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AMC MCQ - You Can Do It!!!!!❤️❤️ > Reviewing > Flashcards

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) 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).

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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.

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:

  1. 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.
  2. 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.
  3. 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.”
  4. 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.
  5. 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.

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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

A
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15
Q

ASTHMA: Salbutamol dose

A
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16
Q

ASTHMA: Management of mild-moderate ATTACK

A
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17
Q

ASTHMA: Management of SEVERE ATTACK

A
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18
Q

TUBERCULOSIS DIAGNOSE ALGORITHM

A
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19
Q

Erythema nodosum SLIDE

A
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20
Q

Tuberculosis: Ghon focus

A
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21
Q

DRUGS that produce gynecomastia

A
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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
Q

OSTEOPENIA CRITERIA FOR TREATMENT

A

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

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26
Q

Osteoporosis CRITERIA FOR TREATMENT

A

 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

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27
Q

Osteoporosis FIRST-LINE Treatment

A
  1. Bisphosphonates
    - Alendronate
    - Risedronate
    - Zoledronic Acid
  2. Denosumab
  3. Strontium ranelate
  4. Raloxifene
  5. MHT
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28
Q

Osteoporosis Treatment: BISPHOSPHONATES General Features

A
  • 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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29
Q

Osteoporosis FIRST-LINE Treatment: BISPHOSPHONATES Alendronate & Risedronate

A
  • Alendronate - weekly dose
  • Risedronate - daily/weekly/monthly

For 5 to 10 years in postmenopausal women.

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30
Q

Osteoporosis FIRST-LINE Treatment: BISPHOSPHONATES Zoledronic Acid

A

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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31
Q

Osteoporosis FIRST-LINE Treatment: Denosumab

A
  • Monoclonal antibody against osteoclast.
  • Given as 6 monthly injections subcutaneously for 36 months.
  • No gastrointestinal side effects.
  • But increases hypocalcemia.
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32
Q

Osteoporosis FIRST-LINE Treatment: Strontium ranelate

A

Given orally 2 grams/day.

Should not be given with calcium supplements.

Reserved for severe osteoporosis because can cause MI

  • Contraindications:
  • DVT
  • Prolonged immobilisation
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33
Q

Osteoporosis FIRST-LINE Treatment: Raloxifene

A
  • 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.
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34
Q

Osteoporosis FIRST-LINE Treatment: MHT

A

In peri or postmenopausal women with osteoporosis associated with other menopausal symptoms

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35
Q

Osteoporosis SECOND-LINE Treatment

A

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

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36
Q

OSTEOPOROSIS
Treatment for people with special circumstances: Corticosteroid therapy

A

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.
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37
Q

OSTEOPOROSIS
Treatment for people with special circumstances: Renal impairment

A

Raloxifene or Denosumab.

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38
Q

Osteoporosis Treatment Follow-up

A

Repeat DEXA in 2 years.

Every year if medication is changed, termination of the treatment or high-risk patient.

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39
Q

Osteopenia Follow-up

A

Repeat DEXA every 2 - 5 years

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40
Q

CTG Baseline rate of the fetal heart

A

Normal: 110-160 bpm

Fetal tachycardia: > 160 bpm

Fetal bradycardia: < 110 bpm.
Severe prolonged: < 80 bpm for more than 3 minutes (severe hypoxia)

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41
Q

CTG Fetal tachycardia CAUSES

A
  1. Fetal hypoxia
  2. Chorioamnionitis
  3. Hyperthyroidism
  4. Fetal or maternal anaemia
  5. Fetal tachyarrhythmia
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42
Q

CTG Fetal Bradycardia CAUSES

A

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

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43
Q

CTG Variability Criteria

A

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

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44
Q

CTG Reduced variability CAUSES

A
  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
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45
Q

CTG Accelerations Criteria

A

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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46
Q

CTG Decelerations Definition

A

Abrupt decrease in the baseline fetal heart rate of greater than 15 bpm for greater than 15 seconds.

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47
Q

CTG Early Deceleration Features

A

Start when the uterine contraction begins and recover when uterine contraction stops.

Physiological due to increased fetal intracranial pressure

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48
Q

CTG Variable Deceleration Features

A

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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49
Q

CTG Variable Deceleration CAUSES

A
  1. Reduced amniotic fluid volume
  2. Umbilical cord compression
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50
Q

CTG Shoulders of Variable Deceleration MEANING

A

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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51
Q

CTG Variable Deceleration 1st management

A

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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52
Q

CTG: Late deceleration Features

A

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).

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53
Q

CTG: Late deceleration CAUSES

A

o Maternal hypotension

o Pre-eclampsia

o Uterine hyper-stimulation

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54
Q

CTG: Late deceleration MANAGEMENT

A

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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55
Q

CTG: Prolonged deceleration

A

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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56
Q

CTG: ABNORMAL Deceleration Features

A

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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57
Q

CTG Sinusoidal pattern FEATURES

A

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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58
Q

CTG Sinusoidal pattern INDICATES

A

o Severe foetal hypoxia
o Severe foetal anaemia
o Foetal/maternal haemorrhage

Immediate C-section is indicated

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59
Q

Diabetes Mellitus Diagnose

A

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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60
Q

Diabetes Mellitus Diagnose FLOW CHART

A
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61
Q

Gestational Diabetes Diagnose

A
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62
Q

Gestational Diabetes Risk factors

A
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63
Q

Diabetes Mellitus Screening

A

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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64
Q

Diabetes Mellitus T2 Treatment: Metformin side effects

A

*gastrointestinal adverse effects

*vitamin B12 deficiency

*lactic acidosis (rare)

CI: Renal Impairment GFR< 30 and liver impairment

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65
Q

Diabetes Mellitus T2 Treatment: Thiazolidinediones

A

GLITAZONE

Side Effects:
Weight gain
Dyslipidemia, CV disease
Osteopenia

Pioglitazone:
Risk for bladder cancer

Rosiglitazone:
Edema —>CHF
MI, Stroke

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66
Q

Diabetes Mellitus T2 Treatment: SGLT2

A

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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67
Q

Diabetes Mellitus T2 Treatment: Sulfonylureas

A

IDE
gliclazide
glipizide
glibenclamide
glimepiride

Side effects:
HYPOGLYCEMIA
Weight gain
Dermatological allergic reactions

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68
Q

Diabetes Mellitus T2 Treatment: DPP-4 inhibitors

A

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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69
Q

Diabetes Mellitus T2 Treatment: GLP-1 receptor agonists

A

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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70
Q

MASTITIS Management

A

∗ 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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71
Q

CAUSES OF POSTPARTUM FEVER

A
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72
Q

Contraindications for Tocolisis

A
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73
Q

Tetanus prophylaxis

A
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74
Q

Common causes of pneumonia by ages

A
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75
Q

Alcohol withdrawal, hallucinosis and delirium tremens timings

A
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76
Q

Cellulitis Treatment

A
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77
Q

Chronic otitis media in aboriginal treatment

A
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78
Q

Acute otitis media treatment

A
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79
Q

RHEUMATIC FEVER JONES CRITERIA

A
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80
Q

paracetamol intoxication protocol

A
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81
Q

Melanoma excision margins

A
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82
Q

NEPHRO: Genetic disorders

A
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83
Q

Testicular tumors

A
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84
Q

Glomerulonephritis by age

A
85
Q

Nephritic Syndrome causes

A
86
Q

Nephrotic Syndrome causes

A
87
Q

CAUSES FOR NEPRHOTIC AND NEPHRITIC SYNDROMES

A
88
Q

PRE RENAL, RENAL AND POST RENAL AKI

A
89
Q

Renal tumor management

A
90
Q

Thromboprofilaxis in pregnancy

A
91
Q

Wernike and Korsackoff

A
92
Q

Warfarin interactions

A
93
Q

Jelly Fish Poisoning TABLE

A
94
Q

Major Box Jelly Fish photo

A
95
Q

Major Box Jelly Fish STING photo

A
96
Q

BLUEBOTTLE JELLY FISH photo

A
97
Q

DISFAGIA FLOW CHART 1/3

A
98
Q

DISFAGIA FLOW CHART 2/3

A
99
Q

DISFAGIA FLOW CHART 3/3

A
100
Q

SEPTIC ARTHRITIS TREATMENT

A
101
Q

Differentials between postpartum depression, blues, and psychosis

A
102
Q

PAEDS: Dehydration severity scale

A
103
Q

Tetanus Vaccination WOUNDS

A
104
Q

Thyroid nodules management

A
105
Q

Pediatric Brain Tumours (picture)

A
106
Q

Pediatric Brain Tumours (table)

A
107
Q

Adrenaline dosage for anaphylaxis

A
108
Q

Prostate cancer staging

A
109
Q

Prostate cancer Management

A
110
Q

Hernias location

A
111
Q

Cyanotic Congenital Heart Disease

A
112
Q

Cholelithiasis Management flow chart

A
113
Q

Suggested AAA surveillance (w/
US) of Abdominal Aortic
Aneurysm

A

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
Q

COVID High risk patients

A
115
Q

COVID Antiviral management Outpatient

A
116
Q

COVID antiviral Management Hospitalized

A
117
Q

MILESTONES Gross and fine motor

A

important 9 and 18 months

118
Q

MILESTONES language and social

A

important 9 and 18 months

119
Q

MILESTONES Red flags

A

important 9 and 18 months

120
Q

Autism spectrum disorder (ASD) Criteria

A
121
Q

Asperger’s criteria

A
122
Q

Tourette Criteria

A
123
Q

Kids Phyc Table Dr Cintia

A
124
Q

Bloody diarrhea differentials

A
125
Q

DIARRHEA PART 1:
Viral
Typhoid – Enteric Fever Salmonella
Giardiasis
Amoebiasis

A
126
Q

DIARRHEA PART 2:
Salmonella sp. (non-Typhoidal)
Shigella
E. coli
Campylobacter jejuni

A
127
Q

DIARRHEA PART 3:
Clostridium difficile
Staph Aureus
Bacillus cereus
Clostridium sp
Clostridium botulinum
Vibrio Cholerae - Cholera

A
128
Q

Scabies management

A
  1. Permethrin.
    If no improv, repeat in 1-2w
  2. Benzyl Benzoate
  3. Oral cephalexin, top mupirocin if
    infection
129
Q

Syphilis Clinical features (1ry, 2ry and 3ry)

A
  • Primary: Single painless ulcer
  • Secondary: Generalised
    nontender lymphadenopathy,
    rash in palms and soles, patchy
    alopecia.
  • Tertiary: Neurosyphilis or
    cardiosyphilis
130
Q

Syphilis Investigations

A

FIRST: Darkfield Microscopy

BEST: RPR and Treponema pallidum hemagglutination assay (TPHA)
Both tests must be (+)

131
Q

Syphilis Treatment

A

Benzilpenicilline

Early syphilis: Single dose

Late syphilis: once weekly for 3 weeks

Tertiary syphilis: IV 4-hourly for 15 days

132
Q

NEONATAL JAUNDICE: Physiological vs Pathological

A
133
Q

NEONATAL JAUNDICE: UNconjugated (INDIRECT) Hyperbilirubinemia CAUSES

A
  • 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
Q

NEONATAL JAUNDICE: Conjugated (DIRECT) Hyperbilirubinemia CAUSES

A
  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
Q

PHYSIOLOGICAL NEONATAL JAUNDICE: Characteristics

A
  • Day 2-14 (> 21 in preterm)
  • Mild
  • Diagnosis of exclusion
  • Resolves in 2w
  • Rarely exceeds 220 micromol/L
136
Q

PATHOLOGICAL NEONATAL JAUNDICE: Characteristics

A
  • 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
Q

NEONATAL JAUNDICE + unwell state, suggests:

A

Sepsis OR GIT obstruction

138
Q

NEONATAL JAUNDICE < 24-48 H UNCONJUGATED suggests:

A

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
  4. Rh incompatibility (Most severe)
    - Peripheral smear: NO spherocytes
    - Direct Coombs (+)
139
Q

NEONATAL JAUNDICE + Family history of hemolytic disease, suggests:

A

G6PD deficiency

OR

Spherocytosis (FxHx of gall stones)

140
Q

NEONATAL JAUNDICE + Dark urine or pale stools OR ↑ DIRECT bilirubin, suggests:

A

Biliary obstruction (Biliary atresia)

141
Q

JAUNDICE + Plethora, suggest:

A

Polycythaemia

142
Q

NEONATAL JAUNDICE + Hepatosplenomegaly, suggest:

A

Hepatitis (↑ liver enzymes)

OR

Metabolic problems (Galactosemia)

143
Q

NEONATAL JAUNDICE: BILIARY ATRESIA Clinical Features (6)

A
  • 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
Q

Breast Milk Jaundice Clinical features

A

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
Q

Breastfeed Jaundice Clinical features

A
146
Q

PHYSIOLOGICAL NEONATAL JAUNDICE: Mechanism (3)

A
  • Shorter lifespan of neonatal red blood cells
  • Immature liver function at birth
  • A relatively high concentration of β-glucuronidase in the small intestine
147
Q

PHYSIOLOGICAL NEONATAL JAUNDICE: Risk factors (4)

A
  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
Q

NEONATAL JAUNDICE: BILIARY ATRESIA Best Investigation

A

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
Q

NEONATAL JAUNDICE: Congenital Hypotiroidism Clinical features (11)

A

listless

 Goitre

 prominent tongue

 hoarse cry

 puffy face

 constipation

 umbilical hernia

 hypothermia

 bradycardia

 dry skin

 failure to thrive

150
Q

NEONATAL JAUNDICE > 24-48 H ↑UNCONJUGATED, suggests:

A
  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
Q

NEONATAL JAUNDICE: Sepsis Management

A

1st Hemocultures

2nd ATB: Wich??

152
Q

Biliary atresia VS Idiopathic Neonatal hepatitis

A
153
Q

Knee trauma differentials

A
154
Q

Pericarditis Clinical Features

A

Chest pain+SOB+viral infection

Kussmaul sign.

S4 Gallop: Cardiac Tamponade

155
Q

Pericarditis Initial Investigations

A
  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
Q

Pericarditis Causes

A
  • 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
Q

Pericarditis Best Investigation

A

Echocardiogram with drainage and culture (Pericardiocentesis)

158
Q

Pericarditis Complications

A

 Constrictive pericarditis.

 Cardiac tamponade

159
Q

Pericarditis Medical Treatment

A

Mild to moderate Pericarditis

Colchicine + AAS or Ibuprofen

2nd line: Prednisone

If infection: ATBs and drainage

160
Q

Pericarditis Surgical Treatment

A

Severe Pericarditis, include admision

  1. Cardiac tamponade: Pericardiocentesis
  2. Severe, Recurrent or Constrictive:
    Pericardiectomy
161
Q

Beck’s triad = Cardiac Tamponade

A

Low blood pressure (weak pulse or narrow pulse pressure)

Muffled heart sounds

Raised jugular venous pressure.

162
Q

Pericarditis Physiopathology

A

Restrictive Cardiomyopathy

Diastolic Dysfunction with impaired filling – relaxation

Normal Ejection fraction + S4 gallop

163
Q

Dressler’s Syndrome risk factors

A
  1. Young age
  2. B-negative blood type
  3. Prior history of pericarditis
  4. Prior treatment with prednisone
164
Q

Dressler’s Syndrome Treatment

A

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.

165
Q

Dressler’s Syndrome investigations

A

Gold Standard: Echocardiogram

UNSTABLE patient: bedside ultrasonographic (E-FAST)

ECG: Same pattern as pericarditis (global ST segment elevation and T wave inversion)

166
Q

Dressler’s Syndrome COMPLICATION

A

Cariac Tamponade

167
Q

Pericarditis Duration: Chronic & Acute

A

Acute (<6w) Chronic (>6w).

168
Q

Kussmaul sign phisical exam

A

Paradoxical: ↑ JVP with insp and ↓ JVP with exp)

Means: constrictive and/or cardiac tamponade.

169
Q

Dressler’s Syndrome definition

A

Pericarditis in the context of major heart attack or heart surgery

170
Q

List 3 Acyanotic + 3 Cyanotic Congenital Heart Diseases

A

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

171
Q

Congenital Heart Disease: VSD - Details & Clinical Features: Hint: different sizes may have varying clinical features

A

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
Q

Congenital Heart Disease: ASD - Details & Clinical Features:

A

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

173
Q

Congenital Heart Disease: PDA - Details & Clinical Features:

A
  • 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
Q

Congenital Heart Disease: TOF - Details & Clinical Features:

A

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
Q

Congenital Heart Disease: HLHD (3)

A
  • 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
Q

Congenital Heart Disease: TGV

A

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.

177
Q

TGV Management

A
  1. The FO can be enlarged with a catheter procedure, called Balloon
  2. Septostomy
178
Q

TGV 1st Investigation & Diagnosis

A

Hyperoxia Test:

ABG after 100% oxygen for 10 minutes. PaO2 will remain low & not rise

179
Q

Hyperoxia Test: Differences between Acyanotic CHD & TGV

A

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
Q

Congenital Heart Disease: VSD - Management & Indications for Surgical Closure:

A
  • 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
Q

Congenital Heart Disease: ASD - Management:

A
  • 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
Q

Congenital Heart Disease: PDA - Management:

A
  1. Indomethacin
  2. Surgical: Ligation or catheter closure by insertion of a device or embolization coils.
183
Q

Congenital Heart Disease: TOF - Management:

A

Corrective Sx at about 6 months

184
Q

SVT STABLE Management

A

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
Q

Hepatic hydatid cyst pathogen

A

Echinococcus tape worm

186
Q

Hepatic hydatid cyst investigation

A

Triphasic abdominal CT Triphasic abdominal CT
Cyst aspiration

187
Q

Hepatic hydatid cyst management

A

Albendazole

188
Q

Secondary - Tertiary (Pituitary) Hypothyroidism CAUSES

A

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
Q

Clinical features of Chronic Lower Limb Ischemia

A
  • Claudication (pain w/ exercise
    and relieved by rest), if pain at
    rest: RED FLAG
  • Shiny hairless legs
  • Muscles atrophied
190
Q

Chronic Lower Limb Ischaemia referral criteria

A

– 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
Q

Chronic Lower Limb Ischemia initial investigation

A
  1. Measure ABI
  2. Duplex US (often the only imaging required to plan endovascular interventions)
192
Q

Chronic Lower Limb
Ischaemia best investigation

A

CT Angiography w/
contrast (Contraindicated in RF)

193
Q

Chronic Lower Limb Ischaemia MEDICAL Management

A

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
Q

Chronic Lower Limb Ischaemia SURGICAL Treatment

A

– Endovascular angioplasty or stenting

– Open surgical reconstruction by bypass or endarterectomy.

195
Q

Clinical features of Acute Lower limb
ischemia

A
  • 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.
  1. Pulselessness.
  2. Pallor.
  3. Paresthesia.
  4. Paralysis:
  • Foot drop = Peroneal nerve paralysis.
  • Most reliable sign requiring Emergency Qx intervention.
196
Q

Acute Lower limb ischemia FIRST investigation

A
  1. Excersice ABI
  2. CT angiogram (Emergency Qx intervention) can be MRI also
  3. Duplex US for contrast Contraindications
197
Q

Acute Lower limb ischemia BEST investigation

A

Digital subtraction arteriography or just arteriography

198
Q

Acute Lower limb ischemia Treatment

A

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.
  1. After acute, give warfarin for 3-6m
199
Q

Esophageal dysplasia Surveillance

A
200
Q

Hyperkalemia Management

A
201
Q

Psudomona treatment (ATB)

A
202
Q

Hyperparathiroidism

A
203
Q

Vertigo differentials

A
204
Q

Light’s criteria

A
205
Q

Cocaine complications

A
206
Q

Transient synovitis

A
207
Q

HPV Vaccination

A
208
Q

Tourette DSM-IV criteria

A
209
Q

Kids rehydration

A

AMC MCQ - You Can Do It!!!!!❤️❤️ (50 decks)

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