Quiz 2 Flashcards

1
Q

What is Pulmonary Embolism?

A
  • an occlusion of a pulmonary vessel
  • life threatening
  • mortality rate as high as 30%
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2
Q

Etiology of pulmonary embolism

A

DVT - deep vein thrombosis
(Popliteal, femoral, iliac)

Other sources:
Air
Fat - from a broken bone
Amniotic fluid - during delivery

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3
Q

P. Embolism patho

A

DVT➡️embolus➡️thrombus in arterial bed➡️impaired perfusion

Ventilation: perf imbalance ➡️ hypoxemia

Platelet degranulation ➡️ bronchial and arterial constriction ➡️ hemodynamics instability

Neurally triggered bronchoconstriction

⬇️ CO

L/O surfactant ➡️ atelectasis

RHF

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4
Q

Mnfts of P. Embolism

A
  • depend on size and sight

- usually: dyspnea, tachypnea, chest pain, tachycardia

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5
Q

Dx of P Embolism

A
  • Hx, Px
  • ABG
  • LDH3 - a lung enzyme lactate dehydrogenase- indicative of cell damage
  • D-dimer - a byproduct of breakdown of protein
  • lung scan
  • CT, MRI
  • pulmonary angiogram
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6
Q

Tx of P Embolism

A

STAT! The larger the vessel, the more problematic

Maintain cardiopulmonary Fx

Thrombolytics, anticoagulants

Address DVT

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7
Q

Pulmonary HTN

A

Persistent elevation in pulmonary arterial pressure >25mmHg

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8
Q

Pulmonary Circuit Qualities

A
  • Low pressure and resistance (makes the circuit compliant)
  • If CO increases, there is minimal increase in pulmonary pressure
  • Pulmonary vasoconstriction increases circuit pressure
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9
Q

Pulmonary HTN Etiology

A

Cardiac and pulmonary disorders
3 categories:
- Increase in pulmonary volume (cardiac septal defects)
- Hypoxemia
- Increase in pulmonary venous pressure (LV dysfx)

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10
Q

Pulmonary HTN Mnfts

A
  • dyspnea
  • chest pain on exertion
  • syncope
  • fatigue
  • mnfts of RHF (right sd pumping against resistance)
  • RV hypertrophy
  • distended pulmonary arteries
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11
Q

Pulmonary HTN Tx

A
  • treat underlying cause
  • vasodilators —Calcium Channel Blockers
  • —prostacyclin—
  • a potent vasodilator
  • prevents regurgitation
  • anti-thrombolytic
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12
Q

Acute Respiratory Distress Syndrome ARDS

A

AKA wet lung

  • severe progressive damage to alveoli and capillaries
  • Rapid onset
  • thick layer of impermeable fluid disallowing gas exchange into capillary bed
  • up to 60% mortality
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13
Q

ARDS Etiology

A
Aspiration
- near drowning
- gastric contents
Inhaled gases
- NH3
Fat Embolism
Severe Burns
Drugs
- free-base cocaine
- heroin
- radiation
Infections
- septicemia
DIC (Disseminated Intravascular Coagulation)
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14
Q

ARDS Patho

A
  • Pulmonary and systemic inflm
  • lung trauma > neutrophil influx > free radicals, phospholipids and protease release > alveolar and cap damage > increase permb > proteins, cells and fluids enter IS and alveoli > decrease compliance and impaired gas exchange
  • Diffuse consolidation
  • Surfactant inactivation > atelectasis
  • Thick exudate lines alveoli
  • Impervious hyaline membrane lines alveoli > no gas exchange
  • Profound hypoxemia
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15
Q

ARDS Mnfts

A
  • Severe respiratory distress
  • dyspnea
  • tachypnea —- early sign
  • marked hypoxemia
  • early resp alkalosis
  • late metb acidosis
  • multi-organ failure
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16
Q

ARDS Tx

A
  • Stat intervention—-provide O2
  • respiratory support to maintain vital organs
  • correct hypoxemia
  • reverse underlying cause
  • treat complx

(Stabalize pt, treat cause)

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17
Q

Lung Cancer

A
  • Primary and Secondary
  • aggressive, invasive, metastic
  • leading cause of CA death
  • mets to bone, liver, brain
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18
Q

4 major types of Lung CA

A
  1. Small cell carcinoma (~12%) SCLC
  2. Large cell carcinoma (~12%) NSCLC
  3. Squamous cell carcinoma (~27%) NSCLC
  4. Adenocarcinoma (~#)%) NSCLC
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19
Q

Lung Cancer Etiology

A
  • Smoking
  • genetic predisposition
  • toxins (asbestos)
  • marijuana
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20
Q

Lung CA Patho in SCLC

A
  • aka oat cell carcinoma
  • 99% in smokers
  • aggressive, invasive, early mets (esp to brain)
  • 70% mets at Dx
  • tiny, oval cells (tumors too small to remove Sx)
  • paraneoplastic syndromes (Cushing’s, SIADH)
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21
Q

Lung CA Patho in adenocarcinoma

A
  • common form in women and non-smokers
    Central > tracheal and bronchi
    Peripheral > smaller airways
  • peripheral origin
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22
Q

Lung CA Patho in squamous cell carcinoma

A
  • Central origin (intraluminal)—-in the bronchi
  • impacts mediastinum
  • spreads to hilar nodes—-only entrance/exit of lungs associated with structures
  • More common in men
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23
Q

Lung CA Patho in large cell carcinoma

A
  • Peripheral origin
  • Large, undifferentiated cells
  • Early mets
  • Poor prognosis
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24
Q

Lung CA mnfts

A
  • based on type, extent, mets, paraneoplastic syndromes
  • if central > impact breathing»coughing, wheezing, dyspnea
    > cardiac mnfts»tumor causes external pressure
    > hemoptysis
    > pain»r/t stimulation of nerves
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25
Q

Lung Cancer Dx

A
  • Hx, Px
  • CXR, US, CT, MRI
  • bronchoscopy, needle biopsy
  • sputum/bronchial wash cytology
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26
Q

Lunc CA Tx

A
  • depends on type
  • chemo and radiation SCLC
  • Sx, radiation, chemo NSCLC
    »»»»POOR PROGNOSIS»»»»»
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27
Q

Cystic Fibrosis

A
  • defective chloride channel in cell membrane
  • leads to fluid hypersecretion
  • GI, resp and reproductive system
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28
Q

CF Etiology

A
  • defective CFTR gene on Chr 7
    &raquo_space;»>Cystic Fibrosis Transmembrane Regulator»»
  • autosomal recessive
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29
Q

CF Patho

A
  • CFTR gene codes chloride channel on cell membrane
  • mutation > defective channel > alters CM CL permb
  • impaired CL transport across CM
  • impact is tissue specific
    »»Chloride gets stuck in the secretory cells- making musous thick and sticky. Giving way for infecx and decreased a/w exchange»»
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30
Q

CF Respiratory

A
  • thick, copius mucous > excessive decrease in mucocilliary Fx
  • a/w obstructed > ventilation impaired
  • bacterial infecx
  • > 90% death from severe pulmonary disease
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31
Q

CF Dx

A
  • Sweat test&raquo_space;» high levels of NaCl in sweat
  • newborn screen (trypsinogen)
    • measured in blood
    • will be increased in a CF+ newborn
  • resp and gi mnfts&raquo_space;> diarrhea, abdm pain
32
Q

CF Tx

A
  • no cure
  • slow progression&raquo_space;> Abx, gamma globulins, mucous (prevent complx)
  • diet mods
  • pancreatic Es
  • mucolytics, anti-inflm
  • chest physio
33
Q

Respiratory Failure

A

Failure of lung function

- hypoxemia and hypercapnia

34
Q

Resp Failure Etiology

A
Hypoxemic
- severe pneumonia
- atelectasis
Hypercapnic/Hypoxemic
- airway obstruction
- tumors
- Guillan Barre
- COPD
Impaired Diffusion
- PE
- ARDS
35
Q

Resp Failure Mnfts

A
  • hypoxemia (PaO2 < 60mmHg N: 80-100
  • hypercapnia (PaCO2 > 45mmHg N: 35-45
  • resp acidosis
  • those of underlying cause
36
Q

Resp Failure Tx

A

Restore resp Fx

  • O2, mechanical ventilation
  • bronchodilators
  • Abx
  • underlying cause
37
Q

Prostate Physiology

A
  • encapsulated accessory organ
  • inferior to and surrounds neck of bladder
  • posterior surface in contact with rectum
  • common site for neoplasms
38
Q

Benign Prostatic Hyperplasia BPH

A
  • most common reproductive disorder in men
  • gradual benign enlargement
    »>periuretheral
  • prevalence increases with age
    • > 40 ~ 20%
    • > 60 ~ 50% As men age, their prostate
    • > 80 ~ 90% enlarges
39
Q

BPH Etiology

A
  • unclear
  • ageing is primary risk
  • hormonal change (androgens)
  • genetics, race, diet
    «<»>High in African Men
40
Q

BPH Patho

A
  • related to changes in testosterone, dihydrotestosterone, and estrogen
  • T changes to DHT by 5 alpha reductase
  • mediated by Es
  • E sensitizes cells to DHT
  • T levels decrease with age
  • relative increase in E oversensitizes cells to DHT > enlargement
  • prostatic IGF-I also implicated (insulin like growth factor)
  • hyperplasia of periuretheral tissue > urethra compressed
  • prostatic smooth muscle also undergo hypertrophy
  • urine flow impeeded
41
Q

BPH Structural Changes (compensatory)

A
  • thickening of the bladder wall (prevent rupture)
  • trabeculations and diverticula form (similar to stomach rugae)
  • ureters distend with urine > hydroureter
    • ureters “fishhook”
  • urine pools in the kidney causing hydronephrosis > distnension of renal pelvis and the caylicys with urine
  • urine stasis > infect and calculi
42
Q

BPH Mnfts

A
  • urinary frequency > gradual
  • hesitancy (difficulty starting flow)
  • weak urine stream
  • post voiding dribble
  • complete obstruction
    - urine retention
    PSAD - density PSAV - velocity
43
Q

BPH Dx

A
  • Hx, Px, mnfts
  • DRE
  • PSA (prostate-specific antigen)
  • US to determine size
  • BUN (blood, urine, nitrogen), creatine (kidney Fx)
44
Q

BPH Tx

A
  • no Tx required in early stages
  • based on severity and complx
  • behavioural > no fluids at HS, avoid alcohol/caffeine
  • drugs:
    • alpha adrenergic antagonist (relax muscles, facilitate voiding)
    • 5-alpha-reductase inhibitor {long term} (decreases DHT by blocking E from converting T > DHT)
    • combination is more effective
  • TURP (transurethral resection of prostate) of laser prostectomy
45
Q

Prostate Cancer —- presents with neoplasia

A
  • common CA in men
  • 3rd in CA death
  • increases after 50yr (85% after 65)
  • early mnfts are absent > delays Dx
46
Q

Prostate CA risks

A
  • mostly adenocarcinomas
    • peripheral, multicentric (tumor is peripheral in origin, reason for absence of mnfts)
    • variable appearance
  • aggressive, invasive, mets quickly, then extension to other organs
  • extension to bladder and seminal vesicles
  • mets to bone, liver, lungs
47
Q

Prostate Mnfts

A
  • appear after invasion or mets
  • dysuria, hematuria
  • prostatitis
  • late: hip and back pain (bone mets)
48
Q

Prostate Dx

A
  • Hx, Px
  • DRE, PSA (screening tests)
  • US (transurethral)
  • biopsy
49
Q

Prostate Tx

A
  • based on stage, grade and age
  • active surveillance if localized and low risk
  • 1st line: antiandrogens (eg: estrogen - withdraws support for growth)
  • radical prostectomy
  • radiation
50
Q

Pelvic Inflammatory Disease PID

A
  • inflm of the upper reproductive tract (beyond cervix)
  • d/t ascending infect
    • uterus endometriosis
    • tubes salpingitis
    • ovary oophoritis
51
Q

PID Etiology

A
  • pyogenic microbes (pus producing)
  • untreated bacterial infect
  • sexually transmitted
    • chlamydia (20%)
    • gonorrhea (10%)
52
Q

PID Patho

A
  • microbes enter cervix (dilated at menstruation)
  • rapid proliferation in uterus as endometrium sloughs
  • microbes ascend to tubes > ovary > peritoneum
53
Q

PID Mnfts

A
  • lower back and abdominal pain
  • heavy, purulent vaginal discharge
  • fever
  • early stages are asymptomatic
  • adnexal tenderness (structures associated with uterus)- leukocytosis
54
Q

PID Complx

A
  • common: pelvic abscesses

- occasional vaginal bleeding

55
Q

PID Dx

A
  • clinical presentation
  • increase in C-Reactive protein
  • increase in ESR (Erythrocyte sedimentation rate)
  • laparoscopy
56
Q

PID Tx

A
  • multiple broad spectrum Abx (90% success)

- Sx for complx

57
Q

Breast CA

A
  • most common CA in women (~ 1 in 10)
  • major cause of death from CA
  • affects men, rarely
58
Q

Breast CA Etiology and Risks

A
  • ageing
  • inherited (5-10%)
    • BRCA1 gene on Chr 17
    • BRCA2 gene on Chr 13
    • autosomal dominant (50%)
  • hormonal factors
    • late menopause
    • early menarche
    • HRT
    • nulliparity
59
Q

Breast CA Patho (Various Forms)

A
  • infiltrating ductal carcinoma ~ 80%
  • infiltrating lobular carcinoma ~ 10-15%
  • medullary carcinoma ~ 5%
  • colloid carcinoma rare
  • tubular carcinoma ~ 2%
  • inflm breast CA ~ 1-3%
60
Q

Ductal carcinoma in situ

A
  • ~20%
  • ductal epithelial
  • non-invasive
  • stage 0
    This is malignant and will progress to another form if not treated
61
Q

Infiltrating ductal carcinoma

A
  • most common from (~75%)
  • ductal origin
  • solid, irregular mass
  • invasive
  • mets to axillary lymph nodes
  • distal mets (eg: liver, bone, brain)
    Far worse than ductal carcinoma in situ
62
Q

Mnfts of Breast CA

A
  • fixed, irregular, painless mass
  • usuall UOQ
  • unilateral by the tail of spence
  • late: discharge, retraction, and edema of the nipple
63
Q

Breast CA Dx

A
  • mammography
  • biopsy
  • SLN assessment (Sentinel Lymph Node) [1st node affected]
  • tumor markers eg: CEA (carcinoembryonic Antigen)
  • Estrogen and Progesterone receptors in biopsy
  • 60% - 70% detected by patient
64
Q

Breast CA Tx (varied)

A
  • H therapy if increase in E & P receptors
    • tamoxifen (anti-E), Es inhibitors
  • Sx, chemo, radiation
  • lumpectomy - mass and surrounding tissue
  • mastectomy - breast
  • quadrantectomy - quadrant
  • radiation - breast and axillary
  • chemo - pre and post Sx
65
Q

Ovarian CA (worst of all reproductive CA)

A
  • most lethal reprod CA in women
  • poor Dx
  • 75% mets at Dx
66
Q

Ovarian CA Etiology and risks

A
  • ageing (usually between ~ 65 - 85 yr)
  • ovulatory age (period from menarche to menopause)
  • some forms are autosomal dominant
  • familial predisposition (ovarian or breast CA)
  • nulliparity??
  • infertility??
67
Q

Ovarian CA patho

A
  • diverse forms
    1. epithelial (most common)
    2. stromal
    3. germ cell
  • silent growth and spread (invasion, extension, seeding, mets)
  • extension: tubes, uterus, ligaments, other ovary
  • seeding: bowel, liver, other organs
    Late:
  • pressure on adjoining organs
  • abdm distension
  • mets vial lymph and blood
68
Q

Ovarian CA mnfts

A
- early: GI disturbances
             Non-specific
             Difficult to detect
- pain (d/t pressure &amp; inflm)
- abdm distension
- urinary &amp; bowel obstr
- ascites &amp; dyspnea
- pelvis mass usually first but late finding
69
Q

Ovarian CA Dx

A

US
Laparoscopy
Exploratory laparotomy

70
Q

Ovarian CA Tx

A
  • Radical Sx (excision of uterus, tubes, ovaries and omentum)
  • then chemo
  • laparotomy 6-12 months later
  • some recover fully
71
Q

Cervical CA

A

100% curable if in situ (not spread)

72
Q

Cervical CA etiology and risks

A
  • HPV (human papillomavirus)
  • > 100 strains
  • ~ 40 are sexually transmitted
  • 6 & 11 responsible for genital warts (90%)
  • 16 & 18 responsible for cervical CA (70%)
  • Gardasil - 3 doses, covers 4 strains, protects for 5 yr
  • Hx of STD
  • early age sex, multiple sex partners
  • smoking (organ specific carcinogens)
73
Q

Cervical CA Patho

A
  • mostly squamous cell origin
  • pre CA lesion: initial dysplasia
  • then carcinoma in situ (epithelial layer)
  • later invasive CA (deeper layers)
  • several years between pre CA & invasive stage
  • levels of Cervical Intraepithelial Neoplasia (CIN)
    1. CIN1 (mild dysplasia) [LSIL}
    2. CIN2 (moderate dysplasia) {HSIL}
    3. CIN3 (severe dysplasia & carcinoma in situ) {HSIL}
  • mets via lymphatics

LSIL - low squamous intraepithelial lesion
HSIL - high squamous intraepithelial lesion

74
Q

Cervical CA Dx

A
  • PAP smear

- colposcopy (scope through the vagina)

75
Q

Cervical CA Mnfts

A
  • metrorrhagia (bleeding between periods)
  • vaginal d/c
  • more frequent menses
    LATE: pelvic/back pain
76
Q

Cervical CA Tx

A
Early: excision (of the lesion)
Invasive: radiation and Sx
- cryosurgery (freeze necrosis)
- conisation (excises cone shaped area)
- laser
- LEEP (loop electro-surgical excision procedure)
- radical hysterectomy