CBL Semester 1 Flashcards
NYHA functional classification of Heart Failure
- HF and no limitation to physical activity
- HF and slight limitation to physical activity
- HF and marked limitation to physical activity
- HF and inability to perform physical activity
Signs of HF on CXR
Alveolar oedema
B lines (kerley) - horizontal lines near base of lungs Cardiomegally
Dilated upper vessels
Effusions (pleural)
1st line Pharmacological HF management
Start
- ACEi (ARB if intolerant)
Once stable - Beta blocker
Still symptomatic - Aldosterone antagonist (spironolactone)
Still symptomatic - Digoxin
Clinical Features of Rheumatic fever
Effects everything apart from the heart only mildly or transiently.
· General - Fever, Recent sore throat
· CNS - Chorea
· Heart - Carditis
· Joints - Pain, migratory arthritis
· Subcutaneous tissue - nodules
· Skin - rash
Rheumatic fever diagnosis criteria
Jones Criteria
Required Criteria
• Evidence of preceding strep infection/ other bacteria that cause it
○ DNAase B
○ Anti-streptolysin O
○ Positive throat culture
○ Rapid Antigen test
Major Criteria - (1 from each involved system)
- Chorea
- Carditis
- Polyarthritis
- Subcutaneous nodules
- Erythema marginatum
Minor Criteria
- Fever
- Arthralgia
- Previous rheumatic fever/ RHD
- Acute phase reactions (CRP, ESR etc)
- Prolonged PR interval
Types of vegetations of RHD and IE
RHD: warty, small along line of closure of valve leaflet
IE: Large friable can extend on chordae tendinae
Clinical Manifestations of IE
- Constitutional - Fever, Malaise, Anorexia/ weight loss
- Emboli- Splinter haemorrhages, Splenic/ renal infracts, Petechiae
- Constant bacteraemia
- IC mediated Glomerulonephritis
Diagnostic Criteria for IE
Dukes Criteria
Major Criteria
· Positive blood cultures
· Echocardiographic changes that suggest IE
Minor
· fever
· predisposing factor: (IV drug use, cardiac lesion)
· emboli evidence: · immunological problems: ( glomerulonephritis)
· positive blood culture that doesn’t meet major diagnostic criteria
Complications of IE
Local - vavular, shunting, heart block
Emboli
Immunocomplexes
Mycotic abscesses
TB medication regime
Rifampicin - 6 months
Isoniazid + VB6 - 6 months
Pyrazinamide 2 months
Ethambutol - 2 months (or until susceptibility tests back) Or streptomycin
All taken orally, daily
TB Medication AEs
Isoniazid:
- Neuropathy - prescribe with vB6 to prevent this
- Hepatitis (<1%, can be fatal)
Ethambutol:
• optic neuritis (colour vision goes first)
Rifampicin:
- staining of body fluids
- P450 inducer
- flu like symptoms - bad
Pyrazinamide:
- Hepatic toxicity,
- Hyperuricaemia
Streptomycin
• Permanent damage to vestibular nerve
Clinical features of acute leukaemia
· Abrupt, stormy onset
· Decreased marrow function (from crowding, competition for growth factors, etc) ○ Anaemia ○ Neutropenia ○ Thrombocytopenia
· Neoplastic infiltration (more in ALL) ○ Lymphadenopathy ○ Bone pain ○ Splenomegaly ○ Hepatomegaly
· CNS involvement - meneingeal spread (> in ALL) ○ Headache ○ Vomiting ○ Nerve palsies ○ Meningism
ALL treatment
Chemotherapy
- induction
- consolidation
- maintainance
Supportive
- stop uric acid rise (fluids, allopurinol)
- Antimicrobials
- Anti-chemo (semen preservation, blood + growth factors, nutrition)
BPH Investigations?
Important
- Urinalysis
- PSA
- International prostate symptom score
- Global bother score
Consider
- Uroflowmetry (pee into a container)
- US - rule out cancer CT
- Urodynamics
- Cystoscopy
BPH Treatment
Depending on IPSS
- Watchful waiting
- Lifestyle management
- Review meds
- Fluid restrictions
- Constipation management
- Urination education
- Drugs
- Alpha Blocker - 1st line
- Alpha adrenergic receptor blockers, alpha 1 is the most common type in the prostate and inhibiting this leads to smooth muscle relaxation. Also effects bladder and sphincter muscles.
- 5- Alpha reductase inhibitors - decrease DHT
- NSAIDs - improve flow and urinary symptoms
- Alpha Blocker - 1st line
- Surgery
- TURP
Prostate Cancer Metastasis sites
- Bone - most common
- Lymph nodes
- Lung
- Liver
- Brain
Heparin MOA
Increases effect of antithrombin III
Inactivates thrombin.
Decreases the conversion of fibrinogen to fibrin.
Prostate cancer treatment (apart from watchful waiting)
Original - surgery, radation
metastatic - androgen deprication
- GNRH agonist (goserelin) + anti-androgen (bicalutamide)
- OR GNRH antagonist
Catrate resistant - Chemotherapy - anthrocyclines
Bone mets- bisphosphinates, RANKLi (denosumab)
HPV protein actions
- E5 - activates growth factors
- E6 - inactivates p53
- E7 - stops retinoblastoma
Sites of Prostate cancer occurance (and %)
- Transitional zone 10-20%
- Central zone 2.5%
- Peripheral zone 70-80%
Microbial causes of UTI in males
KEEPS
Klebsiella, E.coli, Enterococcus, Proteus
Morphology of SIL
Koilocytic atypia (nuclear enlargement and variations in size and peri-nuclear halo)
Hyperchromic (dark staining)
Presence of coarse chromatin granules
Principles of Screening
- Important health problem
- Disease should have recognisable latent or early symptomatic stage
- Well understood natural hx of disease
- Treatment avaliable for those with disease
- Suitable test or examination
- Test acceptable to population
- Agreed policy on who to treat
- Facilities for diagnosis and treatment avaliable
- Costs of screening/diagnosis/treatment economically balanced with other expenses on health care
- Case finding should be a continuing process
Natural Hx of Hep B
Acute: 95% adults, 5-30% children
Chronic: 3-5% adults, 70-95% children
Natural Hx of Hep C
80% from acute to chronic
20% chronic to cirrhosis
1-4% per year HCC
Morphology of cirrhosis
Proliferation of hepatic stellate cells and conversion to fibrogenic cells
Loss of fenestration of sinusoids
Type 1 and 3 collaged deposited in space of Disse –> Bridging fibrous septae
Disruption of liver architecture
Parenchymal nodules
10 steps of outbreak investigation
1 Prepare for field work
2 Extablish existance of outbreak
3 Verify diagnosis
4 Define and identify causes
5 Describe and orient data in time, person, place
6 Develop hypotheses
7 Evaluate hypotheses
8 Refine hypotheses
9 Implement control and preventative methods
10 Communicate findings
Relative risk
Disease incidence in exposed vs Disease incidence in unexposed
a/(a+b) divided by c/(c+d)
Functions of Skin
1 Physical protection
2 Thermoregulation
3 Metabolic function (Vit D production)
4 Cutaneous sensation
5 Physiological and social functions
Local response to burns (zones)
Zone of hyperaemia - increase perfusion, will recover 7-10d
Zone of stasis - decrease perfusion, reversible with fluid or will necrose.
Zone of coagulation - point of max damage and irreversible tissue loss
Healing of burn depths
Superficial - few days
Superficial dermal - 2-3 wks, reepithelialisation, minimal scarring
Deep dermal - longer than 2-3wks, high risk of hypertrophic scarring
Full thickness - no healing, granulation and wound contraction
Microbiology of burns
Early - Gram +ve Staph aureus and strep pyogenes from sweat glands and hair follicles will colonise
Mid - Gram -ve P. aeruginosa, E.coli, Klebsiella from IT URT, hospital environment
Late - Multiresistant bacteria, Candida or Aspergillus (Fungal)
Signs of wound infection
- Change in colour, smell
- Oedema at margin
- Fever >38
- Loss of epithelium from re-epithelialised wounds
- Apprearance of new eschar
- Purulent exudate
Indications for intubation/Inhalation injury
Erythema or swelling of oropharynx
Changes in voice
Stridor tahypnoea or dyspnoea
GCS
Burns to face, neck, upper torso
Singed nasal hair
Soot, Carbonaceous sputum in mouth
Hx burns in enclosed space
Parkland formula
4ml/(%TBSA)/body weight (kg)
50% in first 8 hrs, 50% in next 16 hrs
Urine output measured at 0.5-1.0ml/kg/hr in adults
Hartmanns solution - Na+, Cl+, lactate, K+, Ca2+
Aetiology of Psoriasis
Genetic suseptibility - HLA-Cw6
Immunological- related to high levels of TNF-alpha
Strep throat infection (Guttate psoriasis)
Stress
Physical injury (koebner phenomenon)
HIV
