Lecture 17- Cardiovascular Diseases Flashcards
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
- sporadic variant
- immunodeficient- associated
^ slides 34
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; s37
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
Protease inhibitors
Prevent the assembly of new viruses
Inhibits viral protease required to cleave viral precursor proteins into virion components
Resistance appears quickly; single mutation required
Resistance to AZT= takes months
Protozoa; Toxoplasmosis
Toxoplasma gondii
Associated with cats
Mild symptoms; unless susceptible
Susceptible hosts
*Pregnant; early in = miscarriage, still birth/ birth defects
Later= complications of the infection may develop later; eye damage/risk of brain damage/blindness
*Immunocompromised; headaches, confusion, seizures, chest pains etc
- risk of permanent eye/brain damage
Malaria
Plasmodium vivax, P. Ovale, P. Malaria + P. Falciparum
Anopheles mosquito
Destruction of rbc
-rest of slides
