ELECTIVE - ID and Paeds Flashcards
1
Q
What are NRTIs and how do they work?
A
Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTIs) block HIV’s reverse transcriptase enzyme, preventing viral DNA synthesis.
2
Q
Give examples of NRTIs.
A
Tenofovir (TDF), Emtricitabine (FTC), Zidovudine (AZT).
3
Q
What are NNRTIs and how do they work?
A
Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs) bind directly to reverse transcriptase, stopping it from working.
4
Q
Give examples of NNRTIs.
A
Efavirenz (EFV), Nevirapine (NVP), Doravirine (DOR).
5
Q
What are PIs and how do they work?
A
Protease Inhibitors (PIs) block the HIV protease enzyme, preventing virus assembly.
6
Q
Give examples of PIs.
A
Atazanavir (ATV), Darunavir (DRV), Ritonavir (RTV).
7
Q
What are INSTIs and how do they work?
A
Integrase Strand Transfer Inhibitors (INSTIs) stop HIV DNA from integrating into human DNA.
8
Q
Give examples of INSTIs.
A
Dolutegravir (DTG), Bictegravir (BIC), Raltegravir (RAL).
9
Q
What are Entry/Fusion Inhibitors and how do they work?
A
They prevent HIV from entering human cells.
10
Q
Give examples of Entry/Fusion Inhibitors.
A
Enfuvirtide (T20), Maraviroc (MVC).
11
Q
What is the first-line ART regimen?
A
2 NRTIs + 1 INSTI (e.g., TDF + FTC + DTG).
12
Q
What is the second-line ART regimen?
A
2 NRTIs + 1 Boosted PI (e.g., AZT + 3TC + ATV/r).
13
Q
How is TB diagnosed using a skin test?
A
Tuberculin Skin Test (TST) involves injecting purified protein derivative (PPD) under the skin. A raised bump indicates possible TB exposure.
14
Q
How does a chest X-ray help in TB diagnosis?
A
It checks for lung damage or active TB infection, showing lung infiltrates, cavities, or nodules.
15
Q
What is sputum smear microscopy?
A
A sample of sputum is examined under a microscope to detect TB bacteria (acid-fast bacilli).
16
Q
What is the gold standard for TB diagnosis?
A
Sputum culture, as it grows TB bacteria for confirmation (takes 2–6 weeks).
17
Q
What is NAAT in TB diagnosis?
A
Nucleic Acid Amplification Tests (e.g., GeneXpert) detect TB DNA and drug resistance rapidly.
18
Q
What are IGRAs in TB testing?
A
Interferon-Gamma Release Assays (e.g., QuantiFERON) measure immune response to TB bacteria, useful for latent TB detection.
19
Q
What is TB drug susceptibility testing?
A
It determines if TB bacteria are resistant to drugs (e.g., Rifampicin, Isoniazid).
20
Q
What is the first-line treatment for drug-sensitive TB?
A
Intensive Phase (2 months): RIPE regimen (Rifampin, Isoniazid, Pyrazinamide, Ethambutol). Continuation Phase (4 months): Rifampin + Isoniazid.
21
Q
When treating both TB and HIV, which should be treated first?
A
Treat TB for 2 weeks first, then start HIV treatment.
22
Q
What should be done with ART doses when on Rifampicin?
A
Double the doses of ART.
23
Q
How is HTLV-1 transmitted?
A
Through blood, sexual contact, and breastfeeding.
24
Q
What are the possible diseases caused by HTLV-1?
A
Adult T-cell Leukemia/Lymphoma (ATLL), HTLV-1 Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP), uveitis, dermatitis, arthritis.
25
How is HTLV-1 diagnosed?
Serology (ELISA, Western blot), PCR for viral DNA.
26
What is the treatment for HTLV-1?
No cure; symptom management for ATLL or HAM/TSP.
27
How is Onchocerciasis transmitted?
By blackfly bites (Simulium species) near fast-flowing rivers.
28
What are the symptoms of Onchocerciasis?
Itchy skin, rash, thickened skin ('lizard skin'), depigmented spots ('leopard skin'), eye damage leading to blindness.
29
How is Onchocerciasis diagnosed?
Skin snips, PCR, serology, slit-lamp exam for eye involvement.
30
What is the treatment for Onchocerciasis?
Ivermectin (kills microfilariae; given annually or biannually).
31
What is Nodding Syndrome and its cause?
A neurological disorder linked to Onchocerciasis and possible autoimmune/neuroinflammatory factors.
32
What are the symptoms of Nodding Syndrome?
Nodding seizures triggered by food or cold, cognitive decline, stunted growth, muscle wasting.
33
How is Nodding Syndrome treated?
Anti-epileptic drugs (e.g., sodium valproate), supportive care.
34
How can Nodding Syndrome be prevented?
Onchocerciasis control (Ivermectin distribution).
35
What are the infectious causes of hepatosplenomegaly?
Leishmaniasis (Sandfly), Malaria, HIV, TB, Schistosomiasis, Brucellosis (animal hides, unpasteurized dairy products).
36
What is the incubation period for malaria?
7–30 days after the infective mosquito bite.
37
What are the symptoms of uncomplicated malaria?
Fever (often cyclical), chills, sweating, headache, muscle aches, fatigue, nausea, vomiting, mild diarrhea, enlarged spleen, mild jaundice.
38
What are the features of severe malaria?
Altered consciousness or seizures (cerebral malaria), severe anemia, jaundice, dark urine (hemolysis), respiratory distress, pulmonary edema, shock, kidney failure, multi-organ dysfunction.
39
What is malaria relapse, and which species cause it?
Reappearance of symptoms weeks to months later due to dormant liver-stage parasites; caused by P. vivax or P. ovale.
40
How soon do severe symptoms of malaria develop?
1–2 weeks after an infected mosquito bite (especially P. falciparum).
41
How does gastric acid influence typhoid infection risk?
Gastric acid is protective; reduced acid production (e.g., due to PPIs) increases susceptibility to infection.
42
What are the symptoms of early-stage typhoid (first week)?
Gradual fever onset (stepwise pattern), fatigue, malaise, headache, abdominal discomfort, dry cough.
43
What are the symptoms of mid-stage typhoid (2nd–3rd week)?
High sustained fever, abdominal pain or distension, constipation or diarrhea ('pea soup' stools), rose spots (salmon-colored maculopapular rash), hepatosplenomegaly, altered mental state (dull or psychotic).
44
What are severe complications of untreated typhoid?
Intestinal perforation, hemorrhage, sepsis, shock, altered mental status (typhoid encephalopathy).
45
What are first-line antibiotics for typhoid?
Ceftriaxone, azithromycin, fluoroquinolones (e.g., ciprofloxacin), depending on resistance.
46
What are alternative antibiotics for typhoid in non-resistant areas?
Chloramphenicol, amoxicillin, trimethoprim-sulfamethoxazole.
47
What is neurocysticercosis, and what causes it?
A parasitic CNS infection caused by Taenia solium larvae.
48
What are the common symptoms of neurocysticercosis?
Seizures (most common, focal or generalized), headache (from increased ICP), neurological deficits (ataxia, vision changes), cognitive changes (memory loss, altered mental status).
49
What are severe complications of neurocysticercosis?
Hydrocephalus (ventricular obstruction), meningitis/encephalitis (immune response), stroke-like symptoms (vascular inflammation/vasculitis).
50
What is the normal CD4 count range in healthy individuals?
500–1,500 cells/μL.
51
What is the significance of a CD4 count >500?
Early HIV infection, usually asymptomatic or mild nonspecific symptoms.
52
What happens when CD4 count is 350–500?
Early immune suppression; increased risk of mild infections (seborrheic dermatitis, oral thrush).
53
What are the risks associated with a CD4 count of 200–349?
Moderate immune suppression; higher risk of tuberculosis, oral candidiasis, herpes zoster.
54
What is the AIDS-defining CD4 threshold, and what are the risks?
<200 cells/μL; high risk for opportunistic infections like Pneumocystis jirovecii pneumonia (PJP).
55
What are the risks with a CD4 count <100?
Severe immunosuppression; high risk for Toxoplasmosis, Cryptococcal meningitis.
56
What are the risks with a CD4 count <50?
Advanced AIDS; life-threatening infections like Cytomegalovirus (CMV) retinitis or disseminated Mycobacterium avium complex (MAC).
57
What are the clinical signs of aspiration pneumonia in neonates?
Tachypnea, grunting, nasal flaring, retractions, cyanosis, poor feeding, fever (may be absent in preterm infants), apnea.
58
What are common causes of aspiration pneumonia in neonates?
Inhalation of substances like milk, amniotic fluid, or meconium; GER; weak suck-swallow reflexes; neuromuscular disorders; maternal sedation during delivery.
59
What is the treatment for neonatal aspiration pneumonia?
Oxygen therapy or respiratory support (CPAP/mechanical ventilation in severe cases), broad-spectrum antibiotics, airway clearance, nutritional support via NG tube, management of underlying conditions.
60
What antibiotics are commonly used for neonatal aspiration pneumonia?
Amoxicillin and metronidazole (community-acquired); cefuroxime + gentamicin + metronidazole (hospital-acquired).
61
What is transient tachypnea of the newborn (TTN)?
A temporary respiratory condition in newborns caused by delayed clearance of fetal lung fluid, leading to mild respiratory distress.
62
What are the symptoms of TTN?
Tachypnea (>60 breaths/min), nasal flaring, mild retractions, grunting, mild cyanosis.
63
What are the risk factors for TTN?
Cesarean delivery, prematurity, maternal diabetes.
64
How is TTN treated?
Supportive care: oxygen therapy if needed, nasal CPAP for distress, normal temperature and hydration maintenance.
65
How does macrosomia lead to jaundice?
Increased fetal insulin levels promote excessive growth → polycythemia → excessive RBC breakdown → high bilirubin → neonatal liver struggles to conjugate/excrete bilirubin → jaundice.
66
What are potential long-term complications in macrosomic infants?
Metabolic syndrome, cardiovascular disease, endocrine disorders, neurodevelopmental issues, reproductive health problems, orthopedic problems.
67
What is BIND (Bilirubin-Induced Neurological Dysfunction)?
A spectrum of neurological impairments caused by unconjugated bilirubin crossing the blood-brain barrier, accumulating in the basal ganglia and brainstem nuclei, leading to neurotoxicity.
68
What are the two forms of BIND?
1. Acute Bilirubin Encephalopathy (ABE) – early stage.
2. Kernicterus – chronic, irreversible stage.
69
What are the phases of ABE?
Phase 1: Lethargy, hypotonia, poor feeding, high-pitched cry.
Phase 2: Hypertonia (opisthotonus), fever, irritability, worsening feeding issues.
Phase 3: Apnea, seizures, coma, death if untreated.
70
What happens if ABE is not treated?
It progresses to kernicterus, leading to permanent neurological damage.
71
What are the major complications of kernicterus?
Movement disorders, hearing loss, cognitive impairment, gaze abnormalities, dental enamel hypoplasia.
72
How can kernicterus be prevented?
Early treatment of ABE with phototherapy or exchange transfusion.
73
At what bilirubin levels is neurotoxicity considered high risk in term infants?
>340-350 µmol/L (20 mg/dL).
74
What is a potentially toxic bilirubin level in preterm infants?
>250-300 µmol/L (15-18 mg/dL).
75
At what bilirubin level is immediate exchange transfusion required in term neonates?
>425 µmol/L (25 mg/dL).
76
Why are preterm infants more vulnerable to bilirubin toxicity?
Preterm infants have an immature blood-brain barrier and liver enzyme systems, making them more susceptible to bilirubin toxicity at lower levels.
77
How do low serum albumin levels increase bilirubin toxicity risk?
Low albumin (<3 g/dL) reduces bilirubin binding capacity, leading to increased free bilirubin and higher neurotoxicity risk.
78
How do acidosis and hypoxia contribute to bilirubin toxicity?
Acidosis weakens bilirubin-albumin binding, increasing free bilirubin, while hypoxia disrupts the blood-brain barrier, allowing bilirubin to enter the brain more easily.
79
Why does sepsis increase bilirubin neurotoxicity risk?
Sepsis and infections increase blood-brain barrier permeability, making the brain more vulnerable to bilirubin deposition.
80
What conditions cause rapid hemolysis leading to bilirubin toxicity?
ABO/Rh incompatibility and G6PD deficiency cause rapid hemolysis, overwhelming the liver’s ability to clear bilirubin.
81
Which genetic disorders impair bilirubin conjugation?
Crigler-Najjar and Gilbert syndromes impair bilirubin conjugation, leading to increased bilirubin levels.
82
How does neonatal dehydration increase bilirubin toxicity risk?
Dehydration delays bilirubin clearance and increases enterohepatic circulation, raising bilirubin levels.
83
At what bilirubin levels is phototherapy initiated?
Phototherapy is started at 150-250 µmol/L, depending on gestational age and risk factors.
84
When is exchange transfusion considered for neonatal hyperbilirubinemia?
Exchange transfusion is considered at bilirubin levels of 340-425 µmol/L, depending on clinical signs and risk factors.
85
Why do newborns lose weight in the first few days of life?
Newborns lose weight due to fluid loss, meconium passage, limited initial milk intake, and high metabolic activity.
86
What is the normal amount of weight loss for a newborn in the first 3-5 days?
Up to 7-10% of birth weight loss by day 3-5 is considered normal.
87
When should weight loss in a newborn be a concern?
Weight loss >10%, persistent weight loss beyond day 5, failure to regain birth weight by 14 days, or signs of dehydration should be evaluated.
88
What are signs of dehydration in a newborn?
Dry mouth, fewer than 6 wet nappies per day after day 4, sunken fontanelle, lethargy, and worsening jaundice indicate dehydration.
89
What is the treatment approach for acute chest syndrome in sickle cell disease?
Treatment includes oxygen therapy, hydration, pain management (opioids), blood transfusions, antibiotics, non-invasive ventilation, and inhaled nitric oxide in severe cases.
90
What is the Kramer scale used for?
The Kramer scale estimates bilirubin levels based on the progression of jaundice across different body zones.
91
What bilirubin level corresponds to jaundice limited to the face (Kramer Zone 1)?
Approximately 5 mg/dL.
92
At what bilirubin level does jaundice reach the palms and soles (Kramer Zone 5)?
>15-20 mg/dL, indicating severe jaundice.
93
What is a limitation of the Kramer scale?
It provides a rough estimate and should be confirmed with serum bilirubin measurement for accuracy.
94
When is neonatal jaundice concerning?
When bilirubin levels are too high or rise too quickly, increasing risk of kernicterus.
95
What are red flags for neonatal jaundice?
1. Early onset (<24 hours) - possible hemolysis (ABO/Rh incompatibility, G6PD deficiency). 2. High bilirubin (>95th percentile on Bhutani nomogram). 3. Rapid bilirubin rise (>0.2-0.3 mg/dL/hour or >5 mg/dL/day). 4. Kramer Zone 4 or 5 jaundice. 5. Persistent jaundice (>2 weeks in term, >3 weeks in preterm) - possible liver disease. 6. Signs of acute bilirubin encephalopathy - lethargy, poor feeding, hypotonia, seizures, high-pitched cry.
96
What defines apnoeic spells in neonates?
Episodes where breathing stops for ≥20 seconds or shorter if accompanied by bradycardia (<100 bpm), desaturation (SpO₂ <80–85%), cyanosis or pallor.
97
What are risk factors for apnoeic spells in neonates?
1. Prematurity (<30 weeks) 2. Low birth weight (<1500 g) 3. Neonatal infections 4. Perinatal asphyxia 5. Respiratory distress syndrome 6. Metabolic imbalances 7. Neurological conditions 8. GERD 9. Maternal drug exposure 10. Temperature instability.
98
What are the types of neonatal apnoea?
1. Central - No respiratory effort due to immature brainstem. 2. Obstructive - Upper airway obstruction with respiratory effort but no airflow. 3. Mixed - Central apnoea followed by airway obstruction, most common in preterms.
99
Why does neonatal apnoea occur?
1. Immature brainstem control. 2. Poor CO₂ response. 3. Reduced airway muscle tone. 4. Delayed respiratory reflex maturation.
100
How do you manage an apnoeic episode?
1. Tactile stimulation 2. Reposition airway 3. Supplemental oxygen 4. Positive pressure ventilation if prolonged.
101
What is ongoing management of neonatal apnoea?
1. Supportive care - maintain neutral thermal environment, treat underlying causes, monitor vitals. 2. Pharmacological - Caffeine citrate (first-line), Theophylline (less common). 3. Respiratory support - Nasal CPAP, HFNC, mechanical ventilation if severe.
102
Why do you need an NG tube when ventilating a neonate who has been fed?
To prevent gastric distension and aspiration.
103
What is the Moro Reflex?
Startle reflex - baby extends arms outward, then brings them back in, often with crying. Present at birth, disappears by 4–6 months. Persistence may indicate neurological issues.
104
What is the Rooting Reflex?
Stroking cheek causes baby to turn head toward stimulus and open mouth. Helps with breastfeeding. Present at birth, disappears by 4 months. Absence may indicate neurological impairment.
105
What is the Sucking Reflex?
Touching lips or mouth causes baby to start sucking. Essential for feeding. Develops at 32–36 weeks gestation, disappears by 4 months. Poor reflex may indicate prematurity or CNS depression.
106
What is the Palmar Grasp Reflex?
Placing finger in palm causes baby to grasp. Present at birth, disappears by 4–6 months. Persistence may indicate cerebral palsy; asymmetry may indicate nerve damage.
107
What is the Tonic Neck Reflex?
Turning baby’s head to one side causes arm on that side to extend while opposite arm flexes. Present at birth, disappears by 4–6 months. Persistence may indicate cerebral palsy.
108
What are the Sarnat stages of HIE?
1. Mild (Stage 1) - Hyperalert, normal/increased tone, no seizures. 2. Moderate (Stage 2) - Lethargy, hypotonia, weak suck, possible seizures. 3. Severe (Stage 3) - Coma, severe hypotonia, absent reflexes, poor autonomic function.
109
What is the prognosis for HIE?
Mild HIE usually resolves. Moderate HIE may cause neurological impairment but can improve with therapeutic hypothermia. Severe HIE has high risk of long-term disability or death.
110
Severe Acute Malnutrition (SAM) - Causes
Inadequate intake: Poverty, poor feeding, famine; Increased needs: Infections (HIV, TB), malignancies; Malabsorption/Loss: Celiac disease, diarrhea
111
Severe Acute Malnutrition (SAM) - Signs & Symptoms
Marasmus: Severe wasting, no edema; Kwashiorkor: Edema, swollen abdomen, skin & hair changes; General: Lethargy, infections, hypoglycemia, hypothermia
112
Severe Acute Malnutrition (SAM) - Investigations
Anthropometry: WHZ < -3 SD, MUAC < 11.5 cm, bilateral edema; Blood tests: Glucose, electrolytes, CBC, albumin, CRP; Stool: Rule out infections/malabsorption
113
Severe Acute Malnutrition (SAM) - Management (WHO Protocol)
Stabilization (First 48h): Rehydrate carefully (ReSoMal, NOT ORS), Empirical antibiotics (ampicillin + gentamicin), Correct hypoglycemia & hypothermia; Rehabilitation: Start F-75 (low protein/sodium), then F-100/RUTF for catch-up, Micronutrient supplementation (A, zinc, folic acid); Long-Term Care: Address underlying causes, nutritional support, follow-up
114
Severe Acute Malnutrition (SAM) - Key Considerations
Risk of refeeding syndrome → Start slow; Screen for TB, HIV, chronic disease
115
Hypoxic-Ischemic Encephalopathy (HIE) - Stages
Mild (Stage 1): Hyperalertness, irritability, normal or increased muscle tone, no seizures, resolves within 24 hours; Moderate (Stage 2): Lethargy, hypotonia, weak reflexes, occasional seizures, may last 2–14 days; Severe (Stage 3): Stupor/coma, flaccid tone, absent reflexes (including brainstem reflexes), frequent seizures, high risk of long-term brain injury or death
116
NIPE Exam - Head & Face
Abnormal skull shape/fontanelles → Craniosynostosis, hydrocephalus, microcephaly; Absent red reflex → Congenital cataracts, retinoblastoma; Low-set ears → Down syndrome; Cleft lip/palate → Congenital cleft defects
117
NIPE Exam - Neck & Clavicles
Lumps/swelling → Cystic hygroma, branchial cyst; Clavicle fracture → Birth trauma (e.g., shoulder dystocia)
118
NIPE Exam - Chest
Respiratory distress → Respiratory distress syndrome, congenital pneumonia; Murmurs/abnormal heart sounds → Congenital heart defects (e.g., VSD, ASD, coarctation of the aorta)
119
NIPE Exam - Abdomen
Organomegaly → Congenital infections, metabolic disorders (e.g., storage diseases); Abdominal masses → Wilms tumor, neuroblastoma, hydronephrosis; Delayed umbilical cord separation → Immune disorders (e.g., leukocyte adhesion deficiency)
120
NIPE Exam - Genitalia & Anus
Undescended testes → Cryptorchidism, risk of infertility/cancer; Hypospadias → Urethral developmental anomaly; Imperforate anus → Anorectal malformation (e.g., VACTERL association)
121
NIPE Exam - Spine & Limbs
Sacral dimple with abnormal signs → Spina bifida occulta; Absent/extra digits → Polydactyly, syndactyly (linked to genetic syndromes); Asymmetric limb movement → Erb’s palsy (brachial plexus injury), cerebral palsy
122
NIPE Exam - Hips
Positive Barlow/Ortolani test → Developmental dysplasia of the hip (DDH)
123
NIPE Exam - Reflexes & Tone
Absent Moro reflex → Birth trauma (e.g., brachial plexus injury), brain injury; Hypotonia → Down syndrome, Prader-Willi syndrome, neuromuscular disorders (e.g., SMA); Hypertonia → Cerebral palsy
124
Birth Asphyxia - Definition
Birth asphyxia is a condition where a newborn fails to establish or sustain adequate respiration at birth, leading to hypoxia (low oxygen) and acidosis, which can cause organ damage, particularly to the brain (Hypoxic-Ischemic Encephalopathy, HIE).
125
Birth Asphyxia - Causes
Antenatal: Preeclampsia, eclampsia, diabetes, severe anemia, placental abruption, placenta previa, intrauterine infections; Intrapartum: Prolonged or obstructed labour, umbilical cord prolapse, uterine rupture, fetal distress; Postnatal: Prematurity, severe neonatal infections, congenital abnormalities
126
Birth Asphyxia - Why It Happens
Oxygen supply interruption leads to: Hypoxia → Anaerobic metabolism → Lactic acidosis → Cellular dysfunction and organ damage; Impaired cerebral blood flow → Hypoxic-Ischemic Encephalopathy (HIE); Multi-organ damage → Kidneys, heart, lungs, intestines, liver
127
Birth Asphyxia - Management
Immediate Resuscitation (ABC Approach): Airway → Clear airway, suction if necessary; Breathing → Provide PPV if not breathing spontaneously; Circulation → If HR < 60 bpm, start chest compressions, consider IV adrenaline; Temperature control → Prevent hypothermia; Supportive Care: Oxygen therapy, fluids & glucose, anticonvulsants, therapeutic hypothermia
