Reviewing Flashcards
Cryptogenic organizing pneumonia (COP) CLINICAL FEATURES
Same as bronchiolitis obliterans organizing pneumonia (BOOP)
Malaise, fevers and cough.
Their cough may be dry or productive.
Sputum may be of clear or discolored.
Typically discloses inspiratory crackles, but the exam can be normal.
Fifth to sixth decade of life
Cryptogenic organizing pneumonia Risk factors:
Rheumatoid arthritis
Granulomatosis with polyangiitis and polymyositis
Dermatomyositis
After radiation exposure to lung
Secondary to some medications
Smoking is not considered a risk factor
Cryptogenic organizing pneumonia (COP) Investigations
CXR
FBE, ESR, and CRP
Torax CT
PFT
Bronchoscopy with bronchoalveolar lavage
Lung Biopsy
Diagnosed only after exclusion of any other possible etiology
Cryptogenic organizing pneumonia (COP) Differential
Disruption of the normal lung architecture should also lead to consideration of an alternative diagnosis like Usual Interstitial Pneumonia (UIP) or other Idiopathic Pulmonary Fibrosis (IPF).
Cryptogenic organizing pneumonia (COP) Chest X-ray features
Single or multifocal air space opacities.
Patchy diffuse consolidations mostly involve bilateral lower zones.
Nodular opacities: Migratory, irregular, or linear.
Pleural effusions can also be seen.
Cryptogenic organizing pneumonia (COP) Bloods results
White cell count is typically elevated with neutrophilia.
ESR and CRP are commonly elevated.
When COP is suspected then testing for autoimmune diseases should be undertaken.
Cryptogenic organizing pneumonia (COP) Torax CT features
Atoll sign, also known as the reverse halo sign: Dense outer rim of consolidation around a focal ground-glass opacity.
Non-sensitive or specific. Can be seen in other infectious and inflammatory conditions.
Cryptogenic organizing pneumonia (COP) Pulmonary Function Test features
Typically reveals a restrictive defect with diffusion impairment
Cryptogenic organizing pneumonia (COP) Bronchoscopy with bronchoalveolar lavage Features
Performed to rule out infections, pulmonary hemorrhage, and malignancy.
In COP: Mixed cellularity with neutrophils, lymphocytes, and eosinophils. Significant lymphocyte elevation (approximately 40%) is typical, and CD4/CD8 ratio reveals CD8 predominance.
Cryptogenic organizing pneumonia (COP) Lung Biopsy Features
DEFINITIVE DIAGNOSE: Formation of organized buds of granulation tissue obstructing the alveolar lumen and bronchioles. Leakage of plasma proteins into the alveolar space, results as organized plugs of intraluminal granulation tissue are known as Masson bodies
IMPORTANT NOTE: Treatment can be started without a lung biopsy, after discussion with the patient.
Cryptogenic organizing pneumonia (COP) TREATMENT
Prednisone 1 mg/kg per day and weaning over 6 to 12 months
Second-line agents Cyclophosphamide and Cyclosporine A
Cryptogenic organizing pneumonia (COP) Prognosis
Generally excellent with a good response to systemic corticosteroids
PNEUMONIA MOS COMMON CAUSES (Microorganisms)
Neonatal Respiratory Distress DIFFERENTIALS
ASTHMA: Salbutamol dose
ASTHMA: Management of mild-moderate ATTACK
ASTHMA: Management of SEVERE ATTACK
TUBERCULOSIS DIAGNOSE ALGORITHM
Erythema nodosum SLIDE
Tuberculosis: Ghon focus
DRUGS that produce gynecomastia
Ostoporosis RISK FACTORS
Diet- low in calcium
Low BMI < 19
Lack of exercise
Inadequate exposure to sunlight
SAD and excessive coffee intake
Medications: glucocorticoids, anticonvulsants (phenothiazines), GnRh, aromatase inhibitors (Letrozole, Anastrozole, Exemestane), heparin, Depo, thiazolidinedions (glitazones), PPI’s
Medical conditions: hyperthyroidism, hyperparathyroidism, chronic liver or renal disorders, rheumatoid arthritis, coeliac disease
Menopause
Family history
Ostoporosis First Investigation
25 hydroxy Vitamin D
Ostoporosis Best Investigation
DEXA Scan (Don’t take Ca 24 hours before)
- T-score:
> -1: Normal, - 0.9 to -2.4: Osteopenia
< -2.5: Osteoporosis - Z score: ≤ -2: Investigation for underlying causes
OSTEOPENIA CRITERIA FOR TREATMENT
T score between -1 and -2.5 without minimal trauma fracture
Treat with calcium and Vitamin D supplementation and lifestyle modifications:
1200- 1500 mg/day of calcium
800- 2000 IU/day of Vitamin D
Osteoporosis CRITERIA FOR TREATMENT
Any man or woman with spine or hip fractures after minimal trauma even if the T score is more than -2.5. Treatment may be initiated without confirmation of low bone mineral density.
No fracture but score < or equal to -2.5 if risk factors are present
Osteoporosis due to secondary causes
Treatment with medications has to be started along with Calcium and Vitamin D supplementation
1200- 1500 mg/day of calcium
800- 2000 IU/day of Vitamin D
Notes: Medications increase bone density in the hip approximately by 1-3% and in the spine by 4-8% over 3-4 years
Osteoporosis FIRST-LINE Treatment
- Bisphosphonates
- Alendronate
- Risedronate
- Zoledronic Acid - Denosumab
- Strontium ranelate
- Raloxifene
- MHT
Osteoporosis Treatment: BISPHOSPHONATES General Features
- Decrease bone loss and increase mineral density.
- Measure Vit D and RFT before starting the treatment.
- Useful for vertebral & non-vertebral fractures.
- Contraindicated in pregnancy because it’s teratogenic.
- Side Effects: GI discomfort, oesophagitis, and jaw necrosis
Osteoporosis FIRST-LINE Treatment: BISPHOSPHONATES Alendronate & Risedronate
- Alendronate - weekly dose
- Risedronate - daily/weekly/monthly
For 5 to 10 years in postmenopausal women.
Osteoporosis FIRST-LINE Treatment: BISPHOSPHONATES Zoledronic Acid
Annual infusion for a maximum of 3 years.
Used if patients have Oesophagitis.
Vitamin D levels should be corrected to 50nmol/L before starting the treatment.
Osteoporosis FIRST-LINE Treatment: Denosumab
- Monoclonal antibody against osteoclast.
- Given as 6 monthly injections subcutaneously for 36 months.
- No gastrointestinal side effects.
- But increases hypocalcemia.
Osteoporosis FIRST-LINE Treatment: Strontium ranelate
Given orally 2 grams/day.
Should not be given with calcium supplements.
Reserved for severe osteoporosis because can cause MI
- Contraindications:
- DVT
- Prolonged immobilisation
Osteoporosis FIRST-LINE Treatment: Raloxifene
- Selective estrogen receptor modulator
- Oestrogen-like effect on bone but antagonistic for uterus and breast.
- Can be considered as second-line treatment for postmenopausal women with osteoporosis at risk of breast cancer.
- Reduces risk of vertebral fractures.
Osteoporosis FIRST-LINE Treatment: MHT
In peri or postmenopausal women with osteoporosis associated with other menopausal symptoms
Osteoporosis SECOND-LINE Treatment
Teriparatide:
- Is a recombinant parathyroid hormone.
- Stimulates bone-forming cells.
- Only if other treatments fail.
- Given as daily injections subcutaneously for 18 months.
INDICATIONS: > 1 symptomatic new fracture after 12 months of biphosphonate or if T score is ≤-3
OSTEOPOROSIS
Treatment for people with special circumstances: Corticosteroid therapy
All people above 50 years on corticosteroid therapy of 7.5 mg/day for at least 3 months with a T score of -1.5 or less have to be given bisphosphonates for the duration of therapy.
- First-line: Alendronate and risedronate with adjuvant Calcium and Vit D.
- Second-line: Zoledronic acid.
OSTEOPOROSIS
Treatment for people with special circumstances: Renal impairment
Raloxifene or Denosumab.
Osteoporosis Treatment Follow-up
Repeat DEXA in 2 years.
Every year if medication is changed, termination of the treatment or high-risk patient.
Osteopenia Follow-up
Repeat DEXA every 2 - 5 years
CTG Baseline rate of the fetal heart
Normal: 110-160 bpm
Fetal tachycardia: > 160 bpm
Fetal bradycardia: < 110 bpm.
Severe prolonged: < 80 bpm for more than 3 minutes (severe hypoxia)
CTG Fetal tachycardia CAUSES
- Fetal hypoxia
- Chorioamnionitis
- Hyperthyroidism
- Fetal or maternal anaemia
- Fetal tachyarrhythmia
CTG Fetal Bradycardia CAUSES
100-120 bpm:
1. Postdate gestation
2. Occiput posterior or transverse presentations
Severe prolonged:
1. Prolonged cord compression
2. Cord prolapse
3. Epidural and spinal anesthesia
4. Maternal seizures
5. Rapid fetal descent
CTG Variability Criteria
Normal: 5-25 bpm (Reassuring)
Non-reassuring:
Less than 5 bpm for 50 min
More than 25 bpm for 25 min
Abnormal:
Less than 5 bpm for more than 50 min
More than 25 bpm for more than 25 m
Sinusoidal
CTG Reduced variability CAUSES
- Fetal sleeping: this should last no longer than 40 minutes (this is the most common cause)
- Fetal acidosis (due to hypoxia): more likely if late decelerations are also present Fetal tachycardia
- Drugs: opiates, benzodiazepines, methyldopa and magnesium sulphate
- Prematurity: variability is reduced at earlier gestation (<28 weeks)
- Congenital heart abnormalities
CTG Accelerations Criteria
Accelerations are an abrupt increase in the baseline fetal heart rate of greater than 15 bpm for greater than 15 seconds
The presence of accelerations is reassuring
Accelerations occurring alongside uterine contractions is a sign of a healthy fetus.
CTG Decelerations Definition
Abrupt decrease in the baseline fetal heart rate of greater than 15 bpm for greater than 15 seconds.
CTG Early Deceleration Features
Start when the uterine contraction begins and recover when uterine contraction stops.
Physiological due to increased fetal intracranial pressure
CTG Variable Deceleration Features
Rapid fall in baseline fetal heart rate with a variable recovery phase.
Variable in their duration and may not have any relationship to uterine contractions.
CTG Variable Deceleration CAUSES
- Reduced amniotic fluid volume
- Umbilical cord compression
CTG Shoulders of Variable Deceleration MEANING
Accelerations before and after a variable deceleration. Indicates the fetus is not yet hypoxic and is adapting to the reduced blood flow. Without the shoulders, suggests the fetus is becoming hypoxic
CTG Variable Deceleration 1st management
Variable decelerations can sometimes resolve if the mother changes position
The presence of persistent variable decelerations indicates the need for close monitoring.
CTG: Late deceleration Features
Begin at the peak of uterine contraction and recover after the contraction ends.
Indicates: Insufficient blood flow through the uterus and placenta
(Danger of fetal hypoxia and acidosis).
CTG: Late deceleration CAUSES
o Maternal hypotension
o Pre-eclampsia
o Uterine hyper-stimulation
CTG: Late deceleration MANAGEMENT
The presence of late decelerations is taken seriously and foetal blood sampling for pH is indicated.
If foetal blood pH is acidotic it indicates significant foetal hypoxia and the need for emergency C-section.
CTG: Prolonged deceleration
A deceleration that lasts more than 2 minutes.
If it lasts between 2-3 minutes it is classed as non-reassuring
If it lasts longer than 3 minutes it is immediately classed as abnormal
Action must be taken quickly: Fetal blood sampling or emergency C-section
CTG: ABNORMAL Deceleration Features
Variable decelerations with any concerning characteristics in over 50% of contractions for 30 minutes (or less if any maternal or fetal clinical risk factors).
Late decelerations for 30 minutes (or less if any maternal or fetal clinical risk factors).
Acute bradycardia, or a single prolonged deceleration lasting 3 minutes or more.
CTG Sinusoidal pattern FEATURES
This type of pattern is rare, however if present it is very serious.
It is associated with high rates of foetal morbidity & mortality
It is described as:
o A smooth, regular, wave-like pattern
o Frequency of around 2-5 cycles a minute
o Stable baseline rate around 120-160 bpm
o No beat to beat variability
CTG Sinusoidal pattern INDICATES
o Severe foetal hypoxia
o Severe foetal anaemia
o Foetal/maternal haemorrhage
Immediate C-section is indicated
Diabetes Mellitus Diagnose
FBG:
- If ≥7: DM
- If 5.5-6.9 —->OGTT
OGTT
- If ≥ 11.1: DM
- If 7.8-11Retest in a year
- if ≤7.7: Retest in 3 years
HbA1c:
- If ≥6.5: DM
- If 6-6.4: retest in 1 year
- If ≤5.9 retest in 3 years
Diabetes Mellitus Diagnose FLOW CHART
Gestational Diabetes Diagnose
Gestational Diabetes Risk factors
Diabetes Mellitus Screening
People with known impaired fasting glucose/glucose tolerance (‘prediabetes’)
Age >40 years
> 30 years: family history (first-degree relative with T2D), obesity (BMI >30), high-prevalence ethnic groups
Age >18 years in Aboriginal and Torres Strait Islander people
Previous gestational diabetes
People on long-term steroids or antipsychotics
Polycystic ovarian syndrome, especially if overweight
Previous cardiovascular event
The optimal frequency is every 3 years from age 40 years using AUSDRISK
If the score is ≥12, do fasting blood glucose or HbA1c.
Screen annually in very high-risk groups (including Aboriginal and Torres Strait Islander people and those with prediabetes)
Diabetes Mellitus T2 Treatment: Metformin side effects
*gastrointestinal adverse effects
*vitamin B12 deficiency
*lactic acidosis (rare)
CI: Renal Impairment GFR< 30 and liver impairment
Diabetes Mellitus T2 Treatment: Thiazolidinediones
GLITAZONE
Side Effects:
Weight gain
Dyslipidemia, CV disease
Osteopenia
Pioglitazone:
Risk for bladder cancer
Rosiglitazone:
Edema —>CHF
MI, Stroke
Diabetes Mellitus T2 Treatment: SGLT2
GLIFOZIN
dapagliflozin
empagliflozin
ertugliflozin
Advantages:
weight loss
reduce the rate of secondary cardiovascular events, including
overall mortality
reduce blood pressure
slow the progression of kidney disease
Side effects:
Genital infections (candida)
UTI
reversible increase in creatinine
volume depletion (rare)
diabetic ketoacidosis (uncommon), which may occur without hyperglycemia
Diabetes Mellitus T2 Treatment: Sulfonylureas
IDE
gliclazide
glipizide
glibenclamide
glimepiride
Side effects:
HYPOGLYCEMIA
Weight gain
Dermatological allergic reactions
Diabetes Mellitus T2 Treatment: DPP-4 inhibitors
GLIPTINE
alogliptin
linagliptin
saxagliptin (CI Heart failure)
sitagliptin
vildagliptin
Weith loss
avoid in patients with acute pancreatitis or history of pancreatitis
Side effects:
Headache
Mild respiratory and urinary infections
Weight neutral
Contraindications in Pregnancy and breastfeeding
Diabetes Mellitus T2 Treatment: GLP-1 receptor agonists
TIDE
dulaglutide
exenatide
liraglutide
Subcutaneous administration
Advantages:
weight loss
improve postprandial glucose control
reduce the rate of secondary cardiovascular events, including
overall mortality (liraglutide)
slow the progression of kidney disease (dulaglutide, liraglutide)
CI:
* Acute pancreatitis or history of pancreatitis
* Family history of medullary thyroid cancer or multiple
endocrine neoplasia syndrome type 2 (liraglutide)
* Severe kidney impairment (dulaglutide, exenatide)
* End-stage kidney disease (liraglutide)
MASTITIS Management
∗ Continue breast feeding from affected breast
∗ Place hot washers over breast before starting to feed and cold packs after feeding
∗ Antibiotics: Dicloxacillin Flucloxacillin Cephalexin for 5 days
∗ Analgesics
∗ Check breast feeding technique
∗ Review in 24- 48 h
∗ Basic blood tests and U/S if doubtful of breast abscess or in 48
hours if mastitis is not responding to antibiotics
∗ If Candidial mastitis-Fluconazole orally
CAUSES OF POSTPARTUM FEVER
Contraindications for Tocolisis
Tetanus prophylaxis
Common causes of pneumonia by ages
Alcohol withdrawal, hallucinosis and delirium tremens timings
Cellulitis Treatment
Chronic otitis media in aboriginal treatment
Acute otitis media treatment
RHEUMATIC FEVER JONES CRITERIA
paracetamol intoxication protocol
Melanoma excision margins
NEPHRO: Genetic disorders
Testicular tumors
Glomerulonephritis by age
Nephritic Syndrome causes
Nephrotic Syndrome causes
CAUSES FOR NEPRHOTIC AND NEPHRITIC SYNDROMES
PRE RENAL, RENAL AND POST RENAL AKI
Renal tumor management
Thromboprofilaxis in pregnancy
Wernike and Korsackoff
Warfarin interactions
Jelly Fish Poisoning TABLE
Major Box Jelly Fish photo
Major Box Jelly Fish STING photo
BLUEBOTTLE JELLY FISH photo
DISFAGIA FLOW CHART 1/3
DISFAGIA FLOW CHART 2/3
DISFAGIA FLOW CHART 3/3
SEPTIC ARTHRITIS TREATMENT
Differentials between postpartum depression, blues, and psychosis
PAEDS: Dehydration severity scale
Tetanus Vaccination WOUNDS
Thyroid nodules management
Pediatric Brain Tumours (picture)
Pediatric Brain Tumours (table)
Adrenaline dosage for anaphylaxis
Prostate cancer staging
Prostate cancer Management
Hernias location
Cyanotic Congenital Heart Disease
Cholelithiasis Management flow chart
Suggested AAA surveillance (w/
US) of Abdominal Aortic
Aneurysm
3.0-3.9 cm: e/ 24m
4.0-4.5 cm: e/ 12m
4.6-5.0 cm: e/ 6m
≥5.1 cm: e/3m
If 1st degree rel has it, 20% risk
of getting it. Arrange yearly US from 50yo.
COVID High risk patients
COVID Antiviral management Outpatient
COVID antiviral Management Hospitalized
MILESTONES Gross and fine motor
important 9 and 18 months
MILESTONES language and social
important 9 and 18 months
MILESTONES Red flags
important 9 and 18 months
Autism spectrum disorder (ASD) Criteria
Asperger’s criteria
Tourette Criteria
Kids Phyc Table Dr Cintia
Bloody diarrhea differentials
DIARRHEA PART 1:
Viral
Typhoid – Enteric Fever Salmonella
Giardiasis
Amoebiasis
DIARRHEA PART 2:
Salmonella sp. (non-Typhoidal)
Shigella
E. coli
Campylobacter jejuni
DIARRHEA PART 3:
Clostridium difficile
Staph Aureus
Bacillus cereus
Clostridium sp
Clostridium botulinum
Vibrio Cholerae - Cholera
Scabies management
- Permethrin.
If no improv, repeat in 1-2w - Benzyl Benzoate
- Oral cephalexin, top mupirocin if
infection
Syphilis Clinical features (1ry, 2ry and 3ry)
- Primary: Single painless ulcer
- Secondary: Generalised
nontender lymphadenopathy,
rash in palms and soles, patchy
alopecia. - Tertiary: Neurosyphilis or
cardiosyphilis
Syphilis Investigations
FIRST: Darkfield Microscopy
BEST: RPR and Treponema pallidum hemagglutination assay (TPHA)
Both tests must be (+)
Syphilis Treatment
Benzilpenicilline
Early syphilis: Single dose
Late syphilis: once weekly for 3 weeks
Tertiary syphilis: IV 4-hourly for 15 days
NEONATAL JAUNDICE: Physiological vs Pathological
NEONATAL JAUNDICE: UNconjugated (INDIRECT) Hyperbilirubinemia CAUSES
- Physiological
- Breast milk jaundice
- Breastfeed jaundice
- Sepsis
- Metabolic:
- Gilbert’s syndrome
- Congenital hypothyroidism
- Crigler-Najjar syndrome
- Hemolytic:
- ABO/Rh incompatibility
- Spherocytosis
- G6PD deficiency
- Sickle cell anemia
NEONATAL JAUNDICE: Conjugated (DIRECT) Hyperbilirubinemia CAUSES
- Biliary atresia
- Neonatal hepatitis
- TORCH infection
- Idiopathic
- Metabolic: Galactosemia, Wilson, alpha 1antitripsine.
NOTE:
Always > 24 h
Conjugated bilirubin level >25 micromol/L because this may indicate serious liver disease
PHYSIOLOGICAL NEONATAL JAUNDICE: Characteristics
- Day 2-14 (> 21 in preterm)
- Mild
- Diagnosis of exclusion
- Resolves in 2w
- Rarely exceeds 220 micromol/L
PATHOLOGICAL NEONATAL JAUNDICE: Characteristics
- Too early < 24 hours of age
- Too Long > 10 - 14 days of age (term: 2 weeks / preterm: 3 weeks)
- Too high > 220 micromol/L
- CONJUGATED Hyperbilirubinemia
NEONATAL JAUNDICE + unwell state, suggests:
Sepsis OR GIT obstruction
NEONATAL JAUNDICE < 24-48 H UNCONJUGATED suggests:
Hemolysis
- ABO incompatibility (Most common)
- Mother: O group; Child: A or B
- Direct Coombs (+)
- Peripheral smear: Spherocytes (some) - Spherocytosis
- Peripheral smear: Predominant spherocytes
- Direct Coombs (-)
- FBE:↑ MCHC
- FxHx: Anemia/spherocytosis/gallstones - Sickle Cell
- Peripheral smear: Sickle and target cells
- Direct Coombs (-)
- African descendants - Rh incompatibility (Most severe)
- Peripheral smear: NO spherocytes
- Direct Coombs (+)
NEONATAL JAUNDICE + Family history of hemolytic disease, suggests:
G6PD deficiency
OR
Spherocytosis (FxHx of gall stones)
NEONATAL JAUNDICE + Dark urine or pale stools OR ↑ DIRECT bilirubin, suggests:
Biliary obstruction (Biliary atresia)
JAUNDICE + Plethora, suggest:
Polycythaemia
NEONATAL JAUNDICE + Hepatosplenomegaly, suggest:
Hepatitis (↑ liver enzymes)
OR
Metabolic problems (Galactosemia)
NEONATAL JAUNDICE: BILIARY ATRESIA Clinical Features (6)
- Presentation: since the 1st week
- Prolonged Jaundice (> 14 days in term and > 21 in preterm)
- Dark urine
- Clay-colored stools (even meconium is pale)
- Abdominal pain (crying on changing diapers)
- Hepatosplenomegaly ( >2cm below costal margin)
Breast Milk Jaundice Clinical features
Very common
Develops within 2-4 days of birth, may peak at 7-15 days of age, and may persist for many weeks.
No need to stop breastfeeding
Breastfeed Jaundice Clinical features
PHYSIOLOGICAL NEONATAL JAUNDICE: Mechanism (3)
- Shorter lifespan of neonatal red blood cells
- Immature liver function at birth
- A relatively high concentration of β-glucuronidase in the small intestine
PHYSIOLOGICAL NEONATAL JAUNDICE: Risk factors (4)
- Preterm babies (higher bilirubin levels)
- Exclusive breastfed babies
- Babies with significant bruising or cephalohaematoma: The breakdown of RBCs within the cephalohaematoma causes higher bilirubin levels and predisposes to jaundice.
- Previous sibling with neonatal jaundice requiring phototherapy
NEONATAL JAUNDICE: BILIARY ATRESIA Best Investigation
Percutaneous biopsy (gold-standard):
Bile ductular proliferation (>specific), bile plugging, multinucleated giant cells, focal necrosis of liver parenchyma, extramedullary hemopoiesis, and inflammatory cell infiltrate.
NEONATAL JAUNDICE: Congenital Hypotiroidism Clinical features (11)
listless
Goitre
prominent tongue
hoarse cry
puffy face
constipation
umbilical hernia
hypothermia
bradycardia
dry skin
failure to thrive
NEONATAL JAUNDICE > 24-48 H ↑UNCONJUGATED, suggests:
- Physiological jaundice
Most Common cause in the first week:
- Term: 50%
- Preterm: 80%
finishes in 1-2 weeks (preterm 3 weeks) - Breast milk jaundice
Lasts up to 6 weeks
Diagnose: Suspending breastfeeding for 24-48 hrs = ↓ serum bilirubin - Neonatal sepsis
End of the first week (4-7 days old)
Lethargic + jaundice + hepatosplenomegaly
↑ BOTH, Direct and Indirect bilirubin.
NEONATAL JAUNDICE: Sepsis Management
1st Hemocultures
2nd ATB: Wich??
Biliary atresia VS Idiopathic Neonatal hepatitis
Knee trauma differentials
Pericarditis Clinical Features
Chest pain+SOB+viral infection
Kussmaul sign.
S4 Gallop: Cardiac Tamponade
Pericarditis Initial Investigations
- ECG:
- ST elevation except in AVR & V1
- Reciprocal PR - CXR:
- Pericardial fluid
- Pulmonary congestion - Echocardiogram: Is diagnostic! Chest FAST scan should be done ASAP.
- Cardiac CT
Pericarditis Causes
- Viral infection: Coxsackie B, CMV, influenza, EBV, COVID, HIV
- After a major heart attack or heart surgery: Dressler syndrome.
- Systemic inflammatory disorders: Lupus, rheumatoid arthritis.
- Trauma
Pericarditis Best Investigation
Echocardiogram with drainage and culture (Pericardiocentesis)
Pericarditis Complications
Constrictive pericarditis.
Cardiac tamponade
Pericarditis Medical Treatment
Mild to moderate Pericarditis
Colchicine + AAS or Ibuprofen
2nd line: Prednisone
If infection: ATBs and drainage
Pericarditis Surgical Treatment
Severe Pericarditis, include admision
- Cardiac tamponade: Pericardiocentesis
- Severe, Recurrent or Constrictive:
Pericardiectomy
Beck’s triad = Cardiac Tamponade
Low blood pressure (weak pulse or narrow pulse pressure)
Muffled heart sounds
Raised jugular venous pressure.
Pericarditis Physiopathology
Restrictive Cardiomyopathy
Diastolic Dysfunction with impaired filling – relaxation
Normal Ejection fraction + S4 gallop
Dressler’s Syndrome risk factors
- Young age
- B-negative blood type
- Prior history of pericarditis
- Prior treatment with prednisone
Dressler’s Syndrome Treatment
1st LINE: NSAIDs in high doses (aspirin, ibuprofen, naproxen) tapered over 4 to 6 weeks.
2nd LINE: Corticosteroids (prednisone) tapered over a 4-week period
3rd LINE: Colchicine.
Dressler’s Syndrome investigations
Gold Standard: Echocardiogram
UNSTABLE patient: bedside ultrasonographic (E-FAST)
ECG: Same pattern as pericarditis (global ST segment elevation and T wave inversion)
Dressler’s Syndrome COMPLICATION
Cariac Tamponade
Pericarditis Duration: Chronic & Acute
Acute (<6w) Chronic (>6w).
Kussmaul sign phisical exam
Paradoxical: ↑ JVP with insp and ↓ JVP with exp)
Means: constrictive and/or cardiac tamponade.
Dressler’s Syndrome definition
Pericarditis in the context of major heart attack or heart surgery
List 3 Acyanotic + 3 Cyanotic Congenital Heart Diseases
Acyanotic {Left to the right}
1. VSD - Ventricular Septal Defect*
2. ASD - Atrial Septal Defect
3. PDA - Patent Ductus Arteriosus
Cyanotic {Right to the left}
1. TOF - Tetralogy of Fallot
2. HLHD - Hypoplastic Left Heart Dx
3. TGV - Transposition of the great vessels
Congenital Heart Disease: VSD - Details & Clinical Features: Hint: different sizes may have varying clinical features
Most common congenital heart disease.
Asoc w/ Turner Sx
Presentation age: Infant 5 to 6 weeks
Clinical Features:
2-3/6 harsh holosystolic murmur heard along the LSB more prominent with small VSD and absent with very Large VSD
SMALL - Moderate: 3-6mm
- Asymptomatic
- 50% will close spontaneously at 2y
Mod - LARGE
- Symptomatic & require Sx repair
- SOB with feeding & crying
- Recurrent chest infections
- Heart failure from 3 months of age
- FTT
Congenital Heart Disease: ASD - Details & Clinical Features:
Secundum ASD – Fossa Ovalis, most common
Primum ASD – lower in position, more serious
Clinical Features:
- Initial: NO MURMUR
- PS: Systolic ejection murmur - LSB
- RV heave.
- Fixed widely split S2 (Ao then Pulm Valve closes)
- Asymptomatic or easy fatigability or mild growth failure.
High risk of developing right heart failure with pulmonary HT
Congenital Heart Disease: PDA - Details & Clinical Features:
- Persistence of the Ductus Arteriosus (PA to the Aorta)
- Normally closes in the 1st wk of life.
- Associated with Turner Sx
- Associated with Ao coarctation, VSD, and TORCH inf Rubella!!)
Clinical Features:
- Continuous machinery systolic murmur: Gibson Murmur
- Small PDA: Asymptomatic
- Large PDA: CHF, growth restriction, and FTT.
Congenital Heart Disease: TOF - Details & Clinical Features:
Most common cyanotic CHD
- Pulmonary stenosis (1st worse)
- VSD (2nd worse)
- Overriding Ao
- Right ventricular hypertrophy
Clinical Features:
- Cyanosis after the neonatal period (4m approx) and progressive
- Clubbing fingers(Scharmoth’s sing)
- Hypoxemic spells (“Tet spells”)
- Systolic ejection murmur - LSB (PS)
Congenital Heart Disease: HLHD (3)
- LV and aorta are abnormally small (hypoplastic).
- Early days (2-7d) of life & need urgent Sx to survive.
- HLH is dependent on PDA for survival
Congenital Heart Disease: TGV
The aorta arises from the RV & receives “blue” blood, whilst the Pulmonary Artery arises from the LV.
Immediately after birth, and needs urgent treatment.
Survival depends on the PDA or the FO remaining open in the early days of life until treatment.
TGV Management
- The FO can be enlarged with a catheter procedure, called Balloon
- Septostomy
TGV 1st Investigation & Diagnosis
Hyperoxia Test:
ABG after 100% oxygen for 10 minutes. PaO2 will remain low & not rise
Hyperoxia Test: Differences between Acyanotic CHD & TGV
TGV: ABG after 100% oxygen for 10 minutes. PaO2 will remain low & not rise
◦ Pulmonary disease (not cyanotic CHD) is suspected if the PaO2 increases to more than 150 mm Hg with oxygen.
Congenital Heart Disease: VSD - Management & Indications for Surgical Closure:
- Small VSD: No physical restrictions, reassurance, periodic follow-up & endocarditis prophylaxis.
- Symptomatic VSD: Medical treatment initially with afterload reducers & diuretics.
- Indications for Surgical Closure:
Large VSD w/ medically uncontrolled symptomatology &
continued FTT.
Ages 6-12 mo w/ large VSD & Pulmonary HT
Congenital Heart Disease: ASD - Management:
- Surgical or device closure for Secundum ASD
- Closure performed between ages 2 & 5 years
- Sx correction is done earlier in children w/ CHF or significant
pulmonary HTN.
NOT Endocarditis prophylaxis
Congenital Heart Disease: PDA - Management:
- Indomethacin
- Surgical: Ligation or catheter closure by insertion of a device or embolization coils.
Congenital Heart Disease: TOF - Management:
Corrective Sx at about 6 months
SVT STABLE Management
Step 1:
< 8 yo Modified Valsalva manoeuvre
> 8 yo Carotid massage
Step 2: Adenosine x 2 (2min)
Step 3: Verapamile x 2 (30 min)
Step 3: Direct current (DC) cardioversion or pharmacological cardioversion (amiodarone or overdrive pacing may be required.
Recurrent: Ablation or amiodarone
Hepatic hydatid cyst pathogen
Echinococcus tape worm
Hepatic hydatid cyst investigation
Triphasic abdominal CT Triphasic abdominal CT
Cyst aspiration
Hepatic hydatid cyst management
Albendazole
Secondary - Tertiary (Pituitary) Hypothyroidism CAUSES
Pituitary tumors
Tumors compressing hypothalamus
Sheehan syndrome
Thyroid releasing hormone (TRH) resistance
TRH deficiency
Lymphocytic hypophysitis
Radiation therapy to the brain
Drugs such as dopamine, prednisone, or opioids
Clinical features of Chronic Lower Limb Ischemia
- Claudication (pain w/ exercise
and relieved by rest), if pain at
rest: RED FLAG - Shiny hairless legs
- Muscles atrophied
Chronic Lower Limb Ischaemia referral criteria
– Rest Pain
– Ischemic ulceration
– Gangrene
– Claudication symptoms are limiting day to life, work, and there is no improvement with exercises, risk factor modifications and medical management after 6 M.
Chronic Lower Limb Ischemia initial investigation
- Measure ABI
- Duplex US (often the only imaging required to plan endovascular interventions)
Chronic Lower Limb
Ischaemia best investigation
CT Angiography w/
contrast (Contraindicated in RF)
Chronic Lower Limb Ischaemia MEDICAL Management
ABI:
1-1.4: Normal
0.9: Borderline. Nothing
<0.9:
Risk factor management
- Smoke cessation
- Antiplatelets (aspirin or clopidogrel)
- Statins (even in the absence of dyslipidemia)
- ACE Inhibitors or ARBs.
- Supervised exercise program.
The beta-blockers should be avoided until and unless they are commenced for cardioprotection.
For mixed ulcers (Do not use compression bandage if ABI <0.8)
<0.4: Urgent referral
Chronic Lower Limb Ischaemia SURGICAL Treatment
– Endovascular angioplasty or stenting
– Open surgical reconstruction by bypass or endarterectomy.
Clinical features of Acute Lower limb
ischemia
- Context of a patient with: Thrombosis (most common cause) or Embolus from AF.
- Acute onset of progressive PAIN:
- Calf: Common femoral art / Superficial femoral art (MC site of occlusion).
- Buttock: Common
iliac/external iliac Thrombosis.
- Pulselessness.
- Pallor.
- Paresthesia.
- Paralysis:
- Foot drop = Peroneal nerve paralysis.
- Most reliable sign requiring Emergency Qx intervention.
Acute Lower limb ischemia FIRST investigation
- Excersice ABI
- CT angiogram (Emergency Qx intervention) can be MRI also
- Duplex US for contrast Contraindications
Acute Lower limb ischemia BEST investigation
Digital subtraction arteriography or just arteriography
Acute Lower limb ischemia Treatment
Golden time: 4 hrs
- IV Unfractionated Heparin: 5000 IU then 1250IU/hour. APTT guides further adjustment.
- Surgical treatment:
- Embolectomy: Can cause
reperfusion injury (HyperK, metab
acid, myoglobinuria, increased CK).
Keep pt hydrated and perfused.
Can Be:
A) Angioplasty (Endovascular):
Short obstruction (<10 cm)
Aorto-Illiac location
B) Bypass (grafting)
Long obstruction (> 10 cm)
Location: Infra Popliteal or Common femoral artery
Chronic total oclusion
- Amputation is required only if there are irreversible ischemic changes.
- After acute, give warfarin for 3-6m
Esophageal dysplasia Surveillance
Hyperkalemia Management
Psudomona treatment (ATB)
Hyperparathiroidism
Vertigo differentials
Light’s criteria
Cocaine complications
Transient synovitis
HPV Vaccination
Tourette DSM-IV criteria
Kids rehydration
