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
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
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
4
Q
Cryptogenic organizing pneumonia (COP) Diferential
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).
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.
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.
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.
Cryptogenic Organizing Pneumonia (COP) is a type of lung condition that causes inflammation and scarring in the small airways and air sacs of the lungs. Here are the key features seen on a Thoracic CT scan:
-
Patchy Consolidation:
- Areas of the lung look dense or white on the CT scan, which indicates filled-in spaces where air should be. These patches are often irregular and can move around or change over time.
-
Ground-Glass Opacities:
- These are hazy areas on the CT that aren’t as dense as full consolidations. They look like the glass on a frosted window and indicate partial filling of the air sacs, inflammation, or both.
-
Peribronchial Distribution:
- The areas of consolidation or ground-glass opacities are often located around the bronchi (the large airways in the lungs). This pattern is called “peribronchial.”
-
Subpleural Distribution:
- The abnormalities may also be found near the pleura, which is the lining around the lungs, often near the edges of the lungs.
-
Reverse Halo Sign (less common but characteristic):
- A specific pattern where there’s a ring of consolidation (dense area) with a central area of ground-glass opacity. This looks like a “halo” on the scan and is a more specific sign of COP.
On a CT scan, COP typically shows patchy areas of lung consolidation and ground-glass opacities, often around the airways (peribronchial) or near the edges of the lungs (subpleural). These features reflect the inflammation and scarring characteristic of COP.
This imaging pattern helps differentiate COP from other lung diseases and is key to diagnosis.
8
Q
Cryptogenic organizing pneumonia (COP) Pulmonary Function Test features
A
Typically reveals a restrictive defect with diffusion impairment
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.
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.
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
12
Q
Cryptogenic organizing pneumonia (COP) Prognosis
A
Generally excellent with a good response to systemic corticosteroids
13
Q
PNEUMONIA MOS COMMON CAUSES (Microorganisms)
A
14
Q
Neonatal Respiratory Distress DIFFERENTIALS
A
15
Q
ASTHMA: Salbutamol dose
A
16
Q
ASTHMA: Management of mild-moderate ATTACK
A
17
Q
ASTHMA: Management of SEVERE ATTACK
A
18
Q
TUBERCULOSIS DIAGNOSE ALGORITHM
A
19
Q
Erythema nodosum SLIDE
A
20
Q
Tuberculosis: Ghon focus
A
21
Q
DRUGS that produce gynecomastia
A
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
23
Q
Ostoporosis First Investigation
A
25 hydroxy Vitamin D
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
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
28
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
29
Osteoporosis FIRST-LINE Treatment: BISPHOSPHONATES Alendronate & Risedronate
- Alendronate - weekly dose
- Risedronate - daily/weekly/monthly
For 5 to 10 years in postmenopausal women.
30
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.
31
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.
32
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.
39
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.
46
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
48
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.
49
CTG Variable Deceleration CAUSES
1. Reduced amniotic fluid volume
2. Umbilical cord compression
50
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
51
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.
52
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
54
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.
55
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
56
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.
57
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
58
CTG Sinusoidal pattern INDICATES
o Severe foetal hypoxia
o Severe foetal anaemia
o Foetal/maternal haemorrhage
Immediate C-section is indicated
59
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
60
Diabetes Mellitus Diagnose FLOW CHART
61
Gestational Diabetes Diagnose
62
Gestational Diabetes Risk factors
63
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)
64
Diabetes Mellitus T2 Treatment: Metformin side effects
*gastrointestinal adverse effects
*vitamin B12 deficiency
*lactic acidosis (rare)
CI: Renal Impairment GFR< 30 and liver impairment
65
Diabetes Mellitus T2 Treatment: Thiazolidinediones
GLITAZONE
Side Effects:
Weight gain
Dyslipidemia, CV disease
Osteopenia
Pioglitazone:
Risk for bladder cancer
Rosiglitazone:
Edema --->CHF
MI, Stroke
66
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
67
Diabetes Mellitus T2 Treatment: Sulfonylureas
IDE
gliclazide
glipizide
glibenclamide
glimepiride
Side effects:
HYPOGLYCEMIA
Weight gain
Dermatological allergic reactions
68
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
69
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)
70
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
71
CAUSES OF POSTPARTUM FEVER
72
Contraindications for Tocolisis
73
Tetanus prophylaxis
74
Common causes of pneumonia by ages
75
Alcohol withdrawal, hallucinosis and delirium tremens timings
76
Cellulitis Treatment
77
Chronic otitis media in aboriginal treatment
78
Acute otitis media treatment
79
RHEUMATIC FEVER JONES CRITERIA
80
paracetamol intoxication protocol
81
Melanoma excision margins
82
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
96
BLUEBOTTLE JELLY FISH photo
97
DISFAGIA FLOW CHART 1/3
98
DISFAGIA FLOW CHART 2/3
99
DISFAGIA FLOW CHART 3/3
100
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.
114
COVID High risk patients
115
COVID Antiviral management Outpatient
116
COVID antiviral Management Hospitalized
117
MILESTONES Gross and fine motor
important 9 and 18 months
118
MILESTONES language and social
important 9 and 18 months
119
MILESTONES Red flags
important 9 and 18 months
120
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
128
Scabies management
1. Permethrin.
If no improv, repeat in 1-2w
2. Benzyl Benzoate
3. Oral cephalexin, top mupirocin if
infection
129
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
132
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
134
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.
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Pericarditis Physiopathology
Restrictive Cardiomyopathy
Diastolic Dysfunction with impaired filling – relaxation
Normal Ejection fraction + S4 gallop
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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
167
Pericarditis Duration: Chronic & Acute
Acute (<6w) Chronic (>6w).
168
Kussmaul sign phisical exam
Paradoxical: ↑ JVP with insp and ↓ JVP with exp)
Means: constrictive and/or cardiac tamponade.
169
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
172
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.
174
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)
175
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
176
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
178
TGV 1st Investigation & Diagnosis
Hyperoxia Test:
ABG after 100% oxygen for 10 minutes. PaO2 will remain low & not rise
179
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.
180
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
181
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
182
Congenital Heart Disease: PDA - Management:
1. Indomethacin
2. Surgical: Ligation or catheter closure by insertion of a device or embolization coils.
183
Congenital Heart Disease: TOF - Management:
Corrective Sx at about 6 months
184
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
185
Hepatic hydatid cyst pathogen
Echinococcus tape worm
186
Hepatic hydatid cyst investigation
Triphasic abdominal CT Triphasic abdominal CT
Cyst aspiration
187
Hepatic hydatid cyst management
Albendazole
188
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
189
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
190
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.
191
Chronic Lower Limb Ischemia initial investigation
1. Measure ABI
2. Duplex US (often the only imaging required to plan endovascular interventions)
192
Chronic Lower Limb
Ischaemia best investigation
CT Angiography w/
contrast (Contraindicated in RF)
193
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
194
Chronic Lower Limb Ischaemia SURGICAL Treatment
– Endovascular angioplasty or stenting
– Open surgical reconstruction by bypass or endarterectomy.
195
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.
196
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
197
Acute Lower limb ischemia BEST investigation
Digital subtraction arteriography or just arteriography
198
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
199
Esophageal dysplasia Surveillance
200
Hyperkalemia Management
201
Psudomona treatment (ATB)
202
Hyperparathiroidism
203
Vertigo differentials
204
Light's criteria
205
Cocaine complications
206
Transient synovitis
207
HPV Vaccination
208
Tourette DSM-IV criteria
209
Kids rehydration
