Reviewing Flashcards

1
Q

Cryptogenic organizing pneumonia (COP) CLINICAL FEATURES

A

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

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2
Q

Cryptogenic organizing pneumonia Risk factors:

A

Rheumatoid arthritis
Granulomatosis with polyangiitis and polymyositis
Dermatomyositis
After radiation exposure to lung
Secondary to some medications

Smoking is not considered a risk factor

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3
Q

Cryptogenic organizing pneumonia (COP) Investigations

A

CXR
FBE, ESR, and CRP
Torax CT
PFT
Bronchoscopy with bronchoalveolar lavage
Lung Biopsy

Diagnosed only after exclusion of any other possible etiology

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4
Q

Cryptogenic organizing pneumonia (COP) Differential

A

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).

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5
Q

Cryptogenic organizing pneumonia (COP) Chest X-ray features

A

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.

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6
Q

Cryptogenic organizing pneumonia (COP) Bloods results

A

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.

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7
Q

Cryptogenic organizing pneumonia (COP) Torax CT features

A

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.

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8
Q

Cryptogenic organizing pneumonia (COP) Pulmonary Function Test features

A

Typically reveals a restrictive defect with diffusion impairment

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9
Q

Cryptogenic organizing pneumonia (COP) Bronchoscopy with bronchoalveolar lavage Features

A

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.

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10
Q

Cryptogenic organizing pneumonia (COP) Lung Biopsy Features

A

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.

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11
Q

Cryptogenic organizing pneumonia (COP) TREATMENT

A

Prednisone 1 mg/kg per day and weaning over 6 to 12 months

Second-line agents Cyclophosphamide and Cyclosporine A

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12
Q

Cryptogenic organizing pneumonia (COP) Prognosis

A

Generally excellent with a good response to systemic corticosteroids

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13
Q

PNEUMONIA MOS COMMON CAUSES (Microorganisms)

A
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14
Q

Neonatal Respiratory Distress DIFFERENTIALS

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15
Q

ASTHMA: Salbutamol dose

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16
Q

ASTHMA: Management of mild-moderate ATTACK

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17
Q

ASTHMA: Management of SEVERE ATTACK

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18
Q

TUBERCULOSIS DIAGNOSE ALGORITHM

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19
Q

Erythema nodosum SLIDE

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20
Q

Tuberculosis: Ghon focus

A
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21
Q

DRUGS that produce gynecomastia

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22
Q

Ostoporosis RISK FACTORS

A

 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

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23
Q

Ostoporosis First Investigation

A

25 hydroxy Vitamin D

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24
Q

Ostoporosis Best Investigation

A

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
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25
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
26
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
27
Osteoporosis FIRST-LINE Treatment
1. Bisphosphonates - Alendronate - Risedronate - Zoledronic Acid 2. Denosumab 3. Strontium ranelate 4. Raloxifene 5. MHT
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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
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Osteoporosis FIRST-LINE Treatment: BISPHOSPHONATES Alendronate & Risedronate
- Alendronate - weekly dose - Risedronate - daily/weekly/monthly For 5 to 10 years in postmenopausal women.
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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.
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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.
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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
33
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.
34
Osteoporosis FIRST-LINE Treatment: MHT
In peri or postmenopausal women with osteoporosis associated with other menopausal symptoms
35
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
36
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.
37
OSTEOPOROSIS Treatment for people with special circumstances: Renal impairment
Raloxifene or Denosumab.
38
Osteoporosis Treatment Follow-up
Repeat DEXA in 2 years. Every year if medication is changed, termination of the treatment or high-risk patient.
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Osteopenia Follow-up
Repeat DEXA every 2 - 5 years
40
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)
41
CTG Fetal tachycardia CAUSES
1. Fetal hypoxia 2. Chorioamnionitis 3. Hyperthyroidism 4. Fetal or maternal anaemia 5. Fetal tachyarrhythmia
42
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
43
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
44
CTG Reduced variability CAUSES
1. **Fetal sleeping**: this should last no longer than 40 minutes (this is the most common cause) 2. **Fetal acidosis** (due to hypoxia): more likely if **late decelerations** are also present **Fetal tachycardia** 3. **Drugs**: opiates, benzodiazepines, methyldopa and magnesium sulphate 4. Prematurity: variability is reduced at earlier gestation (**<28 weeks**) 5. **Congenital heart abnormalities**
45
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.
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CTG Decelerations Definition
Abrupt **decrease** in the baseline fetal heart rate of **greater than 15 bpm** for **greater than 15 seconds.**
47
CTG Early Deceleration Features
Start when the uterine contraction begins and recover when uterine contraction stops. Physiological due to increased fetal intracranial pressure
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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.
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CTG Variable Deceleration CAUSES
1. Reduced amniotic fluid volume 2. Umbilical cord compression
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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
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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.
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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).
53
CTG: Late deceleration CAUSES
o Maternal hypotension o Pre-eclampsia o Uterine hyper-stimulation
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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.
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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
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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.
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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
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CTG Sinusoidal pattern INDICATES
o Severe foetal hypoxia o Severe foetal anaemia o Foetal/maternal haemorrhage Immediate C-section is indicated
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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
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Diabetes Mellitus Diagnose FLOW CHART
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Gestational Diabetes Diagnose
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Gestational Diabetes Risk factors
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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)
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Diabetes Mellitus T2 Treatment: Metformin side effects
*gastrointestinal adverse effects *vitamin B12 deficiency *lactic acidosis (rare) CI: Renal Impairment GFR< 30 and liver impairment
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Diabetes Mellitus T2 Treatment: Thiazolidinediones
GLITAZONE Side Effects: Weight gain Dyslipidemia, CV disease Osteopenia Pioglitazone: Risk for bladder cancer Rosiglitazone: Edema --->CHF MI, Stroke
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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
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Diabetes Mellitus T2 Treatment: Sulfonylureas
IDE gliclazide glipizide glibenclamide glimepiride Side effects: HYPOGLYCEMIA Weight gain Dermatological allergic reactions
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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
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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)
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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
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CAUSES OF POSTPARTUM FEVER
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Contraindications for Tocolisis
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Tetanus prophylaxis
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Common causes of pneumonia by ages
75
Alcohol withdrawal, hallucinosis and delirium tremens timings
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Cellulitis Treatment
77
Chronic otitis media in aboriginal treatment
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Acute otitis media treatment
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RHEUMATIC FEVER JONES CRITERIA
80
paracetamol intoxication protocol
81
Melanoma excision margins
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NEPHRO: Genetic disorders
83
Testicular tumors
84
Glomerulonephritis by age
85
Nephritic Syndrome causes
86
Nephrotic Syndrome causes
87
CAUSES FOR NEPRHOTIC AND NEPHRITIC SYNDROMES
88
PRE RENAL, RENAL AND POST RENAL AKI
89
Renal tumor management
90
Thromboprofilaxis in pregnancy
91
Wernike and Korsackoff
92
Warfarin interactions
93
Jelly Fish Poisoning TABLE
94
Major Box Jelly Fish photo
95
Major Box Jelly Fish STING photo
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BLUEBOTTLE JELLY FISH photo
97
DISFAGIA FLOW CHART 1/3
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DISFAGIA FLOW CHART 2/3
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DISFAGIA FLOW CHART 3/3
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SEPTIC ARTHRITIS TREATMENT
101
Differentials between postpartum depression, blues, and psychosis
102
PAEDS: Dehydration severity scale
103
Tetanus Vaccination WOUNDS
104
Thyroid nodules management
105
Pediatric Brain Tumours (picture)
106
Pediatric Brain Tumours (table)
107
Adrenaline dosage for anaphylaxis
108
Prostate cancer staging
109
Prostate cancer Management
110
Hernias location
111
Cyanotic Congenital Heart Disease
112
Cholelithiasis Management flow chart
113
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.
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COVID High risk patients
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COVID Antiviral management Outpatient
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COVID antiviral Management Hospitalized
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MILESTONES Gross and fine motor
important 9 and 18 months
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MILESTONES language and social
important 9 and 18 months
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MILESTONES Red flags
important 9 and 18 months
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Autism spectrum disorder (ASD) Criteria
121
Asperger's criteria
122
Tourette Criteria
123
Kids Phyc Table Dr Cintia
124
Bloody diarrhea differentials
125
DIARRHEA PART 1: Viral Typhoid – Enteric Fever Salmonella Giardiasis Amoebiasis
126
DIARRHEA PART 2: Salmonella sp. (non-Typhoidal) Shigella E. coli Campylobacter jejuni
127
DIARRHEA PART 3: Clostridium difficile Staph Aureus Bacillus cereus Clostridium sp Clostridium botulinum Vibrio Cholerae - Cholera
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Scabies management
1. Permethrin. If no improv, repeat in 1-2w 2. Benzyl Benzoate 3. Oral cephalexin, top mupirocin if infection
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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
130
Syphilis Investigations
FIRST: Darkfield Microscopy BEST: RPR and Treponema pallidum hemagglutination assay (TPHA) Both tests must be (+)
131
Syphilis Treatment
Benzilpenicilline Early syphilis: Single dose Late syphilis: once weekly for 3 weeks Tertiary syphilis: IV 4-hourly for 15 days
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NEONATAL JAUNDICE: Physiological vs Pathological
133
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
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NEONATAL JAUNDICE: **Conjugated** (DIRECT) Hyperbilirubinemia CAUSES
1. Biliary atresia 2. 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**
135
PHYSIOLOGICAL NEONATAL JAUNDICE: Characteristics
* Day 2-14 (> 21 in preterm) * Mild * Diagnosis of exclusion * Resolves in 2w * Rarely exceeds 220 micromol/L
136
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
137
NEONATAL JAUNDICE + unwell state, suggests:
Sepsis OR GIT obstruction
138
NEONATAL JAUNDICE < 24-48 H UNCONJUGATED suggests:
**Hemolysis** 1. ABO incompatibility (Most common) - Mother: O group; Child: A or B - Direct Coombs (+) - Peripheral smear: Spherocytes (some) 2. Spherocytosis - Peripheral smear: Predominant spherocytes - Direct Coombs (-) - FBE:↑ MCHC - FxHx: Anemia/spherocytosis/gallstones 3. Sickle Cell - Peripheral smear: Sickle and target cells - Direct Coombs (-) - African descendants 3. Rh incompatibility (Most severe) - Peripheral smear: NO spherocytes - Direct Coombs (+)
139
NEONATAL JAUNDICE + Family history of hemolytic disease, suggests:
G6PD deficiency OR Spherocytosis (FxHx of gall stones)
140
NEONATAL JAUNDICE + Dark urine or pale stools OR ↑ DIRECT bilirubin, suggests:
Biliary obstruction (Biliary atresia)
141
JAUNDICE + Plethora, suggest:
Polycythaemia
142
NEONATAL JAUNDICE + Hepatosplenomegaly, suggest:
Hepatitis (↑ liver enzymes) OR Metabolic problems (Galactosemia)
143
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)
144
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
145
Breastfeed Jaundice Clinical features
146
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
147
PHYSIOLOGICAL NEONATAL JAUNDICE: Risk factors (4)
1. Preterm babies (higher bilirubin levels) 2. Exclusive breastfed babies 3. Babies with significant bruising or cephalohaematoma: The breakdown of RBCs within the cephalohaematoma causes higher bilirubin levels and predisposes to jaundice. 4. Previous sibling with neonatal jaundice requiring phototherapy
148
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.
149
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
150
NEONATAL JAUNDICE > 24-48 H ↑UNCONJUGATED, suggests:
1. Physiological jaundice Most Common cause in the first week: - Term: 50% - Preterm: 80% finishes in 1-2 weeks (preterm 3 weeks) 2. Breast milk jaundice Lasts up to 6 weeks Diagnose: Suspending breastfeeding for 24-48 hrs = ↓ serum bilirubin 3. Neonatal sepsis End of the first week (4-7 days old) Lethargic + jaundice + hepatosplenomegaly ↑ BOTH, Direct and Indirect bilirubin.
151
NEONATAL JAUNDICE: Sepsis Management
1st Hemocultures 2nd ATB: Wich??
152
Biliary atresia VS Idiopathic Neonatal hepatitis
153
Knee trauma differentials
154
Pericarditis Clinical Features
Chest pain+SOB+viral infection Kussmaul sign. S4 Gallop: Cardiac Tamponade
155
Pericarditis Initial Investigations
1. ECG: - ST elevation except in AVR & V1 - Reciprocal PR 2. CXR: - Pericardial fluid - Pulmonary congestion 3. Echocardiogram: Is diagnostic! Chest FAST scan should be done ASAP. 4. Cardiac CT
156
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
157
Pericarditis Best Investigation
Echocardiogram with drainage and culture (Pericardiocentesis)
158
Pericarditis Complications
 Constrictive pericarditis.  Cardiac tamponade
159
Pericarditis Medical Treatment
Mild to moderate Pericarditis Colchicine + AAS or Ibuprofen 2nd line: Prednisone If infection: ATBs and drainage
160
Pericarditis Surgical Treatment
Severe Pericarditis, include admision 1. Cardiac tamponade: Pericardiocentesis 2. Severe, Recurrent or Constrictive: Pericardiectomy
161
Beck's triad = Cardiac Tamponade
Low blood pressure (weak pulse or narrow pulse pressure) Muffled heart sounds Raised jugular venous pressure.
162
Pericarditis Physiopathology
Restrictive Cardiomyopathy Diastolic Dysfunction with impaired filling – relaxation Normal Ejection fraction + S4 gallop
163
Dressler's Syndrome risk factors
1. Young age 2. B-negative blood type 3. Prior history of pericarditis 4. Prior treatment with prednisone
164
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.
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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)
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Dressler's Syndrome COMPLICATION
Cariac Tamponade
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Pericarditis Duration: Chronic & Acute
Acute (<6w) Chronic (>6w).
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Kussmaul sign phisical exam
Paradoxical: ↑ JVP with insp and ↓ JVP with exp) Means: constrictive and/or cardiac tamponade.
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Dressler's Syndrome definition
Pericarditis in the context of major heart attack or heart surgery
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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
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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
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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
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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.
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Congenital Heart Disease: TOF - Details & Clinical Features:
Most common cyanotic CHD 1. Pulmonary stenosis (1st worse) 2. VSD (2nd worse) 3. Overriding Ao 4. 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)
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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
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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.
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TGV Management
1. The FO can be enlarged with a catheter procedure, called Balloon 2. Septostomy
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TGV 1st Investigation & Diagnosis
Hyperoxia Test: ABG after 100% oxygen for 10 minutes. PaO2 will remain low & not rise
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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.
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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
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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
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Congenital Heart Disease: PDA - Management:
1. Indomethacin 2. Surgical: Ligation or catheter closure by insertion of a device or embolization coils.
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Congenital Heart Disease: TOF - Management:
Corrective Sx at about 6 months
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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
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Hepatic hydatid cyst pathogen
Echinococcus tape worm
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Hepatic hydatid cyst investigation
Triphasic abdominal CT Triphasic abdominal CT Cyst aspiration
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Hepatic hydatid cyst management
Albendazole
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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
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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
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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.
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Chronic Lower Limb Ischemia initial investigation
1. Measure ABI 2. Duplex US (often the only imaging required to plan endovascular interventions)
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Chronic Lower Limb Ischaemia best investigation
CT Angiography w/ contrast (Contraindicated in RF)
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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
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Chronic Lower Limb Ischaemia SURGICAL Treatment
– Endovascular angioplasty or stenting – Open surgical reconstruction by bypass or endarterectomy.
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Clinical features of Acute Lower limb ischemia
- Context of a patient with: Thrombosis (most common cause) or Embolus from AF. 1. Acute onset of progressive PAIN: - Calf: Common femoral art / Superficial femoral art (MC site of occlusion). - Buttock: Common iliac/external iliac Thrombosis. 2. Pulselessness. 3. Pallor. 4. Paresthesia. 5. Paralysis: - Foot drop = Peroneal nerve paralysis. - Most reliable sign requiring Emergency Qx intervention.
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Acute Lower limb ischemia FIRST investigation
1. Excersice ABI 2. CT angiogram (Emergency Qx intervention) can be MRI also 3. Duplex US for contrast Contraindications
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Acute Lower limb ischemia BEST investigation
Digital subtraction arteriography or just arteriography
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Acute Lower limb ischemia Treatment
Golden time: 4 hrs 1. IV Unfractionated Heparin: 5000 IU then 1250IU/hour. APTT guides further adjustment. 2. 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. 3. After acute, give warfarin for 3-6m
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Esophageal dysplasia Surveillance
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Hyperkalemia Management
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Psudomona treatment (ATB)
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Hyperparathiroidism
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Vertigo differentials
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Light's criteria
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Cocaine complications
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Transient synovitis
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HPV Vaccination
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Tourette DSM-IV criteria
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Kids rehydration