Lecture 17- Cardiovascular Diseases Flashcards
(27 cards)
Cardiovascular system and lymphatics system
Blood= transports nutrients to + wastes from cells
Lymphatics= transport interstitial fluid to blood
Lymph nodes= contain fixed macrophages
Sepsis + Bacteraemia
Bacteraemia = presence of viable bacteria in the blood
Septicaemia= multiplication of bacteria in the blood
Sepsis= systemic inflammatory response to septicaemia
- increased/decreased temp or leukocyte count, tachycardia + rapid breathing
Severe sepsis= decrease in bp
Septic shock= low bp cannot be controlled
Sepsis causes
Predominantly bacterial
Decline in incidence of gram - sepsis
Major pathogenic pathways of sepsis;
Bacteria- enters sterile site + are detected by resident cells initiating an inflammatory response
Additional cells= recruited to site of inflammation to assist in pathogen eradication
Physiological alterations in the patient as a result of the inflammatory response cause physiological alterations (sepsis)
Suspected infection
Examination; temp, heart rate, respiratory rate, rash, bp + confusion -> sepsis
Management;
High-flow O2, blood culture + source control, IV antibiotics, IV fluid resuscitation etc
Slide 6
E.coli = largest single organism + is the most common cause of Bacteraemia in high income countries
Puerperal sepsis
Childbirth fever
-streptococcus pyogenes
- transmitted to mother during childbirth by attending physicians and midwives
Bacterial infections of the heart
Endocarditis= inflammation of the endocardium; cells that line the heart
Subacute bacterial endocarditis= alpha-haemolytic streptococci from other infections; develops slowly
Acute bacterial endocarditis= staphylococcus aureus from mouth; rapid development
Endocarditis
Blood clots can protect bacteria from phagocytes
^ forms patches of tissue associated bacteria called vegetations
Damage to heart in part from immune response = can require heart valve replacement
Symptoms;
- high temp, chills, loss of appetite + unexplained weight loss, headache, muscle pain, night sweats, shortness of breath + heart murmurs
Pericarditis
Inflammation of the pericardium; sac-like covering of the heart
Caused by= bacterial, fungal/ viral infections
Common viral pathogens; coxsackievirus, cytomegalovirus, herpesvirus + HIV
Bacterial pathogens; staphylococcus, pneumococcus or tuberculous pericarditis
Fungal pericarditis= due to histoplasmosis
Arthropod transmitted disease
Wide range of blood borne diseases transmitted by arthropods; insects etc
2 hosts= human and animal
Plague
Yersinia pestis, gram - rod
Reservoir; rats, vector
Bubonic plague; bacterial growth in blood + lymph
More= slide 23
Lyme disease
Borellia burgdorferi
Reservoir= deer
Vector= ticks
Common = England + wales
Commonly diagnosed= summer period
First symptom; bulls eye rash + flu like symptoms
Paralysis of the facial muscles; typically on one side of the face; bells palsy
Nerve pains; sharp/prickly
More serious symptoms;
Pain + swelling in joints; inflammatory arthritis
Problems affecting the nervous system; numbness etc
Meningitis; severe headache
Eye problems, patches of abnormal skin+ heart problems
Long term chronic symptoms
Some persist- if treatment is late
Long term impacts; fatigue, joint + muscle pain, poor sleep etc
Human herpes virus 4 infections
Slide 32
Infectious mononucleosis
Symptoms; extreme fatigue, fever, sore throat, aches, swollen lymph nodes etc
Recover= 2 weeks may take longer
Diagnosed= via symptoms
Blood work may show; inc white blood cell count, atypical lymphocytes etc
Burkitt’s lymphoma
Cancer of the lymphatic system
3 clinical variants;
*endemic variant= seen in children in malaria endemic areas
- chronic malaria believed to reduce resistance to EBV
*sporadic variant= seen in places where malaria is non-endemic
- less commonly associated with EBV
*immunodeficient- associated= associated with HIV/ post-transplantation pts
- makes up 40% of HIV infection
Cytomegalovirus infections
Cytomegalovirus; human herpesvirus 5
Infected cells swell
Transmitted via body fluids
Latent in white blood cells; permanent infection
May be asymptomatic/mild; temp, tiredness etc
Can cause serious illness in babies/immunocompromised; transmitted across the placenta
Congenital cytomegalovirus infections
Common infection passed from mother to child
Range of other rare impacts; learning delay, microcephaly + visual impairment
Detected at birth via; blood, urine, saliva test or via a scan
Antivirals= reduce the severity of the infection; not a cure
Viral haemorrhagic fevers
Severe life threatening viral diseases
Enveloped RNA viruses; families arenaviridae, filoviridae, hantaviridae and flaviviridae
Symptoms start general then progress to vascular leakage
Severe symptoms; bleeding under skin, in internal organs + from body orifices
Rare in UK
Capable of person-to-person spread
Lassa fever, Crimean/congo haemorrhagic fever, Ebola + Marburg viruses = treated very seriously
Ebola vaccination
Ervebo; most advanced development stage
- recombinant, replication-competent viral vector vaccine
HIV/AIDS
Retro-viral disease of wbc
Targets any cell expressing CD4l CD4 glycoprotein expressed on the surface of wbc, T helper cells, macrophages, dendritic cells etc
Destruction of CD4 cell population;
- direct viral impact
- host immune response
Immune effects due to HIV infection
Progression of HIV infection -> AIDS
HIV destroys infected cells through cell lysis
Half life of an actively infected T cell= less than 1.5 days
Humoral + cell-mediated immune responses destroy the infected CD4 cells; gradual decline of wbc
- generally impaired immune system
- transition from HIV -> AIDS
Treatment of HIV
Fever, headache, tiredness + enlarged lymph nodes
Treatment;
Cure of HIV= not possible
Viral replication cannot be completely suppressed
Antiretroviral therapy aims;
- suppress viral replication
- restore and/or preserve immune function
- improve quality of life
- reduce HIV- associated morbidity + mortality
PrEP
HIV pre-exposure prophylaxis (PrEP)
Antiretrovirals; tenofovir + emtricitabine
Drug targets
Nucleoside reverse transcriptase inhibitors; NRTIs
Nucleotide reverse transcriptase inhibitors; NtRTIs
Non-nucleoside reverse transcriptase inhibitors; NNRTIS
Protease inhibitors
Fusion + entry inhibitors
Integrase inhibitor
Drug classes
Nucleoside/nucleotide reverse transcriptase inhibitors; cytidine, guanosine, thymidine + adenosine
Non-nucleoside/nucleotide reverse transcriptase inhibitors; bind to the reverse transcriptase enzyme, altering its conformation to prevent DNA building
Protease inhibitors; prevent formation of the mature virion
Fusion and entry inhibitors; targets the CCR5 co-receptor needed for viral entry
Integrase inhibitors; prevent the integration of viral DNA into the cell DNA
Inhibits reverse transcriptase (RT); responsible for viral RNA being reverse transcribed to cDNA
