Quiz 2 Flashcards
What is Pulmonary Embolism?
- an occlusion of a pulmonary vessel
- life threatening
- mortality rate as high as 30%
Etiology of pulmonary embolism
DVT - deep vein thrombosis
(Popliteal, femoral, iliac)
Other sources:
Air
Fat - from a broken bone
Amniotic fluid - during delivery
P. Embolism patho
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
Mnfts of P. Embolism
- depend on size and sight
- usually: dyspnea, tachypnea, chest pain, tachycardia
Dx of P Embolism
- 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
Tx of P Embolism
STAT! The larger the vessel, the more problematic
Maintain cardiopulmonary Fx
Thrombolytics, anticoagulants
Address DVT
Pulmonary HTN
Persistent elevation in pulmonary arterial pressure >25mmHg
Pulmonary Circuit Qualities
- Low pressure and resistance (makes the circuit compliant)
- If CO increases, there is minimal increase in pulmonary pressure
- Pulmonary vasoconstriction increases circuit pressure
Pulmonary HTN Etiology
Cardiac and pulmonary disorders
3 categories:
- Increase in pulmonary volume (cardiac septal defects)
- Hypoxemia
- Increase in pulmonary venous pressure (LV dysfx)
Pulmonary HTN Mnfts
- dyspnea
- chest pain on exertion
- syncope
- fatigue
- mnfts of RHF (right sd pumping against resistance)
- RV hypertrophy
- distended pulmonary arteries
Pulmonary HTN Tx
- treat underlying cause
- vasodilators —Calcium Channel Blockers
- —prostacyclin—
- a potent vasodilator
- prevents regurgitation
- anti-thrombolytic
Acute Respiratory Distress Syndrome ARDS
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
ARDS Etiology
Aspiration - near drowning - gastric contents Inhaled gases - NH3 Fat Embolism Severe Burns Drugs - free-base cocaine - heroin - radiation Infections - septicemia DIC (Disseminated Intravascular Coagulation)
ARDS Patho
- 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
ARDS Mnfts
- Severe respiratory distress
- dyspnea
- tachypnea —- early sign
- marked hypoxemia
- early resp alkalosis
- late metb acidosis
- multi-organ failure
ARDS Tx
- Stat intervention—-provide O2
- respiratory support to maintain vital organs
- correct hypoxemia
- reverse underlying cause
- treat complx
(Stabalize pt, treat cause)
Lung Cancer
- Primary and Secondary
- aggressive, invasive, metastic
- leading cause of CA death
- mets to bone, liver, brain
4 major types of Lung CA
- Small cell carcinoma (~12%) SCLC
- Large cell carcinoma (~12%) NSCLC
- Squamous cell carcinoma (~27%) NSCLC
- Adenocarcinoma (~#)%) NSCLC
Lung Cancer Etiology
- Smoking
- genetic predisposition
- toxins (asbestos)
- marijuana
Lung CA Patho in SCLC
- 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)
Lung CA Patho in adenocarcinoma
- common form in women and non-smokers
Central > tracheal and bronchi
Peripheral > smaller airways - peripheral origin
Lung CA Patho in squamous cell carcinoma
- Central origin (intraluminal)—-in the bronchi
- impacts mediastinum
- spreads to hilar nodes—-only entrance/exit of lungs associated with structures
- More common in men
Lung CA Patho in large cell carcinoma
- Peripheral origin
- Large, undifferentiated cells
- Early mets
- Poor prognosis
Lung CA mnfts
- 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
Lung Cancer Dx
- Hx, Px
- CXR, US, CT, MRI
- bronchoscopy, needle biopsy
- sputum/bronchial wash cytology
Lunc CA Tx
- depends on type
- chemo and radiation SCLC
- Sx, radiation, chemo NSCLC
»»»»POOR PROGNOSIS»»»»»
Cystic Fibrosis
- defective chloride channel in cell membrane
- leads to fluid hypersecretion
- GI, resp and reproductive system
CF Etiology
- defective CFTR gene on Chr 7
»_space;»>Cystic Fibrosis Transmembrane Regulator»» - autosomal recessive
CF Patho
- 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»»
CF Respiratory
- thick, copius mucous > excessive decrease in mucocilliary Fx
- a/w obstructed > ventilation impaired
- bacterial infecx
- > 90% death from severe pulmonary disease
CF Dx
- Sweat test»_space;» high levels of NaCl in sweat
- newborn screen (trypsinogen)
- measured in blood
- will be increased in a CF+ newborn
- resp and gi mnfts»_space;> diarrhea, abdm pain
CF Tx
- no cure
- slow progression»_space;> Abx, gamma globulins, mucous (prevent complx)
- diet mods
- pancreatic Es
- mucolytics, anti-inflm
- chest physio
Respiratory Failure
Failure of lung function
- hypoxemia and hypercapnia
Resp Failure Etiology
Hypoxemic - severe pneumonia - atelectasis Hypercapnic/Hypoxemic - airway obstruction - tumors - Guillan Barre - COPD Impaired Diffusion - PE - ARDS
Resp Failure Mnfts
- hypoxemia (PaO2 < 60mmHg N: 80-100
- hypercapnia (PaCO2 > 45mmHg N: 35-45
- resp acidosis
- those of underlying cause
Resp Failure Tx
Restore resp Fx
- O2, mechanical ventilation
- bronchodilators
- Abx
- underlying cause
Prostate Physiology
- encapsulated accessory organ
- inferior to and surrounds neck of bladder
- posterior surface in contact with rectum
- common site for neoplasms
Benign Prostatic Hyperplasia BPH
- 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
BPH Etiology
- unclear
- ageing is primary risk
- hormonal change (androgens)
- genetics, race, diet
«<»>High in African Men
BPH Patho
- 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
BPH Structural Changes (compensatory)
- 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
BPH Mnfts
- urinary frequency > gradual
- hesitancy (difficulty starting flow)
- weak urine stream
- post voiding dribble
- complete obstruction
- urine retention
PSAD - density PSAV - velocity
BPH Dx
- Hx, Px, mnfts
- DRE
- PSA (prostate-specific antigen)
- US to determine size
- BUN (blood, urine, nitrogen), creatine (kidney Fx)
BPH Tx
- 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
Prostate Cancer —- presents with neoplasia
- common CA in men
- 3rd in CA death
- increases after 50yr (85% after 65)
- early mnfts are absent > delays Dx
Prostate CA risks
- 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
Prostate Mnfts
- appear after invasion or mets
- dysuria, hematuria
- prostatitis
- late: hip and back pain (bone mets)
Prostate Dx
- Hx, Px
- DRE, PSA (screening tests)
- US (transurethral)
- biopsy
Prostate Tx
- 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
Pelvic Inflammatory Disease PID
- inflm of the upper reproductive tract (beyond cervix)
- d/t ascending infect
- uterus endometriosis
- tubes salpingitis
- ovary oophoritis
PID Etiology
- pyogenic microbes (pus producing)
- untreated bacterial infect
- sexually transmitted
- chlamydia (20%)
- gonorrhea (10%)
PID Patho
- microbes enter cervix (dilated at menstruation)
- rapid proliferation in uterus as endometrium sloughs
- microbes ascend to tubes > ovary > peritoneum
PID Mnfts
- lower back and abdominal pain
- heavy, purulent vaginal discharge
- fever
- early stages are asymptomatic
- adnexal tenderness (structures associated with uterus)- leukocytosis
PID Complx
- common: pelvic abscesses
- occasional vaginal bleeding
PID Dx
- clinical presentation
- increase in C-Reactive protein
- increase in ESR (Erythrocyte sedimentation rate)
- laparoscopy
PID Tx
- multiple broad spectrum Abx (90% success)
- Sx for complx
Breast CA
- most common CA in women (~ 1 in 10)
- major cause of death from CA
- affects men, rarely
Breast CA Etiology and Risks
- 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
Breast CA Patho (Various Forms)
- infiltrating ductal carcinoma ~ 80%
- infiltrating lobular carcinoma ~ 10-15%
- medullary carcinoma ~ 5%
- colloid carcinoma rare
- tubular carcinoma ~ 2%
- inflm breast CA ~ 1-3%
Ductal carcinoma in situ
- ~20%
- ductal epithelial
- non-invasive
- stage 0
This is malignant and will progress to another form if not treated
Infiltrating ductal carcinoma
- 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
Mnfts of Breast CA
- fixed, irregular, painless mass
- usuall UOQ
- unilateral by the tail of spence
- late: discharge, retraction, and edema of the nipple
Breast CA Dx
- 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
Breast CA Tx (varied)
- 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
Ovarian CA (worst of all reproductive CA)
- most lethal reprod CA in women
- poor Dx
- 75% mets at Dx
Ovarian CA Etiology and risks
- 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??
Ovarian CA patho
- 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
Ovarian CA mnfts
- early: GI disturbances Non-specific Difficult to detect - pain (d/t pressure & inflm) - abdm distension - urinary & bowel obstr - ascites & dyspnea - pelvis mass usually first but late finding
Ovarian CA Dx
US
Laparoscopy
Exploratory laparotomy
Ovarian CA Tx
- Radical Sx (excision of uterus, tubes, ovaries and omentum)
- then chemo
- laparotomy 6-12 months later
- some recover fully
Cervical CA
100% curable if in situ (not spread)
Cervical CA etiology and risks
- 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)
Cervical CA Patho
- 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
Cervical CA Dx
- PAP smear
- colposcopy (scope through the vagina)
Cervical CA Mnfts
- metrorrhagia (bleeding between periods)
- vaginal d/c
- more frequent menses
LATE: pelvic/back pain
Cervical CA Tx
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