] to [high/low] pressure, making it move from the __ into the ___.

CO2 needs [more/less] pressure to diffuse than O2, which is why this works even when the pressure difference is small.

A

Give the pressures of CO2 when it is…

(1) Inhaled: 0 mmHg (0%)
(2) Alveoli: 40 mmHg (5%)
(3) Capillary (venous): 48 mmHg

Gas diffuses from HIGH to LOW pressure, making it move from the CAPILLARIES into the ALVEOLI.

CO2 needs LESS pressure to diffuse than O2, which is why this works even when the pressure difference is small (8 mmHg).

118
Q

In airway clearance dysfunctions, we see some pathological changes…

(1) Altered character/content of __
(2) Alteration in ___ of conducting airways
(3) Alteration in ___ function
(4) Alteration in ____ production/ efficacy of __

A

In airway clearance dysfunctions, we see some pathological changes…

(1) Altered character/content of MUCUS (e.g. enzyme deficiency)
(2) Alteration in CELLULAR WALL of conducting airways (e.g. chronic bronchitis, chronic asthma)
(3) Alteration in CILIA function (can’t move secretions out)
(4) Alteration in FORCE production/ efficacy of COUGH

119
Q

In airway clearance dysfunctions, we see pathophysiological changes that include…

(1) Abnormal ___ transport
(2) Excessive production of __
(3) Inability to produce/retain ___
(4) Increased resistance to __
(5) Increased work of __ / loss of __ mechanics

A

In airway clearance dysfunctions, we see pathophysiological changes that include…

(1) Abnormal MUCOCILIARY transport
(2) Excessive production of SECRETIONS
(3) Inability to produce/retain SECRETIONS
(4) Increased resistance to AIRFLOW
(5) Increased work of BREATHING / loss of COUGH mechanics

120
Q

How do we know that a patient has an airway clearance dysfunction? (5)
(think sounds, imaging, secretions…)

A

(1) Abnormal/ adventitious BREATH SOUNDS or voice sounds indicative of SECRETIONS
(2) Ineffective COUGH, or effective cough not able to clear the VOLUME OF SECRETIONS
(3) CHEST FILM with evidence fo INFILTRATE (e.g. pneumonia) or consolidation
(4) Mediate PERCUSSION NOTE that confirms presence of retained secretions/ consolidation
(5) PATHOLOGY with chronic retained SECRETIONS: CF, bronchiectasis, chronic bronchitis

121
Q

Is SOB indicative of a cardiopulmonary impairment?

A

NO! It can be attributed to cardiac problems, anxiety, etc. and apply to MULTIPLE impairments

122
Q

Give pathologies that would cause a ventilatory pump dysfunction.

A
  • Diaphragm weakness
  • Fluid in lungs (increased resistance and external pressure that hinders lung expansion)
  • Stiffening of the lung tissue (scarring from repeated infections, asbestos or other exposure, disease process like cystic fibrosis)
  • Broken ribs – can also directly prevent pump from expanding
  • Pain
  • Rigidity of rib cage (e.g. with aging, sarcoidosis – taut tissue that has lost elastic fibers)
  • Spinal deformity (scoliosis, kyphosis, etc.)
  • Collapsed lung
123
Q

Give pathologies that would cause a gas exchange dysfunction.

A
  • LOWER SURFICANT (eg. In babies, aging)
  • SMOKING: smoking substances can deposit in your alveoli, so gas has a longer difference to travel, or it can’t diffuse at all
  • CYSTIC FIBROSIS: secretions in lungs make it hard to diffuse
  • PNEUMONIA
  • CHRONIC BRONCHITIS
  • TUBERCULOSIS
  • ASTHMA: you can get scarring and secretions with chronic asthma, increases distance between alveoli
124
Q

Give pathologies that would cause an airway clearance dysfunction.

A

COPD – AIR TRAPPING, but it has 2 components with different pathologies. Most people will have one or the other, but occasionally you’ll see both:

  • Chronic Bronchitis – inflammatory process, chronic inflammatory rxn in airways, often from smoke/cigarette byproducts. You get an influx of fluid (as you do with all inflammation), and you end up getting secretions. Secretions don’t get cleared, and then they can block air = air trapping. THIS is the airway clearance aspect of COPD, not so much emphazema
  • Emphazema – destruction of the alveoli (destroyed the elastin and things that hold the alveoli) so they can’t stay open. You take a deep breath in, and as you go to breathe out, they collapse early. You start to get build up of quantities of air that get trapped in lungs over time (over years) = air trapping

ALSO:
- Stroke, Myesthenia gravis, ALS, etc = loss of motor control/strength so you can’t generate enough force to create an effective cough

  • Someone who can’t protect airway
125
Q

Asthma is characterized by:

  • Increased __ (with this we see increases in what cells?)
  • Airway hyper-____ (with this we see what changes in smooth muscle and nerves?)
  • Increased ___ (because of increased ___ cells and __ glands)
A

Asthma is characterized by:
- Increased INFLAMMATION (with this we see increases in MAST CELLS, EOSINOPHILS, T-CELLS, MACROPHAGES, AND NEUTROPHILS (in smokers)

  • Airway hyper-RESPONSIVENESS (with this we see INCREASED VOLUME & CONTRACTILITY OF SMOOTH MUSCLE, LIMITED MODULATION ABILITY, OVERSENSITIVE SENSORY NN)
  • Increased SECRETIONS (because of increased GOBLET cells and SUBMUCOSAL glands)
126
Q

Asthma is manifested by __, __, __, and inability to __.

A

Asthma is manifested by COUGH, DYSPNEA, WHEEZING, and inability to EXPEL AIR.

127
Q

__% of the population is affected by asthma, and ~40% develop it before age __, with another 30% developing it before age __. What time(s) of day do most people experience increased symptoms?

A

4% of the population is affected by asthma, and ~40% develop it before age 10, with another 30% developing it before age 40. Most people experience increased symptoms at NIGHT and in the MORNING

128
Q

35-55% of patients with asthma have an __ component. Most provoking symptoms are ___ and occur within __-__ mins of exposure. _____-induced asthma can exacerbated by the environment, including __ and __.

A

35-55% of patients with asthma have an ALLERGIC component. Most provoking symptoms are AIRBORNE and occur within 30-60 mins of exposure. EXERCISE-induced asthma can exacerbated by the environment, including COLD AIR and ALLERGENS.

129
Q

Potential exacerbating factors for asthma include… (7)

A
  • Exercise (exercise > 90% HRmax, 6-8 mins after starting activity)
  • Viral respiratory tract infections
  • Occupations: cotton, bakers, metal salts, wood and vegetable dusts, pharmaceutic agents, industrial chemicals, plastics, biologic enzymes, animal/bird/fish/insect proteins
  • Weather changes: cold or dampness
  • High levels of air pollution
  • Pharmacologic agents: aspirin, drug additives (tartrazine –> yellow dye #5) and food preservatives (sulfites)
  • Emotional or psychological factors
130
Q

Is asthma a ventilatory pump, gas exchange, or airway clearance problem?

A

Can be all 3!

  • Gas exchange (can’t get air down b/c bronchoconstriction or secretions)
  • Vent. pump (airway constriction)
  • Airway clearance (secretions)
131
Q

Atelectasis describe the ______ of a lung (or part of a lung). The __ never fully expand.

A

Atelectasis describe the INCOMPLETE EXPANSION OR COLLAPSE of a lung (or part of a lung). The ALVEOLI never fully expand.

132
Q
Atelectasis is caused by...
- Dz with [incr/decr] chest wall compliance
- \_\_\_ weakness
- Loss of \_\_\_
....plus \_\_, \_\_, or \_\_\_.

Also, in a post-op patient, it can be due to…

  • ___
  • ____ due to pain
  • Irritation from __ and ___ on the airways
A
Atelectasis is caused by...
- Dz with DECREASED chest wall compliance
- RESPIRATORY MUSCLE weakness
- Loss of SURFACTANT
....plus BEDREST, SECRETIONS, or TUMOR.

Also, in a post-op patient, it can be due to…

  • BEDREST
  • SPLINTING due to pain
  • Irritation from ANESTHESIA and ENDOTRACHIAL TUBE on the airways
133
Q

COPD stands for ___. They describe disease of the respiratory tract that __ and can be further classified as __ or __.

A

COPD stands for CHRONIC OBSTRUCTIVE PULMONARY DZ. They describe disease of the respiratory tract that OBSTRUCT AIRFLOW and can be further classified as CHRONIC BRONCHITIS or EMPHYSEMA.

134
Q

Chronic bronchitis is defined as hypersecretion of mucus causing a ___ most days for __ (#) months x __ (#) consecutive years. This begins in [large/small] airways [with/ without] obstruction and progresses to [larger/smaller] airways [with/without] obstruction. The more [large/small] airways that are involved, the more disability.

This is more common in [men/women] over ___ y/o and occurs in __-__% of adults.

A

Chronic bronchitis is defined as hypersecretion of mucus causing a PRODUCTIVE COUGH most days for 3 months x 2 consecutive years. This begins in LARGE] airways WITHOUT obstruction and progresses to SMALLER airways WITH obstruction. The more SMALL airways that are involved, the more disability.

This is more common in MEN over 40 y/o and occurs in 10-25% of adults.

135
Q

How does chronic bronchitis happen?
Inflammation and scarring of ___ which then does 2 things: __ and __. Then, we see changes in a number of cells:
- [Incr/decr] diameter of bronchial lumen
- [Incr/decr] # of ciliated cells
- [Incr/decr] smooth muscle in the bronchial wall
- Atrophy of the __ in the bronchial wall
- Increase ___ production in the airways
- [ Incr/decr] goblet cells peripherally in the bronchioli

A

Inflammation and scarring of BRONCHIAL LINING which then does 2 things:

(1) OBSTRUCTS AIRWAY FLOW
(2) INCREASES MUCUS PRODUCTION (hypertrophy and hyperplasia in submucosal glands and trachea)

Then, we see changes in a number of cells:

  • DECREASED diameter of bronchial lumen
  • DECREASED # of ciliated cells
  • INCREASED smooth muscle in the bronchial wall (think: constricting!)
  • Atrophy of the CARTILAGE in the bronchial wall
  • Increase MUCUS production in the airways
  • INCREASED goblet cells peripherally in the bronchioli
136
Q

The pathogenesis (cause) of chronic bronchitis generally involves chronic ___ due to __. This happens due to epithelial [hypo/ hyper] secretion and defective ___ function

Other causes include…(4)

A

The pathogenesis (cause) of chronic bronchitis generally involves chronic INFLAMMATION due to SMOKING. This happens due to epithelial HYPERsecretion and defective MUCOCILIARY function

Other causes include…
- Air pollution
- 2nd hand smoke
- Occupational exposure to dusts (gold, coal, fluospar, asbestos)
- Occupational exposure to vegetable dusts (cotton, flax, hemp)
MAY have a genetic component

137
Q

Emphysema is described as the abnormal and [permanent/ temporary] [narrowing/ enlargement] of air spaces [proximal/distal] to terminal non-respiratory bronchioles with concomitant destruction of the __.

A

Emphysema is described as the abnormal and PERMANENT ENLARGEMENT of air spaces DISTAL to terminal non-respiratory bronchioles with concomitant destruction of the ALVEOLAR WALLS.

138
Q

Emphysema is manifested by loss of ___, excessive collapse of airways on [inhalation/ exhalation], and chronic ___.

So basically, we have an accumulation of ___ in the tissues (called ____)

A

Emphysema is manifested by loss of ELASTIC RECOIL (destruction of elastin), excessive collapse of airways on EXHALATION, and chronic AIRFLOW OBSTRUCTION.

Accumulation of air in tissues. Loss of elasticity –> narrowing or collapse of bronchioles –> trapping inspired air in lungs

139
Q

In emphysema, we see ___ when pockets of air form between the ___ and within the ___. This results in increased ventilatory ___.

A

In emphysema, we see AIR-TRAPPING when pockets of air form between the ALVEOLAR SPACES and within the LUNG PARENCHYMA. This results in increased ventilatory DEAD SPACE.

140
Q

Clinical features of emphysema include…
(think breathing pattern, muscle changes, bone changes, skin changes, imaging)
- ___: [fast/slow] [deep/shallow] pattern, [scant/ lots of] sputum
- [Incr/decr] subcostal angle, [angled/horizontal] ribs ([hyper/hypo] inflation)
- “___”: [thick/thin], __ skin tones
- On chest XR: may be normal or [hyper/hypo] inflation, [lordosis/kyphosis], [incr/decr] retrosternal air, __ diaphragm

A
  • SOB: RAPID SHALLOW pattern, SCANT sputum
  • DECREASED subcostal angle, HORIZONTAL ribs, HYPERINFLATION
  • “PINK PUFFER”: THIN, CACHETIC, ROSY skin tones
  • On chest XR: may be normal or HYPERinflation, KYPHOSIS, INCREASED retrosternal air, FLATTENED diaphragm
141
Q

Average life expectancy of CF is ~__ years; it mainly affects ___ (race). Genetically, it is an ____ [dominant/recessive] disorder resulting from a defect in the __ gene (> ___ (#) mutations)

A

Average life expectancy of CF is ~37 years; it mainly affects CAUCASIANS OF EUROPEAN DECENT. Genetically, it is an AUTOSOMAL RECESSIVE disorder resulting from a defect in the CFTR gene (> 15,000 mutations)

142
Q

In cystic fibrosis, [incr/decr] water secretion makes mucus ___. This collects in [large/small] airways beginning at __ (what stage of life?). This is called ___, and it begins in [prox/distal] airways and progresses [prox/distally] over time creating areas of ___ and ___. The lung is chronically colonized by several ___ which results in increased resistance to __ over time. Involves MULTIPLE systems.

A

In cystic fibrosis, DECREASED water secretion makes mucus THICK & STICKY. This collects in SMALL airways beginning at INFANCY. This is called MUCUS PLUGGING, and it begins in DISTAL airways and progresses PROXIMALLY over time creating areas of CHRONIC BRONCHITIS and BRONCHIECTASIS. The lung is chronically colonized by several BACTERIA which results in increased resistance to ANTIBIOTICS over time. Involves MULTIPLE systems.

143
Q

Rib fractures generally occur in ribs __-__. They are attached [anteriorly/ post/ both] and are not as protected as ribs __-__. Restricted movement is a result of __ which decreases after about __ (#) weeks. Fractures can be associated with __ –> __ –> ___

A

Rib fractures generally occur in ribs 5-9. They are attached BOTH ANTERIORLY AND POSTERIORLY and are not as protected as ribs 1-4. Restricted movement is a result of PAIN which decreases after about 2 weeks. Fractures can be associated with HEMOTHORAX –> EFFUSION –> EMPYEMA

144
Q

In ___, we see free floating segments of ribs due to a fracture in [anterior/post/both] aspect(s) of a rib. This results in a __ breathing pattern moving [inward/outward] with inspiration and [inward/outward] with expiration. This condition is often associated with lung ___ (local pulmonary ____ damage with __ and __ moving into alveoli) due to force of trauma. __% of patients have long-term pain, deformity of the __, ___ on exertion, and/or mild restrictive pathology.

A

In FLAIL CHEST, we see free floating segments of ribs due to a fracture in BOTH ANTERIOR AND POSTERIOR aspect(s) of a rib. This results in a PARADOXICAL breathing pattern moving INWARD with inspiration and OUTWARD with expiration. This condition is often associated with lung CONTUSION (local pulmonary MICROVASCULATURE damage with RBC and PLASMA moving into alveoli) due to force of trauma. 60% of patients have long-term pain, deformity of the CHEST WALL, DYSPNEA on exertion, and/or mild restrictive pathology.

145
Q

Kyphocoliosis is a combination of excessive ___ and __ (directions) curve of the thoracic spine. It occurs in __% of the population and within that population, __% have pulmonary dysfunction. In 85% of these cases, the cause is ___. It occurs in females to males in a __:___ ratio. Most arise during __ (life period)

A

Kyphocoliosis is a combination of excessive ANTEROPOSTERIOR and LATERAL curve of the thoracic spine. It occurs in 3% of the population and within that population, 3% have pulmonary dysfunction. In 85% of these cases, the cause is IDIOPATHIC. It occurs in females to males in a 4:1 ratio. Most arise during ADOLESCENCE (life period)

146
Q

___ is fluid that abnormally accumulates in the pleural space. Normally, ~__cc of pleural fluid is present to lubricate the __ and __ that rub against each other during respiration. The increased fluid pushes on the lung tissue and [incr/decr] compliance.

A

PLEURAL EFFUSION is fluid that abnormally accumulates in the pleural space. Normally, ~5cc of pleural fluid is present to lubricate the VISCERAL and PARIETAL PLEURA that rub against each other during respiration. The increased fluid pushes on the lung tissue and DECREASES compliance.

147
Q

Clinical signs of pleural effusion include:

  • [Pain/ no pain] (if yes, describe it)
  • [Long/short] inspiratory phase of breathing
  • [Incr/decr] breath sounds
  • ___ __ __ present on auscultation
A

Clinical signs of pleural effusion include:

  • PAIN (varies from sharp to dull and non-focal, may be assoc. with deep breath or cough)
  • SHORT inspiratory phase of breathing
  • DECREASED breath sounds
  • PLEURAL FRICTION RUB present on auscultation
148
Q

Aspiration pneumonia is the inflammation of ___ and ___ due to inhalation of foreign material, usually __, __, __, __. This can lead to ___, ___ or ___.

Increased risk with [older/younger], as well as other risk factors…

Most common in [L/R] [upper/middle/lower] lobe due to anatomy.

A

Aspiration pneumonia is the inflammation of LUNGS and BRONCHIAL TUBES due to inhalation of foreign material, usually FOOD, LIQUIDS, VOMIT, ORAL SECRETIONS. This can lead to INFLAMMATORY RXN, PNEUMONIA or LUNG ABCESS.

Increased risk with:

  • Advanced age
  • Dental problems
  • Sedatives
  • Anesthesia
  • Coma
  • Impaired gag
  • Impaired cough
  • Impaired ciliary movement
  • EtOH/drug use

Most common in R UPPER LOBE due to anatomy.

149
Q

Describe the 5 phases in bacterial pneumonia pathophysiology

A

(1) Bacteria & microbes enter lower respiratory tract
(2) Outpouring of edema fluid
(3) Influx of leukocytes with active phagocytosis of bacteria
(4) Fibrin deposited in inflamed area
(5) Day 5, antibodies in area are fighting infection

150
Q

Bacterial pneumonia is a(n) [abrupt/ gradual] onset with what clinical signs?

A

Bacterial pneumonia is a(n) ABRUPT onset with what clinical signs?

  • Lobar consolidation
  • High fever
  • Chills
  • Dyspnea
  • Tachypnea
  • Productive cough
  • Pleuritic pain
  • Leukocytosis
151
Q

In viral pneumonia, the virus localizes in respiratory __ cells which leads to destruction of __ and __ and results in loss of __ function. If it reaches the alveoli, you might see what clinical signs?

Insidious onset with [consolidated/patchy & diffuse] infiltrates, and what other clinical signs?

A

In viral pneumonia, the virus localizes in respiratory EPITHELIAL cells which leads to destruction of CILIA and MUCOSAL SURFACE and results in loss of MUCOCILIARY function. If it reaches the alveoli, you might see what clinical signs?

  • Edema
  • Hemorrhage
  • Hyaline membrane formation
  • Development of ARDS

Insidious onset with PATCHY AND DIFFUSE infiltrates, and what other clinical signs?

  • Moderate fever
  • Dyspnea
  • Tachypnea
  • Nonproductive cough
  • Myalgia
  • NORMAL WBC
152
Q

General clinical signs of pneumonia

A
  • Increased RR
  • Crackles, wheezes, diminished breath sounds
  • Fever/chills
  • Tachycardia
  • Hypoxia
  • Frequent productive cough
  • Purulent secretions
  • Pleuritic pain
  • Myalgias and/or malaise
153
Q

Pulmonary edema is an increase in the ____, affecting the ___ first and then affecting the ___.

A

Pulmonary edema is an increase in the AMOUNT OF FLUID IN THE LUNG, affecting the INTERSTITIUM first and then affecting the ALVEOLAR SPACES.

154
Q

2 causes of pulmonary edema include…

A

(1) Increase in PULMONARY CAPILLARY HYDROSTATIC PRESSURE due to LV FAILURE

(2) Increased ALVEOLAR CAPILLARY MEMBRANE PERMEABILITY (by loss of integrity of pulmonary capillary endothelial cells) due to various causes:
- Gases (toxic levels of O2, sulfur dioxide)
- Liquids (e.g aspirated water)
- Microorganisms (viruses)
- Medications
- Shock/trauma

155
Q

In pulmonary edema, you see [incr/decr] pressure in microcirculation due to back flow from the [R/L] [ventricle/atrium]. Also see [incr/decr] transvascular flow into the interstitium of the lung where it can accommodate ~ __mL excess fluid. The lymph system helps out until the [R/L] [atrium/ventricle] pressure >__mmHg and further progresses into alveoli. So then, increased pressures force fluid in the ___ to flood ___, leading to flooding in the ___ and then ___. Pulmonary edema has increased __ concentrations.

A

In pulmonary edema, you see INCREASED pressure in microcirculation due to back flow from the LEFT VENTRICLE. Also see INCREASED transvascular flow into the interstitium of the lung where it can accommodate ~ 500mL excess fluid. The lymph system helps out until the LEFT ATRIUM pressure >30 and further progresses into alveoli. So then, increased pressures force fluid in the CAPILLARIES to flood ALVEOLAR SPACES, leading to flooding in the VISCERAL PLEURA and then PLEURAL EFFUSIONS. Pulmonary edema has increased PROTEIN concentrations.

156
Q

A pulmonary embolism (PE) occurs when there is a [arterial/venous] thrombosis which travels to the __ then to the __ then gets stuck in the ___ arteries. 95% of these are from the [UE/LE/trunk] and the rest are from the ___. __% of PE are fatal.
Risk factors include…

A
A pulmonary embolism (PE) occurs when there is a VENOUS thrombosis which travels to the RA then to the RV then gets stuck in the PULMONARY ARTERIES.  95% of these are from the LE and the rest are from the THORAX.  10% of PE are fatal.  
Risk factors include...
- Bedrest
- Long periods of travel
- Fx stabilization
- Increased age
- Heart failure
- Obesity
- Cancer
- Chronic venous insufficency
- Trauma
- CVA
- BCP
- Anemia
- Thrombocytosis
157
Q

In PE, an occlusion of the ___ arterial branch causes __ and __ into surrounding lung tissue, leading to ___ of alveolar walls. The alveoli fill with __ and lead to an inflammatory response. There is [incr/decr] alveolar dead space (area being ventilated but not ___), leading to pseudoconstriction and decreased __ due to hyperventilation. Alveolar surfactant [incr/decr], leading to alveolar collapse and regional __. Causes acute V/Q mismatch, [incr/decr] in lung compliance and gas exchange impairment. Necrosis and infarction of lung tissue is [common/rare] because occlusion is in artery and lungs receive oxygen from pulmonary vascular system, bronchial vascular system, and alveolar gas exchange.

A

In PE, an occlusion of the PULMONARY arterial branch causes EDEMA and HEMORRHAGE into surrounding lung tissue, leading to COAGULATIVE NECROSIS of alveolar walls. The alveoli fill with ERYTHROCYTES and lead to an inflammatory response. There is INCREASE alveolar dead space (area being ventilated but not PERFUSED), leading to pseudoconstriction and decreased CO2 due to hyperventilation. Alveolar surfactant DECREASES, leading to alveolar collapse and regional ATELECTASIS. Causes acute V/Q mismatch, DECREASE in lung compliance and gas exchange impairment. Necrosis and infarction of lung tissue is RARE because occlusion is in artery and lungs receive oxygen from pulmonary vascular system, bronchial vascular system, and alveolar gas exchange.

158
Q

Interstitial pulmonary fibrosis (IPF) is present with what diseases or after what interventions? It is a(n) ___ process involving all parts of the ___ wall. This allows __ to enter the alveolar spaces which leads to scarring. ___ clogs the alveoli. Life expectancy is

A

Interstitial pulmonary fibrosis is present with OCCUPATIONAL DUST DZ, POST RADIATION CHANGES It is a(n) INFLAMMATORY process involving all parts of the ALVEOLAR WALL. This allows FIBRIN to enter the alveolar spaces which leads to scarring. INFLAMMATORY EXUDATE clogs the alveoli. Life expectancy is

159
Q

Changes in IPF lead to [thinning/thickening] of alveolar walls, [increasing/decreasing] distance gas travels to diffuse into/out of arterial blood. SO [gas exchange/vent pump/airway clearance] is impaired. Scarring and fibrin [incr/decr] elasticity of lungs and [incr/decr] lung compliance and [incr/decr] work of breathing.

A

Changes in IPF lead to THICKENING of alveolar walls, INCREASING distance gas travels to diffuse into/out of arterial blood. SO GAS EXCHANGE is impaired. Scarring and fibrin INCREASES elasticity of lungs and INCREASES lung compliance and INCREASES work of breathing.

160
Q

Smoke inhalation can lead to injury…

(1) ___ injury to the upper airways
(2) __ injury to the tracheobronchial tree
(3) ____ poisoning due to carbon monoxide or __

A

Smoke inhalation can lead to injury…

(1) THERMAL injury to the upper airways
(2) CHEMICAL injury to the tracheobronchial tree
(3) SYSTEMIC poisoning due to carbon monoxide or CYANIDE

161
Q

Thermal and chemical injury in smoking are the result of a __ process that causes edema and sometimes blistering. May need ___ until inflammation subsides.

A

Thermal and chemical injury in smoking are the result of an INFLAMMATORY process that causes edema and sometimes blistering. May need INTUBATION until inflammation subsides.

162
Q

In carbon monoxide poisoning, hemoglobin has a higher affinity for __ than __ (>___x). This causes __ throughout the body. Clinically, we give increased supplemental __ to increase the pressure and binding capabilities.

A

In carbon monoxide poisoning, hemoglobin has a higher affinity for CO than O2 (>250x). This causes HYPOXIA throughout the body. Clinically, we give increased supplemental O2 to increase the pressure and binding capabilities.

163
Q

In cyanide poisoning, ___ is inhibited. We can’t measure it quick enough for it to be useful, but it’s treated in patients post-burn if it’s suspected.

A

In cyanide poisoning, AEROBIC METABOLISM is inhibited. We can’t measure it quick enough for it to be useful, but it’s treated in patients post-burn if it’s suspected.

164
Q

Tell the spinal cord innervation levels for the following:

INSPIRATORY

  • Diaphragm
  • External intercostals
  • SCM
  • Scalenes
A

INSPIRATORY

  • Diaphragm: C3, 4, 5 (phrenic n)
  • External intercostals: T1-T12
  • SCM: CN XI (spinal accessory)
  • Scalenes C1, C2
165
Q

Tell the spinal cord innervation levels for the following:

EXPIRATORY

  • Internal intercostals
  • Abdominals
A

EXPIRATORY

  • Internal intercostals: T1-T12
  • Abdominals: T7-L1
166
Q

What pulmonary clinical signs do we see with spinal cord injuries?

A
  • Ineffective cough (incr pulm infections)
  • Inspiratory muscle weakness –> incr atelectasis
  • Loss of sigh reflex –> incr atelectasis & alveolar collapse
  • Paradoxical breathing
  • Pulmonary and chest wall compliance decrease over time
167
Q

Give values for HTN classifications:

  • Normal
  • Pre-hypertensive
  • Stage I HTN
  • Stage II HTN
  • Hypertensive Crisis
A
  • Normal: =160 / >=100

- Hypertensive Crisis >180 / >=110

168
Q

Risk factors for HTN include ___ and isolated >= DBP ___mmHg in patients over age __. Treatment for HTN includes ___, __, __, and __.

A

Risk factors for HTN include BLOOD PRESSURE VARIABILITY and isolated >= DBP 90 mmHg in patients over age 50. Treatment for HTN includes MEDICATIONS, EXERCISE, STRESS MGMT, and DIET

169
Q

Atherosclerosis occurs in the __ layer of a vessel and causes ___ of coronary [artery/vein] walls. It results in [incr/decr] flow through coronary aa and also affects vascular __. It involves an __ process.

A

Atherosclerosis occurs in the INTIMA layer of a vessel and causes THICKENING & HARDENING of coronary ARTERY walls. It results in DECREASED flow through coronary aa and also affects vascular TONE. It involves an INFLAMMATORY process.

170
Q

Risk factors for atherosclerosis include…(7)

A
  • Elevated cholesterol and trygliceride levels
  • High blood pressure
  • Smoking
  • Diabetes
  • Obesity
  • Sedentary lifestyle
  • High fat diet
171
Q

Angina is caused by [incr/decr] supply of ___ to the ___. Symptomatically, it is usually described as ___ but can also consist of __ or __. May include __, __, or __. PT implications are that you should only exercise patients with __ angina. Pts should take their ___ tabs to manage their angina if they’re on them! Angina may look different in different patients.

A

Angina is caused by DECREASED supply of OXYGEN to the MYOCARDIUM. Symptomatically, it is usually described as CHEST PAIN but can also consist of BURNING or PRESSURE. May include SOB, DIAPHORESIS, N/V. PT implications are that you should only exercise patients with STABLE angina. Pts should take their SUBLINGUAL NITROGLYCERIN tabs to manage their angina if they’re on them! Angina may look different in different patients.

172
Q

What are the 4 types of angina? Describe each.

A

(1) Unstable angina = occurs with or without effort, leading to MI; can’t predict when it’ll happen. Person needs medical intervention, NO PT treatment. Medical intervention could = mediations, catheterization, or surgery.
(2) Stable angina = angina that comes on at a predicted workload (e.g. not at 2 mph but chest pain at 2.5 mph) – at a given workload, we can predict that you’ll have ischemia. (reproducible with effort/stress)
(3) Asymptomatic/Silent Ischemia – unknown ischemia common in patients with diabetic neuropathy, they might not feel pain with angina. Symptoms may instead include general malaise, SOB.
(4) Variant/Prinzmetal Angina – occurs at REST due to coronary artery spasms treated with Ca2+ channel blocker to stop spasms. Usually happens at a similar time of day (generally morning). Coronary aa spasm → vaso constriction → decreased blood flow. Meds stop spasms and keep Ca2+ channels open and you’re fine!

173
Q

Myocardial infarctions (MI) occur due to ___ or __ of cardiac muscle usually due to [artery/vein] occlusion due to __, __ or coronary [artery/vein] __. Low blood flow can also occur with __ or __. Demand MI occurs in patients with ___ with increased systemic stress.

A

Myocardial infarctions (MI) occur due to CELL DEATH or NECROSIS of cardiac muscle usually due to ARTERY occlusion due to THROMBUS, EMBOLUS, or coronary ARTERY OCCLUSION. Low blood flow can also occur with HEMORRHAGE or HYPOVOLEMIA. Demand MI occurs in patients with UNDERLYING CARDIAC DZ with increased systemic stress.

174
Q

Myocardial infarctions involve [incr/decr] blood flow to a zone, called the ___. The immediate surrounding tissue is called the ___, which is surrounded by the __. These two surrounding zones [can/cannot] heal.

A

Myocardial infarctions involve DECREASED blood flow to a zone, called the ZONE OF INFARCTION (NONCONTRACTILE SCAR TISSUE). The immediate surrounding tissue is called the ZONE OF INJURY, which is surrounded by the ZONE OF ISCHEMIA. These two surrounding zones [can/cannot] heal.

175
Q

[High/low] cardiac enzymes (including __, __, __, and __) indicate myocardial cell death. Cardiac enzymes are drawn every __ hrs after a cardiac event until they are trending [up/down], at which point you can treat the patient.

A

HIGH cardiac enzymes (including CREATINE KINASE, CK-MB, TROPONIN I, & TROPONIN T) indicate myocardial cell death. Cardiac enzymes are drawn every 8 hrs after a cardiac event until they are trending DOWN, at which point you can treat the patient WITH PT

176
Q

PT implications Post-MI:

- Intensity must be

A

PT implications Post-MI:

  • Intensity must be
177
Q

How do you diagnose MI?

A
  • Rise and/or fall of cardiac biomarkers (preferably cardiac troponin) with one value >99th percentile upper limit

AND

  • One of the following:
  • -Symptoms of ischemia
    • New ST or T wave changes, Left bundle branch block or Q waves
    • Imaging evidence of new loss of viable myocardium or regional wall abnormality
    • Identification of intracoronary thrombus
178
Q

In DM, exercise elicits [incr/decr] sensitivity and responsiveness of peripheral tissues to insulin which compensates for the [incr/decr] exercise-induced insulin secretion and increment in counterregulatory hormone secretion.

We see [hyper/hypo] glycemia due to [incr/decr] food intake, rapid absorption of __ at injection site, and exercising at time of peak ___.

How can hyperglycemia occur with exercise?

A

In DM, exercise elicits INCREASED sensitivity and responsiveness of peripheral tissues to insulin which compensates for the DECREASED exercise-induced insulin secretion and increment in counterregulatory hormone secretion.

We see HYPOglycemia due to DECREASED food intake, rapid absorption of INSULIN at injection site, and exercising at time of peak INSULIN EFFECT.

HYPERGLYCEMIA with exercise: if insulin deficit and hyperglycemia are present at onset of exercise, it can lead to the muscle being unable to uptake insulin, so the liver produces MORE glucose –> increased hyperglycemia

179
Q

In DM, we see atherosclerosis due to blood vessel abnormalities due to damage to the ___. HTN is __x as likely in DM with accelerated __ and __ complications. Clinically, we see ___ ischemia or shown as __ and __. Mortality is __-__x > DM

A

In DM, we see atherosclerosis due to blood vessel abnormalities due to damage to the BASEMENT CAPILLARY MEMBRANE. HTN is 2X as likely in DM with accelerated MICROVASCULAR AND MACROVASCULAR complications. Clinically, we see SILENT ischemia or shown as SOB and FATIGUE. Mortality is 2-3X > DM

180
Q

Resting HR is [incr/decr] in the presence of autonomic dysfunction in DM and CAD. These patients tend to be [hyper/hypo] tensive with exercise and [hyper/hypo]tensive post exercise. In DM I, we see a blunted __ response and reach [aerobic/ anaerobic] metabolism at lower HRs.

A

Resting HR is INCREASED in the presence of autonomic dysfunction in DM and CAD. These patients tend to be HYPERtensive with exercise and HYPOtensive post exercise. In DM I, we see a blunted HR response and reach ANAEROBIC metabolism at lower HRs.

181
Q

An aortic dissection is a tear in the __ layer of the aorta. This allows blood flow in the __ layer which can extend along the aorta lining due to __ within the aorta. This usually occurs close to the __ due to loss of __ and __ in the vessel. Untreated, can lead to rupture with [high/low] mortality rate.

A

An aortic dissection is a tear in the INTIMA layer of the aorta. This allows blood flow in the MEDIA layer which can extend along the aorta lining due to HIGH PRESSURES within the aorta. This usually occurs close to the AORTIC VALVE (ASCENDING AORTA) due to loss of COLLAGEN and ELASTIN in the vessel. Untreated, can lead to rupture with HIGH (80%) mortality rate.

182
Q

Symptoms of aortic dissection include…

A
  • Severe, sudden onset chest or back pain (chest pain = ascending aorta dissection, back pain = descending aorta dissection)
  • Distinguished from MI by no ECG changes or HF
  • Distal aortic dissection associated with HTN (>70%), but proximal has ~ equal amounts hyper and hypotension
  • Pulsate mass
183
Q

PT implications for aortic dissection include recognizing symptoms: [gradual/acute] onset, and unrelenting __/__ pain. If patient has a hx of aortic dissection, they will usually have __ and __ parameters to reduce pressure

A

PT implications for aortic dissection include recognizing symptoms: ACUTE onset, and unrelenting BACK/CHEST pain. If patient has a hx of aortic dissection, they will usually have BLOOD PRESSURE and HR parameters to reduce pressure

184
Q

In a(n) ___, a guide wire with a balloon is threaded from the leg to the coronary aa. At the region of plaque, a baloon is inflated to increase vessel lumen size.

A

ANGIOPLASTY

185
Q

A __ involves the same procedure as an angioplasty. The wire __ is on the end of a guide wire that keeps the vessel lumen open. Some of these are drug eluding to prevent ___

A

A STENT involves the same procedure as an angioplasty. The wire STENT is on the end of a guide wire that keeps the vessel lumen open. Some of these are drug eluding to prevent BUILD-UP OF ATHEROSCLEROSIS

186
Q

A __ is indicated for valve stenosis. A guide wire with a balloon is threaded from a vein or artery, and the balloon is inflated to stretch the valve.

A

A VALVULOPLASTY is indicated for valve stenosis. A guide wire with a balloon is threaded from a vein or artery, and the balloon is inflated to stretch the valve.

187
Q

PT Implications Post-Cardiac Catheterization:

  • With groin access, pts must be on bedrest for __hrs after procedure
  • With brachial artery access, may mobilize [early/late], but may be limited with arm activities for __-__ days
  • ___ restrictions for subclavian site
  • Patients are usually on ___ (drug) post op, so consider the risk of ___
  • Usually lesions >__-__% are intervened on, so there may still be dz after intervention!
A
  • With groin access, pts must be on bedrest for 8 HOURS after procedure
  • With brachial artery access, may mobilize EARLY, but may be limited with arm activities for 5-7 days
  • NO restrictions for subclavian site
  • Patients are usually on PLAVIX (drug) post op, so consider the risk of FALLING
  • Usually lesions >60-70% are intervened on, so there may still be dz after intervention!
188
Q

Blockages in coronary arteries are bypassed using ___ vessels in a ____ graft. Usually, this involves harvesting the __ vein or __ artery.

A

Blockages in coronary arteries are bypassed using NATIVE VESSELS in a CORONARY ARTERY BYPASS GRAFT (CABG) graft. Usually, this involves harvesting the SAPHENOUS VEIN or LEFT INTERNAL MAMILLARY ARTERY (LIMA).

189
Q

A valve replacement may be required due to valve __ or __. Mechanical or porcine valves can be used.

A

A valve replacement may be required due to valve STENOSIS or REGURGITATION. Mechanical or porcine valves can be used.

190
Q

In aortic __, there isn’t enough volume flowing through the valve to create aortic distention. This results in a decrease in systemic and coronary artery pressures. Aortic __ –> blood forced back into [R/L] [Atria/ventricle] –> decreases in coronary artery driving pressures
- The ___ acts as a secondary pump to dilatation during [dyastole/systole]

A

In aortic stenosis, there isn’t enough volume flowing through the valve to create aortic distention. This results in a decrease in systemic and coronary artery pressures. Aortic REGURGITATION –> blood forced back into L VENTRICLE –> decreases in coronary artery driving pressures
- The AORTA acts as a secondary pump to dilatation during SYSTOLE

191
Q

PT implications post-sternotomy include…

  • Unable to lift > __ lbs for _–__ weeks
  • [Unilateral/bilateral] UE tasks put less stress through sternal incision than [unilat/bilat] tasks
  • Pt will have temporary __ and/or ___ postop
  • Increased risk for postop ___ (ie >40% of pts have atrial fibrillation)
  • Increased risk for pneumonia due to __ and __
A
  • Unable to lift > 10 lbs for 6-8 weeks
  • UNILATERAL UE tasks put less stress through sternal incision than BILATERAL tasks
  • Pt will have temporary PACEMAKER and/or CHEST TUBES postop
  • Increased risk for postop ARRYTHMIAS (ie >40% of pts have atrial fibrillation)
  • Increased risk for pneumonia due to ATELECTASIS and PLEURAL EFFUSIONS
192
Q

Venous stasis is caused by ___ or __. Clinical symptoms include [LE/UE] edema, ___ veins; chronic edema can lead to [UE/LE] pigmentation changes. You treat this with __ and __.

A

Venous stasis is caused by PHLEBITIS or DVT. Clinical symptoms include LE edema, VARICOSE veins; chronic edema can lead to LE pigmentation changes. You treat this with ELEVATION AND COMPRESSION STOCKINGS

193
Q

A __ is a blood clot that forms within the venous system. What are the 2 large risks when this happens? What are PT implications?

A

A DVT is a blood clot that forms within the venous system.

2 large risks:

  • Piece can break off, travel to LUNGS and cause a PULMONARY EMBOLISM (PE)
  • Clot can extend and OCCLUDE BLOOD FLOW

PT implications:

  • Must be treated with a lytic agent, anticoagulant/antithrombotic and/or IVC filter placement - not our job!
  • Communicate with MD re: activity
  • Know that the risk of PE is the SAME if pt is on bedrest or is mobile
  • Recommendation: no PT until pt has initiated anticoagulant/thrombotic therapy, with an INR of 2-3
194
Q

DVTs can be predicted clinically using the ___. A high probability of a DVT is a total score >= __. Moderate = __, and Low = ___. The ___, an alternative test, should NOT be used as it isn’t sensitive and increases risk of PE.

A

DVTs can be predicted clinically using the WELL’S CRITERIA. A high probability of a DVT is a total score >= 3. Moderate = 1 or 2, and Low t sensitive and increases risk of PE.

195
Q

Causes of DVT fall into 3 main categories. (think about what would cause blood to hang out in an area). Name them and give specific examples for each.

A

STASIS

  • Immobility
  • Surgery
  • Obesity

TRAUMA

  • Fx
  • Injury to vein
  • Bruise

HYPERCOAGULABILITY

  • Medications: BCP
  • Smoking
  • Genetics
  • Cancer
  • Polycythemia
196
Q

DVT symptoms include…

  • Changes in skin temperature?
  • Changes in color?
  • Changes in texture?
  • HR & systemic responses?
  • Pain?
A
  • SWELLING and/or warm skin in leg
  • RED discolored or white skin
  • CORD in leg vein that can be felt (superficial phlebitis)
  • TACHYcardia
  • Slight FEVER
  • Dull ACHE, tightness, tenderness or PAIN in leg (may occur only when walking or standing)
197
Q

What’s the goal of an inferior vena cava filter (IVC)?

A
  • Placed to prevent passing clots from passing from the LE to the LUNGS
  • Removed once clot risk decreases
198
Q

Atherosclerosis affects coronary, peripheral, and cerebral vessels [the same/differently]. Arterial PVD is defined as decreased ___ to meet the demand of activity, leading to increased __. Lots of people (~__ million) are effected. Symptoms of Arterial PVD include:

  • Changes in the skin (temp? skin quality? hair?)
  • [Incr/decr] pulses in legs and feet
  • Non-healing __ or __
  • Changes in muscles?
  • Pain? (with activity? at rest?)
  • Color change in skin when legs are elevated vs hanging down
A

Atherosclerosis affects coronary, peripheral, and cerebral vessels THE SAME. Arterial PVD is defined as decreased VASCULAR SUPPLY to meet the demand of activity, leading to increased PAIN. Lots of people (~10 million) are effected.

Symptoms of Arterial PVD include:
- Changes in the skin: 
DECREASED temperature
THIN brittle or shiny skin
HAIR LOSS
  • DECREASED pulses in legs and feet
  • Non-healing WOUNDS or GANGRENE
  • NUMBNESS, WEAKNESS, OR HEAVINESS in muscles
  • PAIN (burning or aching) at REST in toes and at night when lying flat
  • PALLOR when legs are elevated
  • Reddish-blue discoloration (RUBOR) when extremities are hanging down
199
Q

An ABI, or __ __ __, compares __ in the arm and ankle. Pressures should be [same/different]. ABI = [SBP/DBP] of the ___ divided by [SBP/DBP] of the ___.

A

An ABI, or ANKLE-BRACHIAL INDEX, compares BLOOD PRESSURE in the arm and ankle. Pressures should be SAME. ABI = SBP of the LEG divided by SBP of the ARM.

200
Q

Give ABI values and descriptions

A

> 1.40 = non-compliant aa

  1. 0-1.4 = NORMAL
  2. 91-0.99 = Multi-level PVD, intermittent claudication

=< 0.9 = Abnormal

=< 0.5 = Severe arterial dz, may have pain at rest

201
Q

The toe brachial index is calculated in __ patients. An ABI >1.30 indicates ___.

A

The toe brachial index is calculated in DIABETIC patients. An ABI >1.30 indicates CALCIFIED ARTERIES.

202
Q

Claudication is __ that occurs [at rest/ with activity] in the __, __ or __. It indicates ___. Incidence is ~12% and increases to 30% in patients who are >__y/o or patients >__ y/o who __ or have __.

Describe the Claudication scale.

A

Claudication is PAIN that occurs WITH ACTIVITY in the CALF, THIGH or BUTTOCKS. It indicates BLOCKAGE IN ARTERIES INHIBITING BLOOD SUPPLY. Incidence is ~12% and increases to 30% in patients who are >70 y/o or patients >50 y/o who SMOKE or have DM.

Claudication scale:
0 = NO pain
1 = Minimal pain
2 = Moderate pain (can be distracted)
3 = Intense pain
4 = UNBEARABLE pain
203
Q

What types of stenoses would qualify a patient for peripheral vascular surgery?

A
  • Pts with LONG lesions >= 0.5cm
  • MULTIPLE stenoses
  • Very critical single stenosis in diffusely irregular segment or occlusion
204
Q

A ___ ___ is performed to deal with high grade stenosis (>__-__% occluded). This is performed through an incision near the __ muscle where plaque is removed at the ___ (what point in the vessel?). PTs should monitor ___ response post-op due to likelihood of comorbid cardiac dz and should also look for __ (body system) complications.

A

A CAROTID ENDARTERECTOMY (CEA) is performed to deal with high grade stenosis (>60-70% occluded). This is performed through an incision near the STERNOCLEIDOMASTOID muscle where plaque is removed at the CAROTID BIFURCATION. PTs should monitor HEMODYNAMIC response post-op due to likelihood of comorbid cardiac dz and should also look for NEUROLOGIC complications.

205
Q

After a peripheral revascularization (eg. a graft to bypass an occluded vessel), a PT should consider the __ of the revascularization, positioning of the __ and __ in the context of prolonged sitting, and look for signs of graft failure likely caused by __ or __.

A

After a peripheral revascularization (eg. a graft to bypass an occluded vessel), a PT should consider the LOCATION of the revascularization, positioning of the LE and UE in the context of prolonged sitting, and look for signs of graft failure likely caused by ISCHEMIA or INFECTION.

206
Q

A transmetatarsal amputation is the amputation of ___ (which toes?) and the closure of the wound with a [plantar/dorsal] flap. With any digit amputation, PTs should consider that the ___ is usually restricted (especially with __ amputations or amputation of which toe?) to allow healing. Remember that __ is likely to be impaired. Shoe inserts or different sized shoes can accommodate for amputation.

A

A transmetatarsal amputation is the amputation of ALL TOES and the closure of the wound with a PLANTAR flap. With any digit amputation, PTs should consider that the WEIGHT BEARING STATUS is usually restricted (especially with TRANSMETATARSAL amputations or amputation of HALLUX to allow healing. Remember that BALANCE is likely to be impaired. Shoe inserts or different sized shoes can accommodate for amputation.

207
Q

Below (abbrev:__) and above (abbrev: __) knee amputations are used in the management of critical limb __, __, and __. Below knee amputations can be done at what two points? Above knee amputations can be done at what 3 points?

PTs should consider ___ restrictions depending on wound integrity and healing; increased ___ of mobility and gait; and the need for a follow up with ___.

A

Below (BKA and above (AKA) knee amputations are used in the management of critical limb ISCHEMIA,MALIGNANCY, and TRAUMA.

BKAs:

  • Transtibial
  • Knee disarticulation

AKAs:

  • Transfemoral
  • Hip disarticulation
  • Hemi-pelvectomy

PTs should consider WEIGHT BEARING restrictions depending on wound integrity and healing; increased ENERGY COST of mobility and gait; and the need for a follow up with PROSTHETIST.

208
Q

We see a better outcome following peripheral vascular intervention in patients with [claudication OR critical limb ischemia]. Angioplasty can be effective in pts wtih [how long of an occlusion?] with mild [proximal/distal] dz.

A

We see a better outcome following peripheral vascular intervention in patients with CLAUDICATION vs. critical limb ischemia.

Angioplasty can be effective in pts wtih SHORT to MODERATE-LENGTH disease with mild PROXIMAL dz.

209
Q

Rank the following peripheral vascular interventions from least to most invasive:

  • Angioplasty
  • Bypass
  • Endarterectomy
A

(1) Endarterectomy (roto-rooter!)
(2) Angioplasty (put in stent, holds plaque to edges of vessel wall to restore blood flow
(3) Bypass with graft

210
Q

In a patient with claudication, what do check for and then what do you do? If you do activity, at what intensity level should you do it?

A
  • Are they perfusing well? If NO, send them straight to the ER
  • If YES, then they will benefit from exercise! If you train a pt around their ischemic threshold, they develop collateral circulation (to go around blockage). Walking is a great exercise – walk to point of pain, then sit and rest (pain will go away b/c O2 is restored as demand decreases). Interval training (go to pain, stop rest, pain goes away) and repeat to where they can go for 15-20 (or 30!) mins a day is a GREAT intervention! Walking below that threshold is NOT as effective and won’t evoke growth of lateral circulation.
211
Q

__ and __ are both pain due to ischemia (lack of __).

A

CLAUDICATION and ANGINA are both pain due to ischemia (lack of O2).

212
Q

Stress involves a combination of the __, the __, and the __

A

PERSON
STRESSOR
ENVIRONMENT

213
Q

There are 4 different factors that can contribute to stress. List and give examples!

A

“PEPS”

PSYCHOLOGICAL

  • Personality type, aggressive, hostile, Type A
  • Lack of faith/spirituality
  • Relationship or work conflict, high job demands or low control
  • Hx of abuse

ENVIRONMENTAL

  • Physical work environment
  • Exposure to chemicals, dust, pathogens
  • Rotating shift work

PHYSICAL

  • Sleep disturbance/deprivation
  • Chemical or biological trigger (foods, poor nutrition, caffeine)
  • Medical events, change in personal health, injury
  • No exercise/excessive exercise

SITUATIONAL

  • Poor social support
  • Exposure to safety hazards
  • Recent life changes
214
Q

Stress risk factors include… (elaborate on the following)

  • Age?
  • Enviorment/Social
  • Gender
  • [Early/late] life stressful events
A
  • Very OLD and YOUNG have less of a threshold to accommodate for stress
  • Social supports act as a buffer
  • Women are at greater risk of stress than MEN (BP in women elevated post work); BUT women talk about stressors and benefit from more social support than men
  • EARLY stressful life events
  • Negative life events
215
Q

Describe the Neurologic stress response in the ANS

A
  • Incr HR, BP, RR
  • Pupil dilation
  • Sweating
  • Blood flow to muscles, heart, lungs
  • Gastric fxn decreased (shunts blood to vital organs)

*Recruits sympathetic division of ANS (fight or flight!)

216
Q

Describe the Neurologic stress response in the Thalamus

A
  • Intensifies sensory input: vision, hearing, smell
217
Q

Describe the Neurologic stress response in the Cerebral Cortex

A
  • Intense focus
  • Planning
  • Attention
  • Persistence
218
Q

Describe the Neurologic stress response in the Limbic System

A
  • Regulates emotions (fear, anxiety, anger)

- Stimulates reticular system

219
Q

Hormonal response to stress involving cortisol…

The ___ releases CRH (___ __ __). CRH stimulates the release of ACTH (___ ___ ___ ___) from the ___. ACTH then stimulates ___ to secrete ___. Cortisol increases ___, regulates ___, and acts as an ___.

A

The HYPOTHALAMUS releases CRH (CORTICOTROPIN RELEASING HORMONE). CRH stimulates the release of ACTH (ADRENOCORTICOTROPIC HORMONE) from the PITUITARY. ACTH then stimulates ADRENAL GLANDS to secrete CORTISOL. Cortisol increases METABOLISM, regulates BLOOD GLUCOSE, and acts as an ANTI-INFLAMMATORY.

220
Q

Hormonal response to stress involving ANS…

The [parasympathetic/sympathetic] NS stimulates the release of catecholemines including __, __, and __. This induces the ___ response. We see increased __, __, __, and level of ___. We also see the activation of ___ muscles and blood flow shunted from the __ and __.

A

The SYMPATHETIC NS stimulates the release of catecholemines including EPINEPHERINE, NOREPINEPHRINE, and DOPAMINE. This induces the NEUROLOGIC response. We see increased HR, BP, RR, and level of ALERTNESS. We also see the activation of SKELETAL muscles and blood flow shunted FROM the SKIN and STOMACH.

221
Q

Symptoms of stress might include (12). Stress [aggravates/ causes] these symptoms.

A

Stress AGGRAVATES these symptoms.

  • Hypertension
  • Chest pain
  • Headache
  • Myalgia, arthralgia, fibromyalgia
  • Allergic responses
  • GI symptoms
  • Depression, anxiety, panic attacks
  • Discouragement, boredom
  • Eating disorder
  • Prolonged fatigue (chronic fatigue syndrome)
  • Poor work or school performance, errors in judgment
  • Sleep disturbance
222
Q

There are some stress-related dz and conditions. Provide some for each organ system:

  • Cardiovascular
  • Connective tissue
  • GI
  • Integument
  • Endocrine
  • CNS
  • Pulmonary
  • Muscular
  • Immune
A
  • Cardiovascular: HTN, CAD
  • Connective tissue: Inflammation, RA
  • GI: Ulcer, diarrhea, irritable bowel, impotence, diuresis
  • Integument: eczema, acne
  • Endocrine: DM, amenorrhea
  • CNS: Fatigue, depression, insomnia, substance abuse
  • Pulmonary: hypersensitivity rxns (asthma)
  • Muscular: Unconscious muscular contraction, tension headache
  • Immune: Immunosuppression
223
Q

General adaptation syndrome consists of 3 phases related to stress response. In the first phase, ___, we see a protective __ response that [continues/subsides] when the stressor is removed. The second phase, ___, occurs when the stressor is not removed and the body requires long term __.. Here, we see increased __ and __ production. This can lead to disease states due to __, __, __, and __. The third stage is ___ in which there are no further reserves of body __ or __, leading to risk of organ damage.

A

General adaptation syndrome consists of 3 phases related to stress response. In the first phase, ALARM PHASE (fight, flight, or freeze), we see a protective AUTONOMIC response that SUBSIDES when the stressor is removed. The second phase, RESISTANCE or ADAPTATION, occurs when the stressor is not removed and the body requires long term PROTECTION. Here, we see increased BLOOD SUGAR and CORTICOSTEROID production. This can lead to disease states due to FATIGUE, CONCENTRATION LAPSES, IRRITABILITY, AND LETHARGY. The third stage is EXHAUSTION in which there are no further reserves of body ENERGY or IMMUNITY, leading to risk of organ damage.

224
Q

__ helps to reduce the effects of hormones and secretions to facilitate return to homeostatic state.

A

EXERCISE

225
Q

The ___ Scale can be used to score a patient’s stress related to risk of serious illnesses in the next year. Scoring:
___ points = __% chance

A

The HOLMES & RAHE LIFE EVENTS SCALE can be used to score a patient’s stress related to risk of serious illnesses in the next year. Scoring:
300 points = 80% chance

226
Q

Examples of direct PT interventions to help patients with stress

A
  1. Progressive muscle relaxation
  2. Soft tissue mobilization
  3. Breathing exercises
  4. Physical activity and exercise
  5. Behavior modification
  6. Biofeedback
    * *Biofeedback involves using electronic instrumentation to signal selected somatic signals. Surface electrodes are sensitive to small changes in electrical activity of the muscles, signaling to the patient by way of sight or sound the need to practice physiologically quieting techniques.
227
Q

Ativan, Xanax, Klonopin, and Valium are medications to treat ___

A

ANXIETY

228
Q

Medications to assist with stress relief may be lumped into a few larger categories (4)…

A
Anti-anxiety
Sleep aids (e.g Ambien)
Muscle relaxants (e.g. Flexeril)
Beta Blockers (e.g Propanolol, Tenormin)
229
Q

PTSD occurs after exposure to a traumatic event that is an overwhelming personal experience causing changes in ___ patterns. It is often [acute/delayed] onset (time = ___). Patients have one or more symptoms, including… (4, list and describe)

A

PTSD occurs after exposure to a traumatic event that is an overwhelming personal experience causing changes in NEURAL ACTIVATION patterns. It is often DELAYED onset (time = >6 MONTHS). Patients have one or more symptoms, including…

(1) INTRUSION: re-experiencing traumatic event
(2) AVOIDANCE: decreased responsiveness
(3) AROUSAL: hyperaroused state
(4) Variety of Autonomic, Dysphoric, or cognitive symptoms
* Chronic pain is frequently co-occurring

230
Q

Describe the 4 types of HTN

A

Labile - HTN just happening randomly, doesn’t respond to traditional meds, Stress-triggered (no patterns)
Essential - same as primary HTN, normally idiopathic, 95% of people with HTN have this one
Secondary - due to medications or other patholoiges (renal and cardiac), other health issues
White-Coat - increase in BP when at the MD