Download Medical Notes: Respiratory, Bone, and Gynecological Conditions and more Study Guides, Projects, Research Nursing in PDF only on Docsity!
Patho Exam 5
sexually transmitted diseases commonly responsible for PID
- chlamydia (also gonorrhea)
- chlamydia bc it also has few s/s until it’s a big problem
- PID can cause infertility
STIs can cause infertility for M/W
- Chlamydia: Can damage the fallopian tubes and lead to pelvic inflammatory disease (PID). PID can cause tubal factor infertility (TFI), which is a common cause of infertility. Can reduce sperm quality and motility
- Gonorrhea: Can damage the fallopian tubes and lead to PID. Can cause epididymitis, which can lead to infertility
- Mycoplasma genitalium: Can cause PID and lead to TFI.
- Syphilis: Can cause infertility if left untreated. Syphilis can also cause other serious problems, including brain damage, blindness, and paralysis. Can cause epididymitis and erectile dysfunction, and damage the epididymis during the tertiary stage of infection
- also genital herpes - causing low sperm count, HIV, hepatitis
testicular torsion S/S and immediate management
- Sudden, severe pain in one testicle, swelling and redness in the scrotum, nausea and vomiting, testicle may appear higher than normal, pain in the lower abdomen or groin
- surgery to untwist spermatic cord and prevent testicle death
pulmonary disease most common S/S
- Shortness of breath: A common symptom of many pulmonary diseases, including COPD, pulmonary embolism, and pulmonary hypertension
- Coughing: A chronic cough, sometimes with phlegm, is a common symptom of COPD
- Wheezing: A common symptom of COPD
- Fatigue: A common symptom of COPD
- Chest pain: A symptom of pulmonary hypertension
- Low blood oxygen levels: A symptom of pulmonary embolism
- Swelling in the feet: A symptom of some lung diseases
- Increasing chest discomfort: A symptom of pleural effusion
chronic hypoxia can lead to what long-standing changes in the body conditions causing alveolar dead space
- due to conditions like pulmonary vascular remodeling, resulting in uneven blood flow to the alveoli, as well as structural changes in the lung tissue like fibrosis, which can impair gas exchange and effectively create areas of the lung that are ventilated but not perfused, contributing to increased dead space ventilation
Pulmonary hypertension: chronic hypoxia triggers pulmonary vasoconstriction, leading to increased pulmonary arterial pressure and eventually pulmonary hypertension. This can cause uneven blood flow distribution in the lungs, with some alveoli receiving less blood than others, creating areas of alveolar dead space.
Alveolar destruction: In conditions like COPD, chronic hypoxia can lead to destruction of alveolar walls, resulting in larger, less efficient alveoli and a reduction in the overall surface area available for gas exchange, further increasing dead space
Fibrosis: Prolonged hypoxia can stimulate the production of collagen fibers in the lung tissue, leading to fibrosis which stiffens the lung parenchyma and impairs gas exchange, contributing to increased dead space
Ventilation-perfusion mismatch: primary mechanism behind increased dead space in chronic hypoxia, where areas of the lung are adequately ventilated with air but poorly perfused with blood, leading to inefficient gas exchange
Clinical implications of chronic hypoxia:
- Decreased exercise tolerance: Increased dead space limits the amount of oxygen that can be taken up by the blood, leading to shortness of breath during physical activity - Cyanosis: A bluish discoloration of the skin due to low oxygen saturation in the blood, which can be a sign of severe chronic hypoxia - Right ventricular failure In advanced stages, pulmonary hypertension caused by chronic hypoxia can lead to right ventricular strain and potential heart failure
acute respiratory distress syndrome (ARDS) a life-threatening lung condition that occurs when the lungs are severely injured and can't provide enough oxygen to the body:
- Symptoms: severe shortness of breath, rapid breathing, low blood oxygen, and clicking, bubbling, or rattling sounds in the lungs
- Causes: sepsis, pneumonia, trauma, inhaling chemicals, lung transplant
- treatment: supplemental oxygen, fluid management, and medication, mechanical ventilator
- swelling causes fluid to build up in alveoli
- Excessive ROS generated by the injured endothelium/epithelium as well as recruited leukocytes plays a major role in ARDS progression and lung damage - ROS upregulate the expression of pro-inflammatory cytokines and adhesion molecules amplifying the tissue damage and pulmonary edema
- Prostaglandins , particularly those of the E series (PGE), are pro-inflammatory mediators, and elevated levels can contribute to the inflammatory cascade seen in ARDS, leading to lung tissue damage and impaired gas exchange
- Neutrophils are activated, release inflammatory mediators like cytokines (TNF-alpha, IL-1, IL-8) and chemokines, which recruit additional inflammatory cells to the lungs
- inflammatory mediators damage the pulmonary endothelial cells lining the capillaries, causing increased permeability and allowing fluid to leak into the alveolar spaces
primary emphysema
- related to smoking AND … by a mutation in the SERPINA1 gene, which is located on the 14th chromosome. This mutation results in a deficiency of alpha-1-antitrypsin, a protein that protects the lungs from damage
TB’s evading mechanisms
- Phagosome manipulation: Mtb can block the fusion of phagosomes with lysosomes, which prevents the organism from being exposed to bactericidal components
- Modulation of autophagy : Mtb can modulate autophagy, which is a process that kills intracellular pathogens in autophagic lysosomes
- Hijacking the host's ubiquitin: Mtb can hijack the host's ubiquitin to prevent inflammatory responses
- Interference with antigen presentation: Mtb can interfere with the presentation of antigens to T cells, which can prevent or alter the quality of T-cell responses
- Disrupting innate responses : Mtb can disrupt innate responses such as apoptosis, inflammasome activation, and the production of antimicrobial peptides
- Inducing detrimental cytokine secretion: Mtb can induce the secretion of detrimental type I interferon or excessive TNF
- Impairing dendritic cell maturation : Mtb can impair or misregulate dendritic cell maturation
- Delaying CD4 T cell priming: Mtb can delay the priming of CD4 T cells
TB - how does mycobacterium tuberculosis remain in system w/o symptoms?
- isolation of bacteria: immune system successfully "walls off" the bacteria in latent infection
hydrothorax aka hepatic hydrothorax :
- first-line treatments: Na restriction, diuretics, thoracentesis
- second line: transjugular intrahepatic portosystemic shunt (TIPS), repeated thoracentesis, pleurodesis, chronic indwelling pleural catheter placement
- transudate : watery fluid that diffuses out of capillaries beneath the pleurae
- associated with CV disease causing HTN, liver or kidney diseases that disrupt plasma protein production, causing hypoproteinemia → decreased oncotic pressure
pneumothorax management
- O2: can help the lung re-expand and speed up air reabsorption
- thoracentesis/needle aspiration to remove air from the chest
- chest tube drainage to reduce air in the pleural space and help lung re-expand and heal
- chemical pleurodesis: talcum powder or doxycycline, is used to attach the lung to the chest cavity to prevent future collapse
- surgery/ video-assisted thoracoscopy (VATS)
empyema : collection of pus in the pleural space
osteoblasts: actively synthesize and secrete the components of the bone matrix, including collagen fibers and calcium phosphate minerals, leading to new bone formation
osteocytes: once osteoblasts become surrounded by the bone matrix, they transform into osteocytes which reside in small spaces called lacunae and are connected to each other through canaliculi for nutrient exchange
osteoclasts: large cells responsible for bone resorption, breaking down old or damaged bone tissue to release calcium into the bloodstream
process of bone healing / stages
- Hematoma Formation (Initial Stage): bone breaks, blood vessels are damaged, causing bleeding and forming a blood clot (hematoma) at the fracture site. Clot acts as a temporary stabilizer for the broken bone ends
- Soft Callus Formation (Reparative Stage): inflammatory cells arrive at the fracture site, cleaning up debris and initiating the formation of granulation tissue. Osteoblasts and chondroblasts begin producing a soft, cartilaginous tissue called a "soft callus" which helps bridge the gap between the broken bone ends. New blood vessels develop to supply nutrients for healing
- Hard Callus Formation (Ossification): soft callus gradually transforms into a hard callus as osteoblasts deposit minerals like calcium, forming new bone tissue. This hard callus is not yet fully shaped and provides stability to the fracture site.
- Bone Remodeling: the hard callus is remodeled by osteoclasts and osteoblasts to reshape the bone, restoring its original structure and strength. This stage can last for months or even years depending on the severity of the fracture.
types of joints/arthroses
rhabdomyolysis patho
- damaged muscle releases toxic proteins and electrolytes into the bloodstream
- calcium imbalance: muscle injury causes calcium ions to leak into the intracellular space, which activates proteases and increases muscle cell contractility
- muscle cell death: inc calcium causes a pathologic interaction of actin and myosin, which leads to muscle cell death
- release of intracellular components: damaged muscle cells release substances like myoglobin, creatine kinase, aldolase, and lactate dehydrogenase into the bloodstream.
- kidney damage: excess substances released by damaged muscles can cause kidney damage
bone density T-score between -1 and -2.5 indicates osteopenia (low bone mass), while a T-score of -2.5 or lower indicates osteoporosis
- T-score of -1 or higher is normal bone density
most common initial sign of osteoporosis - broken bone
osteoporosis risk factors: early menopause, low E/T, family history, white or asian, low peak bone mass, inadequate calcium or vit. D intake, low body weight, hypogonadism, endocrine diseases (hormone imbalances, diabetes, hyperparathyroidism, hyperthyroidism), medications (such as heparin, corticosteroids, phenytoin, barbiturates, lithium), and other substances (including tobacco and ethanol), also rheumatoid disease, HIV, malignancies, malabsorption syndromes, liver or kidney disease
osteomyelitis patho
- what causes blockage of small vessels within the bone
osteosarcoma - characteristic S/S: pain prior to soft tissue swelling and an enlarging bone mass
- x ray findings - management: systemic chemotherapy and surgery
- high levels of alkaline phosphatase (AP) and lactate dehydrogenase (LDH), biopsy
osteoarthritis
- initial S/S: “Pain and stiffness in one or more weight bearing or load-bearing joints are often the first symptoms of the disease”
- pain, especially when moving the joint, stiffness, especially after resting, swelling around the joint, especially after use, feeling like the joint is unstable, reduced ability to move the joint
- initial management: weight loss, physical therapy & exercise, vit. D, K, chondroitin
gout dietary changes, fluid intake recommendations
- no alcohol, decrease purine-rich foods, such as organ meats, pork, some fish
- decrease sugar-sweetened foods and high fructose
- dairy, coffee, vit. C are protective against gout
endometriosis: DNC or C-section can precipitate endometriosis
endometrial cancer risk factors
- obesity and increased estradiol levels
- estrogen w/o progesterone to oppose it, never being pregnant, early menarche, late menopause
- sedentary lifestyle
- PCOS
- postmenopausal (peak 50s - 60s)
- incidence higher in white women, mortality higher in Black women
- diabetes, gallbladder disease, and hypertension
testicular cancer s/s: painless testicular enlargement
cryptorchidism inc risk of testicular cancer
BPH - urine stream narrows, dribbling of urine
- does not block urethra completely
bacterial prostatitis s/s, confirmatory diagnostic measure
- systemic signs of infection and a positive urine culture
syphilis stages:
- Stage I, primary syphilis—local invasion: Treponema pallidum multiplies in epithelium, producing granulomatous tissue reaction (chancre); lymph-containing microorganisms drain into adjacent lymph nodes and stimulate immune responses. painless lesion/bump in genital area, can mistake for ingrown hair
- Stage II, secondary syphilis—systemic disease: blood-borne bacteria spread to all major organ systems; immune system suppresses infection and symptoms regress spontaneously. low fever, malaise, sore throat, rash on palms and soles of feet
- Stage III, latent syphilis—silent infection: transmission of infection possible even though there are no clinical signs of infection
- Stage IV, tertiary syphilis—noninfectious disease: significant morbidity and mortality occur; destructive skin, bone, and soft tissue lesions, or gummas, result from severe hypersensitivity; cardiovascular complications (aneurysms, heart valve insufficiency, heart failure) and neurosyphilis develop
- treatment - penicillin G
- if allergic - doxycycline is alternative
- pregnant - desensitize against penicillin, treat in hospital
herpes & herpetic lesions, s/s, treatment
- virus affecting nerve endings
- Regulating alveolar size: surfactant spreads out over the surface of the liquid as the alveoli increase in size, which slows down their expansion, causing all the alveoli to expand at the same rate
- prevents excess fluid accumulation
pulmonary microbiome - lungs are not sterile
heart failure and dyspnea
bronchiolitis - common among newborns, prematurity
- diffuse inflammation of the small airways or bronchioles
- RSV
- rapid ventilatory rate; marked use of accessory muscles; low-grade fever; dry, nonproductive cough; and hyperinflated chest
pneumoconiosis:
- represents any change in the lung caused by inhalation of inorganic dust particles
- treatment: bronchodilators, oxygen therapy, pulmonary rehabilitation, anti-fibrotic agents, lung transplant
acute viral bronchitis common s/s: coughing, with or without mucus, chest soreness, feeling tired, mild headache, mild body aches, sore throat
- lower lung involvement is rare
pneumococcal pneumonia classic s/s, patho:
- community-acquired pneumonia Streptococcus pneumoniae bacteria that produces a lobar pneumonia healing by resolution
- chest pain with breathing, SOB, tachypnea, malaise, in the elderly, drowsiness, confusion, or AMS, typically a preceding viral illness followed by fever with chills and rigors, shortness of breath, and an increasingly productive cough,sometimes with blood or rust-colored phlegm, empyema
- pneumococci can colonize the nasopharynx of 5–90% of healthy people
- invade the bloodstream and cross the blood-brain barrier
- can establish intracellular niches to evade the immune system, can survive in vacuoles within host cells
- cause inflammation which can lead to difficulty breathing
- 4 phases: consolidation, red hepatization, gray hepatization, resolution
- adherence to alveolar macrophages: exposure of cell wall components
- inflammatory response: attraction of neutrophils, release of inflammatory mediators, accumulation of fibrinous exudate, red blood cells, and bacteria
- red hepatization and consolidation of lung parenchyma
- leukocyte infiltration
- gray hepatization and deposition of fibrin on pleural surfaces, phagocytosis in alveoli
- resolution of infection: macrophages in alveoli ingest and remove degenerated neutrophils, fibrin, and bacteria
- after beginning antibiotic treatment, pneumolysin is released from the lysed bacterial cells - cytotoxic to all lung cells - worsens clinical symptoms
- usually limited to 1-2 lobes
functions of sex hormones (androgens in women, estrogens in men?)
androgens: maintenance of reproductive competency, cardiac health, appropriate bone remodeling and mass retention, muscle tone and mass, and brain function, contribute to prepubertal growth spurt, pubic and axillary hair growth, and activation of sebaceous glands
estrogens: maintaining bone health, regulating sperm production, supporting healthy cardiovascular function, influencing sexual behavior and libido, and contributing to proper brain development
factors influencing puberty
precocious puberty concerns:
- diagnosing and treating intracranial disease, arresting maturation until developmentally appropriate, maximizing eventual adult height, and reducing emotional problems
- central precocious puberty: treated with GnRH agonist analogs, which induce reversible, selective suppression of the HPG axis
PCOS usual s/s: irregular ovulation, elevated levels of androgens (e.g., testosterone), and the appearance of polycystic ovaries on ultrasound
- anovulation, hyperandrogenism, and insulin resistance and include dysfunctional bleeding or amenorrhea, hirsutism, acne, acanthosis nigricans, and infertility
secondary amenorrhea (cessation of periods for 3+ months) causes:
- Pregnancy
- Hormonal changes
- Rapid weight loss or gain
- Medications for schizophrenia or psychosis
- An overactive thyroid gland
- Polycystic ovarian syndrome (PCOS)
- Reduced ovarian function
cystocele: descent of a portion of the posterior bladder wall and trigone into the vaginal canal
rectocele: bulging of the rectum and posterior vaginal wall into the vaginal canal
- clue cells are considered pathognomonic for BV
- vaginal epithelial cells that are covered with bacteria, causing them to look as if they were sprinkled with pepper
bursitis s/s: dull, achy pain that can occur in or around the joint, or even in the surrounding area, swelling, stiffness, redness, warmth, difficulty moving, fever, pain at night
pap smear mild dysplasia - may clear if healthy and nonsmoking
- does not require intervention
aging and pulmonary system function and elasticity dec w age
trichomoniasis (parasite) classic s/s in women? yellow/green discharge, strawberry spots on cervix
- mainly asymptomatic
- itching, burning, redness or soreness of the genitals, discomfort when peeing
- clear, white, yellowish, or greenish vaginal discharge, fish smell
how bronchi are situated/angled R vs L
- reasons for types of respiratory conditions R vs L
- based on anatomy
- Right main bronchus: short, wide, and vertically oriented bronchus leads to the right lung. It's more directly in line with the trachea than the left main bronchus - right lung more likely to have aspirational problems
- Left main bronchus: long, narrow, and more horizontally oriented bronchus leads to the left lung. The heart's position causes the left lung to be longer and narrower than the right lung
