---

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4th INTERNAL ASSESSMENT - RGUHS STYLE 10-MARKER NOTES

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1. AETCOM TOPICS

Definition

The Four Pillars

┌─────────────────────────────────────────────────────────────┐
│                    A E T C O M                              │
├──────────┬──────────────┬──────────────────┬────────────────┤
│ ATTITUDE │   ETHICS     │ COMMUNICATION    │    MODULE      │
├──────────┼──────────────┼──────────────────┼────────────────┤
│ Empathy  │ Beneficence  │ Verbal & Non-    │ Integrated     │
│ Respect  │ Autonomy     │ verbal skills    │ curriculum     │
│ Humility │ Non-         │ Breaking bad     │ across all     │
│ Honesty  │ maleficence  │ news (SPIKES)    │ 9 semesters    │
│ Equity   │ Justice      │ Informed consent │                │
└──────────┴──────────────┴──────────────────┴────────────────┘

SPIKES Protocol (Breaking Bad News)

S → Setting      : Private room, sit down, tissues ready
P → Perception   : "What have you been told so far?"
I → Invitation   : "How much detail would you like?"
K → Knowledge    : Give information in small chunks, simple language
E → Emotions     : Acknowledge - "I understand this is difficult"
S → Summary      : Recap plan, offer follow-up, leave door open

Case Scenarios Tested

Key Points for RGUHS

• AETCOM is NOT a separate subject - integrated longitudinally
• Builds "Doctor as a professional" and "Doctor as a communicator" competencies
• Reflective journals, role plays, case-based discussions are assessment tools

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2. CIRRHOSIS AND PORTAL HYPERTENSION

Definition

Etiology

                    CAUSES OF CIRRHOSIS
                           │
          ┌────────────────┼────────────────┐
          │                │                │
      ALCOHOLIC      VIRAL HEPATITIS    METABOLIC
      (most common   B & C              NASH/NAFLD
       in India)     (most common       Wilson's disease
                     globally)          Hemochromatosis
                                        Alpha-1 AT deficiency
          │
    OTHERS: Autoimmune hepatitis, PBC, PSC, Budd-Chiari

Pathophysiology of Portal Hypertension

Fibrosis + Regenerative nodules
            │
            ↓
  ↑ Intrahepatic vascular resistance
            │
            ↓
  ↑ Portal venous pressure (>12 mmHg)
            │
    ┌───────┴────────┐
    │                │
Portosystemic     Splanchnic
collaterals       vasodilation
develop           (↑ NO, ↑ glucagon)
    │                │
Varices, etc.    Hyperdynamic
                 circulation →
                 Ascites

Portal Pressure Values

Complications - ABCDE

A → Ascites
B → Bleeding varices (esophageal/gastric)
C → Coagulopathy + Caput medusae
D → Hepatic enDopathy (Encephalopathy)
E → Endocrine changes + Edema

Also:
→ SBP (Spontaneous Bacterial Peritonitis)
→ Hepatorenal Syndrome (HRS)
→ Hepatocellular Carcinoma (HCC)
→ Hepatopulmonary Syndrome

Management Flowchart - Variceal Bleeding

ACUTE VARICEAL BLEED
        │
        ↓
Resuscitate + Terlipressin IV + Antibiotic prophylaxis (Ceftriaxone)
        │
        ↓
   Endoscopy within 12 hrs
        │
        ↓
  Band ligation (EVL)  ──→  Failure ──→  TIPSS
        │
        ↓
  Secondary prophylaxis:
  Non-selective β-blocker (Propranolol/Carvedilol) + EVL

Child-Pugh Score

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3. DEMENTIA

Definition

Cognitive Domains Affected

           MEMORY
              │
LANGUAGE ─────┼───── EXECUTIVE FUNCTION
              │
   VISUOSPATIAL ────── ATTENTION/PROCESSING

Types of Dementia - Comparison Table

Alzheimer's Pathology Diagram

Normal neuron → Amyloid precursor protein (APP) cleaved
                        │
                ↓ (beta + gamma secretase)
           Amyloid-β (Aβ42) accumulates
                        │
              Senile plaques (EXTRACELLULAR)
                        │
        + Tau protein hyperphosphorylation
                        │
        Neurofibrillary tangles (INTRACELLULAR)
                        │
            Neuronal death → Atrophy
            (hippocampus first → neocortex)

MMSE Scoring Guide

Orientation (time + place)    : 10 points
Registration (3 words)        :  3 points
Attention (serial 7s / WORLD) :  5 points
Recall (3 words)              :  3 points
Language + Construction       :  9 points
                         TOTAL: 30 points

Scoring: 24-30 = Normal | 18-23 = Mild | 10-17 = Moderate | <10 = Severe

Management

REVERSIBLE CAUSES FIRST (treat and cure):
Hypothyroidism, B12 deficiency, Normal Pressure Hydrocephalus,
Subdural hematoma, Neurosyphilis, Depression (pseudodementia)

PHARMACOLOGICAL (Alzheimer's):
Mild-Moderate → Cholinesterase inhibitors:
  Donepezil (once daily, most used)
  Rivastigmine (patch - preferred in Parkinson's dementia)
  Galantamine

Moderate-Severe → Add Memantine (NMDA antagonist)

NON-PHARMACOLOGICAL:
Cognitive stimulation, structured routine, caregiver support,
safety assessment, advance care planning

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4. ECMO (Extracorporeal Membrane Oxygenation)

Definition

ECMO Circuit

Patient Blood
    │
    ↓
[DRAINAGE CANNULA] ──→ [CENTRIFUGAL PUMP] ──→ [MEMBRANE OXYGENATOR]
                                                      │
                                               O2 added
                                               CO2 removed
                                               Blood warmed
                                                      │
                                               [RETURN CANNULA]
                                                      │
                                               Back to Patient

VV vs VA ECMO

┌─────────────────────────────────────────────────────────────┐
│              VV-ECMO              │        VA-ECMO           │
├───────────────────────────────────┼─────────────────────────┤
│ Vein → Oxygenator → Vein         │ Vein → Oxygenator →     │
│                                   │ Artery                  │
│ Supports: LUNGS ONLY              │ Supports: HEART + LUNGS │
│                                   │                         │
│ Indications:                      │ Indications:            │
│ • Severe ARDS (P/F <80)           │ • Cardiogenic shock     │
│ • COVID pneumonia                 │ • Cardiac arrest (E-CPR)│
│ • Status asthmaticus              │ • Massive PE            │
│ • Bridge to transplant            │ • Post-cardiotomy shock │
│                                   │ • Bridge to LVAD/Tx     │
│ Heart function MUST be intact     │ Supports both           │
└───────────────────────────────────┴─────────────────────────┘

Complications

ECMO Weaning

VV-ECMO WEANING:
Reduce FiO2 on membrane → Trial clamp → If SpO2 maintains → Decannulate

VA-ECMO WEANING:
Reduce flow gradually → Echo assessment of cardiac function
→ If EF recovering → Decannulate

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5. ROLE OF PHYSICIAN IN COMMUNITY

Levels of Prevention

┌─────────────────────────────────────────────────────┐
│              LEVELS OF PREVENTION                   │
├─────────────────────────────────────────────────────┤
│ PRIMORDIAL    : Prevent risk factors from arising   │
│                e.g., healthy food policy, no-tobacco│
│                zone                                 │
├─────────────────────────────────────────────────────┤
│ PRIMARY       : Prevent disease before it occurs    │
│                e.g., vaccination, health education  │
├─────────────────────────────────────────────────────┤
│ SECONDARY     : Early detection + treatment         │
│                e.g., screening, cervical Pap smear  │
├─────────────────────────────────────────────────────┤
│ TERTIARY      : Reduce disability, rehabilitation   │
│                e.g., cardiac rehab, physiotherapy   │
└─────────────────────────────────────────────────────┘

Physician's Community Roles (Wheel Model)

                    CLINICIAN
                       │
RESEARCHER ────── PHYSICIAN ──────── HEALTH EDUCATOR
                       │
              DISEASE SURVEILLANCE
                       │
        ┌──────────────┼──────────────┐
   ADVOCATE      GATEKEEPER      TEAM LEADER
(social determinants) (referral)  (PHC team)

Indian Healthcare Team at PHC Level

Notifiable Diseases (Physician's Legal Duty)

Must report to CMO/District Health Officer:
• Cholera, Plague, Yellow Fever (International)
• Tuberculosis, Leprosy, Malaria, Dengue
• Polio, Measles, Diphtheria, Pertussis
• Rabies, Meningitis, Typhoid
• COVID-19 (added 2020)

Alma-Ata Declaration (1978) - PHC Principles

1. Equitable distribution
2. Community participation
3. Focus on prevention & promotion
4. Intersectoral coordination
5. Appropriate technology
   → Goal: "Health for All by 2000" (now SDG 2030)

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6. ETHICS - PRINCIPLES (PRINCIPLISM)

The Four Principles (Beauchamp & Childress, 1979)

┌──────────────────────────────────────────────────────────────┐
│                  FOUR PRINCIPLES OF BIOETHICS                │
├──────────────┬───────────────────────────────────────────────┤
│ AUTONOMY     │ Patient's RIGHT to make their own decisions   │
│              │ Basis of INFORMED CONSENT                     │
│              │ Competent adult can refuse life-saving Rx     │
├──────────────┼───────────────────────────────────────────────┤
│ BENEFICENCE  │ ACT in patient's BEST INTEREST                │
│              │ "Do good" - positive obligation               │
│              │ Basis for treatment recommendations           │
├──────────────┼───────────────────────────────────────────────┤
│ NON-         │ "PRIMUM NON NOCERE"- First, do no harm        │
│ MALEFICENCE  │ Negative obligation - avoid harm              │
│              │ Weigh risk vs benefit of every intervention   │
├──────────────┼───────────────────────────────────────────────┤
│ JUSTICE      │ FAIR treatment of all patients                │
│              │ Equitable resource distribution               │
│              │ No discrimination (race, religion, gender)    │
└──────────────┴───────────────────────────────────────────────┘

Informed Consent - Components

Valid Informed Consent requires ALL of the following:

  DISCLOSURE ──→ Doctor explains diagnosis, treatment, alternatives, risks
       │
  COMPREHENSION ──→ Patient understands (in their language)
       │
  VOLUNTARINESS ──→ No coercion or undue influence
       │
  COMPETENCE ──→ Patient has decision-making capacity
       │
  DECISION ──→ Patient makes a choice (accept or refuse)

When Consent Cannot Be Obtained

Ethical Conflicts - Resolution Framework

Autonomy vs Beneficence:
  → Competent patient → AUTONOMY wins
  → Incompetent patient → BENEFICENCE wins (best interests)

Confidentiality vs Duty to Warn:
  → Tarasoff principle: duty to warn identifiable third party
  → HIV disclosure to sexual partners after counseling

Double Effect Principle:
  → Morphine in terminal cancer (relieves pain but may hasten death)
  → Intent = relieve suffering (acceptable)

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7. OSTEOPOROSIS

Definition

WHO Diagnostic Criteria (T-score on DEXA)

          T-score
          ≥ -1.0     →  NORMAL
     -1.0 to -2.5   →  OSTEOPENIA (low bone mass)
          ≤ -2.5     →  OSTEOPOROSIS
   ≤ -2.5 + fracture → SEVERE OSTEOPOROSIS

Pathophysiology

BONE REMODELING CYCLE:
  Osteoclasts (resorb bone) ←──── RANKL (stimulates)
         ↑                         OPG (inhibits)
  Imbalance: ↑ Resorption > ↑ Formation
         │
         ↓
  Progressive bone loss
         │
    ┌────┴────────────────────┐
    │                         │
Trabecular bone (spine)  Cortical bone (hip, radius)
Loses first              Loses later

Risk Factors

NON-MODIFIABLE              MODIFIABLE
────────────────            ────────────────
Female sex                  Smoking
Age (>65 F, >70 M)          Alcohol
Post-menopause              Low calcium/vit D diet
Family history              Sedentary lifestyle
Prior fragility fracture    Low body weight
Asian/Caucasian ethnicity   Prolonged corticosteroid use
                            Excess thyroid/PTH

FRAX Tool

FRAX = 10-year probability of major osteoporotic fracture (%)
Inputs: Age, Sex, BMI, BMD, steroid use, smoker, alcohol, prior fracture, parental hip Fx, RA, secondary osteoporosis
→ Treatment threshold: FRAX hip fracture ≥3% OR major fracture ≥20%

Treatment Algorithm

OSTEOPOROSIS DIAGNOSED
        │
        ↓
Calcium 1000-1200mg/day + Vitamin D 800-1000 IU/day (ALL patients)
+ Weight-bearing exercise + Fall prevention + Smoking/alcohol cessation
        │
        ↓
Pharmacotherapy:
        │
  ┌─────┴──────────────────────────────────┐
  │ ANTIRESORPTIVE            ANABOLIC     │
  │                                         │
  │ Bisphosphonates           Teriparatide  │
  │ (FIRST LINE)              (severe OP,  │
  │ Alendronate 70mg/week     high fracture │
  │ Risedronate 35mg/week     risk)         │
  │ Zoledronic acid IV yearly               │
  │                           Romosozumab   │
  │ Denosumab (RANKL inhib)   (new - anti- │
  │ 60mg SC q6 months         sclerostin)  │
  │                                         │
  │ Raloxifene (SERM) -                     │
  │ post-menopausal women                   │
  └─────────────────────────────────────────┘

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8. COPD

Definition (GOLD 2023)

Pathological Types

┌────────────────────────────────────────────────────────────┐
│  CHRONIC BRONCHITIS          │  EMPHYSEMA                  │
│  ("Blue Bloater")            │  ("Pink Puffer")            │
├──────────────────────────────┼─────────────────────────────┤
│  Cough + sputum ≥3 months    │  Abnormal enlargement of    │
│  in ≥2 consecutive years     │  airspaces DISTAL to        │
│                              │  terminal bronchioles       │
│  Airway inflammation         │  Destruction of alveolar    │
│  Mucus gland hypertrophy     │  walls - LOSS of elastic    │
│  (Reid index >0.4)           │  recoil                     │
│                              │                             │
│  Hypoxic, hypercapnic        │  Near-normal PaO2, thin,    │
│  overweight, cyanotic        │  breathless, pursed lips    │
│  cor pulmonale               │  barrel chest               │
└──────────────────────────────┴─────────────────────────────┘
Emphysema types:
  Centriacinar → Smoking (upper lobes)
  Panacinar → Alpha-1 AT deficiency (lower lobes)
  Paraseptal → Spontaneous pneumothorax in young

GOLD Spirometric Classification

GOLD ABE Groups (2023)

Symptom Assessment:
  mMRC ≥2 or CAT ≥10 = More symptoms

Exacerbation History:
  0-1 (no hospitalization) = Low risk
  ≥2 or ≥1 hospitalization = High risk

         Symptoms
          Low    │    High
         ────────┼────────
High  E  │  E   │   E   │
Risk     ├───────┼───────┤
Low   A  │  A   │   B   │
Risk     └───────┴───────┘

Step-Up Treatment Algorithm

ALL COPD:
  Smoking cessation (most important ever)
  Influenza + Pneumococcal vaccines
  Pulmonary rehabilitation
        │
GROUP A → BRONCHODILATOR (SABA or SAMA)
        │
GROUP B → LABA or LAMA (prefer LAMA)
        │
GROUP E → LABA + LAMA
        │  (if eos ≥300 or frequent exacerbations → add ICS)
        ↓
  TRIPLE THERAPY: LABA + LAMA + ICS
        │
  Roflumilast (PDE4 inhibitor) if FEV1<50% + chronic bronchitis
  Azithromycin prophylaxis (frequent exacerbators, ex-smokers)

LTOT: if PaO2 ≤55mmHg or SaO2 ≤88% → O2 ≥15 hrs/day

Acute Exacerbation Management

AECOPD:
  1. Controlled O2 → target SpO2 88-92% (avoid CO2 retention)
  2. SABA ± SAMA nebs (salbutamol + ipratropium)
  3. Prednisolone 40mg/day × 5 days
  4. Antibiotics if ≥2 of: ↑ dyspnea, ↑ sputum, ↑ purulence
     (Amoxicillin-clavulanate or Doxycycline or Azithromycin)
  5. NIV if pH <7.35 + PaCO2 >45 (GOLD STANDARD for type 2 RF)
  6. Intubation if NIV fails

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9. MEDICO-LEGAL ISSUES WITH RESEARCH

Foundational Documents

┌─────────────────────────────────────────────────────────────┐
│  NUREMBERG CODE (1947)                                      │
│  → First code after Nazi experiments                        │
│  → Voluntary consent is ABSOLUTELY essential                │
├─────────────────────────────────────────────────────────────┤
│  DECLARATION OF HELSINKI (WMA, 1964, last revised 2013)    │
│  → Ethical principles for medical research on humans       │
│  → IRB/IEC approval mandatory                              │
│  → Research interest NEVER > welfare of subject            │
├─────────────────────────────────────────────────────────────┤
│  BELMONT REPORT (USA, 1979)                                 │
│  → 3 principles: Respect, Beneficence, Justice             │
├─────────────────────────────────────────────────────────────┤
│  ICMR NATIONAL ETHICAL GUIDELINES (India, 2017)            │
│  → New Drugs & Clinical Trials Rules (2019)                │
│  → Audio-visual consent for illiterate subjects            │
│  → CTRI registration mandatory                             │
└─────────────────────────────────────────────────────────────┘

Clinical Trial Phases

PHASE 0 → Microdosing, PK study (<10 subjects)
   │
PHASE I → Safety, dose-finding (20-100 healthy volunteers)
   │
PHASE II → Efficacy + safety (100-300 patients)
   │
PHASE III → Large RCT vs placebo/standard (1000-3000)
   │           → Required for DRUG APPROVAL
PHASE IV → Post-marketing surveillance (safety, rare ADRs)

Medico-Legal Issues Checklist

Informed Consent in Research - Special Populations

VULNERABLE GROUPS needing EXTRA PROTECTION:
  • Children → Parent/guardian consent + child assent
  • Prisoners → No coercion, independent oversight
  • Pregnant women → Special risk-benefit analysis
  • Mentally ill → Legally authorized representative
  • Students/employees → Ensure voluntary, not pressured

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10. DEGENERATIVE JOINT DISEASE (OSTEOARTHRITIS)

Definition

Pathophysiology

Mechanical stress / aging / obesity
            │
            ↓
Chondrocyte activation
            │
            ↓
↑ MMPs (matrix metalloproteinases) + ADAMTS enzymes
            │
            ↓
Proteoglycan depletion → Collagen type II breakdown
            │
            ↓
CARTILAGE FIBRILLATION → EROSION → EBURNATION (ivory bone)
            │
     ┌──────┴───────────────┐
     │                      │
Subchondral sclerosis   Osteophyte
+ Subchondral cysts     formation
(Geode formation)       at joint margins

Clinical Features

Pain: worse with USE, relieved by REST (unlike RA)
Morning stiffness: < 30 minutes (unlike RA >1 hour)
Crepitus on movement
Bony enlargement of joints
Joint deformity (varus/valgus at knee)

HAND OA signs:
  Heberden's nodes = DIP joint osteophytes
  Bouchard's nodes = PIP joint osteophytes
  Squaring of thumb base (1st CMC OA)

X-Ray Features (LOSS Mnemonic)

L → Loss of joint space (asymmetric - weight-bearing side)
O → Osteophytes (bony spurs at joint margins)
S → Subchondral Sclerosis (increased density)
S → Subchondral cysts (geodes - fluid-filled)

(NO periarticular osteopenia, NO erosions - unlike RA)

OA vs RA - Comparison

Management

Non-pharmacological (FIRST LINE):
  Weight loss (every 1kg lost = 4kg less knee force)
  Exercise (quadriceps strengthening, water aerobics)
  Walking aids, knee braces, shoe inserts

Pharmacological:
  Topical NSAIDs / Diclofenac gel → First line mild-moderate
  Oral NSAIDs / COX-2 inhibitors (Celecoxib) → Moderate
  Intraarticular corticosteroid → Acute flares
  Intraarticular hyaluronic acid → Some benefit (controversial)
  Duloxetine → Chronic knee OA with central sensitization

Surgical:
  Arthroscopy → Minimal benefit (not recommended routinely)
  Osteotomy → Young patients with malalignment
  Total Knee/Hip Replacement → Severe, refractory disease

---

11. FRACTURES IN ELDERLY + VISION LOSS IN ELDERLY

A. FRACTURES IN ELDERLY

Why Elderly Fracture Easily

AGE-RELATED CHANGES:
  ↓ Bone density (osteoporosis)
  ↓ Muscle mass (sarcopenia)
  ↓ Balance and coordination
  ↓ Vision
  Polypharmacy (sedatives, antihypertensives → falls)
  Cognitive impairment

Common Fragility Fractures

HIP FRACTURE (most serious)
  ├── Intracapsular (femoral neck)
  │     → Disrupts blood supply to femoral head
  │     → Risk of avascular necrosis (AVN)
  │     → Tx: Hemiarthroplasty or THR
  │
  └── Extracapsular (intertrochanteric/subtrochanteric)
        → Blood supply intact
        → Tx: Dynamic Hip Screw (DHS) or IM nail

VERTEBRAL FRACTURE
  → Thoracic spine most common
  → Acute back pain + height loss
  → Tx: Pain management, brace; severe: vertebroplasty

COLLES FRACTURE (distal radius)
  → FOOSH (fall on outstretched hand)
  → "Dinner fork" deformity
  → Tx: Cast immobilization; displaced: ORIF

Hip Fracture Mortality

30-day mortality     : ~10%
1-year mortality     : 20-30%
Risk factors for death: Age >80, dementia, cardiac disease,
                        delay to surgery >48 hours
→ ORTHOGERIATRIC CO-MANAGEMENT improves outcomes

B. VISION LOSS IN ELDERLY

Causes Summary

┌──────────────────────────────────────────────────────────────┐
│ CATARACT (most common overall)                              │
│  → Clouding of lens; painless, progressive                  │
│  → Risk: Age, diabetes, steroids, UV exposure               │
│  → Treatment: Phacoemulsification + IOL implant             │
├──────────────────────────────────────────────────────────────┤
│ AMD (Age-related Macular Degeneration)                      │
│  → CENTRAL vision loss; scotoma; straight lines bent        │
│  → DRY (atrophic, drusen) vs WET (neovascular - urgent!)   │
│  → Wet AMD: Anti-VEGF intravitreal injections              │
│    (Ranibizumab, Bevacizumab, Aflibercept)                  │
├──────────────────────────────────────────────────────────────┤
│ GLAUCOMA (silent thief of sight)                            │
│  → PERIPHERAL vision loss first (tunnel vision)             │
│  → ↑ IOP → optic disc cupping → ganglion cell death        │
│  → Primary open-angle (most common; chronic, painless)      │
│  → Primary angle-closure (acute: red eye + headache + vomit)│
│  → Rx: Timolol drops, latanoprost, trabeculectomy          │
├──────────────────────────────────────────────────────────────┤
│ DIABETIC RETINOPATHY                                        │
│  → Non-proliferative (dot-blot hemorrhages, hard exudates) │
│  → Proliferative (neovascularization → vitreous hemorrhage)│
│  → Rx: Glycemic control, laser photocoagulation, anti-VEGF │
├──────────────────────────────────────────────────────────────┤
│ RETINAL ARTERY/VEIN OCCLUSION                               │
│  → CRAO: Sudden painless, cherry-red spot, box-car vessels  │
│  → CRVO: "Blood and thunder" fundus                         │
└──────────────────────────────────────────────────────────────┘

---

12. HYPERTENSION: EMERGENCY, URGENCY, PRIMARY, SECONDARY

HTN Emergency vs Urgency

┌─────────────────────────────────────────────────────────────┐
│              BP USUALLY > 180/120 mmHg                     │
├────────────────────────┬────────────────────────────────────┤
│   HTN URGENCY          │     HTN EMERGENCY                  │
├────────────────────────┼────────────────────────────────────┤
│ NO end-organ damage    │ ACUTE end-organ damage (TOD)        │
│                        │                                     │
│                        │ HYPERTENSIVE ENCEPHALOPATHY        │
│                        │ HAEMORRHAGIC / ISCHAEMIC STROKE    │
│                        │ ACUTE AORTIC DISSECTION            │
│                        │ ACUTE MI / UNSTABLE ANGINA         │
│                        │ ACUTE LVF / PULMONARY OEDEMA       │
│                        │ ECLAMPSIA / SEVERE PRE-ECLAMPSIA   │
│                        │ ACUTE RENAL FAILURE                │
│                        │ MICROANGIOPATHIC HAEMOLYTIC ANAEMIA│
├────────────────────────┼────────────────────────────────────┤
│ Oral agents            │ IV agents in ICU                   │
│ Reduce BP over 24-48h  │ Reduce MAP 10-20% in 1st hour     │
│ No ICU needed          │ Then 25% in 2-6 hrs → target 160/100 in 24h│
└────────────────────────┴────────────────────────────────────┘

IV Drugs for HTN Emergency

SPECIAL RULE - Aortic Dissection: Reduce systolic to <120 mmHg in 20 minutes using labetalol IV or esmolol + nitroprusside.

Primary vs Secondary Hypertension

┌──────────────────────────────────────────────────────────┐
│  PRIMARY (ESSENTIAL)         │  SECONDARY                │
│  90-95% of all HTN           │  5-10% of HTN             │
├──────────────────────────────┼───────────────────────────┤
│  No identifiable cause       │  Identifiable cause       │
│  Multifactorial:             │                           │
│  Genetics + sodium +         │  RENAL (most common):     │
│  RAAS activation +           │  Renovascular HTN         │
│  SNS overactivity            │  (RAS - fibromuscular     │
│  + obesity                   │  dysplasia in young F,    │
│                              │  atherosclerosis in old)  │
│  Gradual onset               │  CKD / PCKD               │
│  Middle-aged adults          │                           │
│                              │  ENDOCRINE:               │
│                              │  Primary aldosteronism    │
│                              │  (Conn's - hypokalemia!)  │
│                              │  Phaeochromocytoma        │
│                              │  (paroxysmal symptoms)    │
│                              │  Cushing's syndrome       │
│                              │  Hypothyroidism           │
│                              │                           │
│                              │  OTHERS:                  │
│                              │  Coarctation of aorta     │
│                              │  OSA                      │
│                              │  OCP, NSAIDs, steroids    │
└──────────────────────────────┴───────────────────────────┘

WHEN TO SUSPECT SECONDARY HTN

Red Flags:
  • Age <30 with no family history
  • Resistant HTN (≥3 drugs including a diuretic)
  • Sudden onset / severe / accelerated HTN
  • Hypokalemia without diuretics → Conn's (24hr urinary aldosterone)
  • Paroxysmal symptoms (sweating, headache, palpitations) → Pheo
  • Abdominal bruit → Renovascular
  • Truncal obesity, striae, moon face → Cushing's
  • Absent femoral pulses → Coarctation

---

13. ABG AND ACID-BASE DISORDERS

Normal ABG Values

┌──────────────────────────────────────────────────────┐
│  pH        : 7.35 - 7.45                            │
│  PaCO2     : 35 - 45 mmHg     (respiratory)         │
│  HCO3-     : 22 - 26 mEq/L    (metabolic)           │
│  PaO2      : 80 - 100 mmHg                          │
│  SaO2      : 95 - 100%                              │
│  Base excess: -2 to +2 mEq/L                        │
└──────────────────────────────────────────────────────┘

5-Step Systematic ABG Interpretation

STEP 1: Is pH ACIDEMIA (<7.35) or ALKALEMIA (>7.45)?

STEP 2: Identify PRIMARY disorder:
         CO2 ↑  →  Respiratory Acidosis
         CO2 ↓  →  Respiratory Alkalosis
         HCO3 ↓ →  Metabolic Acidosis
         HCO3 ↑ →  Metabolic Alkalosis

STEP 3: Is there COMPENSATION?
  Met Acidosis → CO2 = 1.5(HCO3) + 8 ± 2 (Winter's formula)
  Met Alkalosis → CO2 ↑ 0.7 per 1 mEq ↑ HCO3 (up to 55)
  Resp Acidosis (acute) → HCO3 ↑ 1 per 10 CO2 ↑
  Resp Acidosis (chronic)→ HCO3 ↑ 3.5 per 10 CO2 ↑

STEP 4: If Metabolic Acidosis → Calculate ANION GAP
  AG = Na - (Cl + HCO3)   [Normal = 8-12 mEq/L]

STEP 5: If high AG → Check Delta-Delta for MIXED disorder
  Delta ratio = (AG - 12) / (24 - HCO3)
  <0.4 → Hyperchloremic NAGMA coexisting
  0.4-0.8 → Mixed HAGMA + NAGMA
  1-2 → Pure HAGMA
  >2 → HAGMA + Metabolic alkalosis

High AG Metabolic Acidosis - MUDPILES

M → Methanol
U → Uremia (CKD)
D → Diabetic Ketoacidosis
P → Propylene glycol / Paraldehyde
I → Isoniazid / Iron / Inborn errors
L → Lactic acidosis (most common in ICU)
E → Ethylene glycol
S → Salicylates

Normal AG (Hyperchloremic) Metabolic Acidosis - HARDUPS

H → Hyperalimentation (TPN)
A → Addison's disease
R → Renal tubular acidosis (RTA)
D → Diarrhea (loss of HCO3 - most common cause)
U → Ureteral diversion (ileal conduit)
P → Pancreatic fistula
S → Saline infusion excess

Respiratory Failure Types

TYPE 1 (Hypoxemic):  PaO2 <60, PaCO2 normal or ↓
  → Causes: Pneumonia, PE, ARDS, pulmonary edema
  → Treat: O2, treat cause

TYPE 2 (Hypercapnic): PaO2 ↓ AND PaCO2 >45
  → Causes: COPD, asthma, neuromuscular disease
  → Treat: NIV (BiPAP), controlled O2, treat cause

---

14. ACUTE RHEUMATIC FEVER + INFECTIVE ENDOCARDITIS

A. ACUTE RHEUMATIC FEVER (ARF)

Pathogenesis

Group A Streptococcal Pharyngitis (Strep. pyogenes)
            │
     Immune response
            │
   Molecular mimicry:
   Anti-streptococcal antibodies cross-react with:
            │
  ┌─────────┼─────────────────┐
  │         │                 │
Heart     Joints             Brain
valves    synovium           (caudate nucleus)
  │         │                 │
Carditis  Arthritis         Chorea

Jones Criteria (2015 AHA Revision)

MAJOR CRITERIA ("CASES"):
  C → Carditis (clinical or subclinical echo)
  A → Arthritis:
       Low-risk populations: Migratory polyarthritis
       High-risk populations: Monoarthritis
  S → Sydenham's Chorea (involuntary purposeless movements)
  E → Erythema Marginatum (skin rash, evanescent)
  S → Subcutaneous Nodules (over bony prominences)

MINOR CRITERIA:
  Fever >38.5°C
  Elevated ESR >60mm/hr and/or CRP >3mg/dL
  Prolonged PR interval on ECG
  Arthralgia (only if arthritis NOT major)
  
EVIDENCE OF GAS INFECTION:
  • Positive throat culture / rapid Ag test
  • Elevated / rising ASO titre (>200 IU/mL adults)
  • Anti-DNase B elevated

DIAGNOSIS: 2 Major OR 1 Major + 2 Minor + GAS evidence

Management

1. Eradicate GAS: Penicillin V PO 10 days OR
                  Benzathine Penicillin G IM single dose
2. Arthritis: Aspirin 50-70mg/kg/day × 2-4 weeks
3. Carditis (without CCF): Aspirin or Prednisolone
4. Severe carditis with CCF: Prednisolone 2mg/kg/day × 2-3 weeks
5. Chorea: Carbamazepine / Valproate; haloperidol if severe

SECONDARY PROPHYLAXIS (Benzathine PCN G 1.2 MU IM q3-4 weeks):
  No carditis: 5 years or age 21 (whichever longer)
  Carditis - no residual valve disease: 10 years or age 21
  Carditis + residual valve disease: 10 years or age 40
  Severe valve disease: LIFELONG

B. INFECTIVE ENDOCARDITIS

Modified Duke Criteria

PATHOLOGICAL CRITERIA (definite IE):
  • Microorganism cultured from vegetation
  • Pathological lesion confirmed at surgery/autopsy

CLINICAL CRITERIA (Definite IE = 2 Major OR 1 Major+3 Minor OR 5 Minor):

MAJOR CRITERIA:
  Blood cultures: Typical organisms ×2 (Viridans strep,
                  S.bovis, HACEK, S.aureus, Enterococcus)
                  OR persistently positive cultures
  Echo: Vegetation, abscess, new valve dehiscence,
        new valvular regurgitation

MINOR CRITERIA:
  Predisposing condition (valve disease, IVDU, prosthetic)
  Fever >38°C
  Vascular phenomena (Janeway, septic emboli, ICH)
  Immunological phenomena (Osler nodes, Roth spots, RF+)
  Positive blood culture not meeting major

Classic Signs

Osler's Nodes    → Painful, tender nodules - FINGER PADS/TOES
                   (immune complex deposition)
Janeway Lesions  → Painless, flat hemorrhages - PALMS/SOLES
                   (septic microemboli)
Roth Spots       → Retinal hemorrhage with pale center
Splinter Hemorrhages → Subungual, linear
Clubbing         → Chronic IE

Treatment Principles

EMPIRICAL: Vancomycin + Gentamicin (native valve)
            Vancomycin + Rifampicin + Gentamicin (prosthetic)

SPECIFIC (after cultures):
  Viridans strep: Penicillin G ± Gentamicin × 4 weeks
  S. aureus (MSSA): Flucloxacillin × 6 weeks
  S. aureus (MRSA): Vancomycin × 6 weeks
  
SURGICAL INDICATIONS (SAVE mnemonic):
  S → Severe heart failure from valve dysfunction
  A → Abscess / fistula / prosthetic valve involvement
  V → Vegetation >10mm with embolic risk
  E → Failure to Eradicate (persistent bacteremia >1 week)

---

15. ACUTE RENAL FAILURE (AKI) + CKD

A. AKI

KDIGO Definition & Staging

DEFINITION (any one):
  • ↑ S.Creatinine ≥0.3 mg/dL within 48 hours
  • ↑ S.Creatinine ≥1.5× baseline within 7 days
  • Urine output <0.5 mL/kg/hr for >6 hours

STAGING:
  Stage 1: Cr ×1.5-1.9 baseline OR ↑0.3 mg/dL; UO <0.5mL/kg/h >6h
  Stage 2: Cr ×2.0-2.9 baseline; UO <0.5mL/kg/h >12h
  Stage 3: Cr ×3 or >4mg/dL; UO <0.3mL/kg/h >24h; anuria >12h

Classification

PRE-RENAL (55-60%)             INTRINSIC (35-40%)
Hypovolemia                    ATN (most common):
Heart failure                    Ischemia
Sepsis (relative)                Nephrotoxins (contrast, amino-
Hepatorenal syndrome             glycosides, NSAIDs, cisplatin)
Artery stenosis                AIN (interstitial nephritis)
                               Glomerulonephritis
                               Vasculitis, TTP/HUS

POST-RENAL (5-10%)
BPH, urethral stricture
Bladder tumor
Bilateral ureteric obstruction (stones, malignancy)
Cervical/prostate cancer

Pre-renal vs ATN - Differentiation

AEIOU - Indications for Emergency Dialysis

A → Acidosis (pH <7.1, refractory to treatment)
E → Electrolytes (Hyperkalemia >6.5 with ECG changes)
I → Intoxication (salicylates, methanol, ethylene glycol, lithium)
O → Overload (pulmonary edema refractory to diuretics)
U → Uremia (encephalopathy, pericarditis, bleeding)

B. CKD

KDIGO CKD Classification

GFR CATEGORIES:            ALBUMINURIA CATEGORIES:
G1: ≥90 (normal)           A1: <30 mg/g (normal)
G2: 60-89 (mildly ↓)       A2: 30-300 (moderately ↑)
G3a: 45-59                 A3: >300 (severely ↑)
G3b: 30-44
G4: 15-29 (severely ↓)
G5: <15 (kidney failure)

CKD Complications & Management

┌──────────────────────────────────────────────────────────────┐
│  COMPLICATION          CAUSE              TREATMENT          │
├──────────────────────────────────────────────────────────────┤
│  Anemia               ↓ EPO               ESA + IV iron     │
│  Hypertension         Na/H2O retention    ACEi/ARB + diuretic│
│  Metabolic acidosis   ↓ H+ excretion      Sodium bicarbonate │
│  Hyperkalemia         ↓ K+ excretion      Low K diet, patiromer│
│  Hyperphosphatemia    ↓ PO4 excretion     Sevelamer, restrict │
│  Secondary hyperPTH   ↑ PTH due to ↓ Ca   Calcitriol, cinacalcet│
│  Renal osteodystrophy ↓ Vit D activation  Active Vit D      │
│  Uremia               Toxin accumulation  Dialysis           │
└──────────────────────────────────────────────────────────────┘

---

16. COMMUNICATION AND MEDIA MANAGEMENT

Levels of Communication in Healthcare

INTRAPERSONAL → Self-reflection; doctor's own biases and emotions
INTERPERSONAL → Doctor-patient; doctor-family; team communication
ORGANIZATIONAL → Referral letters; discharge summaries; MDT meetings
PUBLIC/MEDIA → Press conferences; social media; health campaigns

Calgary-Cambridge Model of Consultation

INITIATING THE SESSION
  → Greet, introduce, establish rapport
  → Identify reason for visit (open-ended)
        │
GATHERING INFORMATION
  → ICE: Ideas, Concerns, Expectations
  → Verbal and non-verbal cues
        │
PHYSICAL EXAMINATION
        │
EXPLANATION AND PLANNING
  → Chunking and checking
  → Shared decision-making
        │
CLOSING THE SESSION
  → Safety netting, follow-up plan

Breaking Bad News - SPIKES

S → Setting up: Private, sit down, turn off phone, support person
P → Perception: "What do you understand about your illness?"
I → Invitation: "Would you like me to explain the full picture?"
K → Knowledge: "I'm afraid the news is not good... the biopsy shows cancer"
E → Emotions/Empathy: Pause, acknowledge, "I can see this is very hard"
S → Strategy/Summary: Treatment plan, next steps, offer hope realistically

Media Management

TRADITIONAL MEDIA (TV, newspaper):
  → Designate ONE spokesperson
  → Stick to facts, avoid speculation
  → Never discuss individual patient details (HIPAA/MCI rules)
  → Have institutional communications team involved

SOCIAL MEDIA (Instagram, X/Twitter, YouTube):
  → NEVER post identifiable patient information
  → Maintain professional dignity at all times
  → Medical misinformation: rebut with evidence-based sources
  → Telemedicine consults: document, consent, limitations stated

HEALTH COMMUNICATION CAMPAIGNS:
  → SBCC (Social Behaviour Change Communication)
  → IEC (Information, Education, Communication) materials
  → Tailored to literacy level and local language

Documentation (Medico-legal importance)

"If it's not documented, it didn't happen"

Essential documents:
  • Medical records (maintain 3 years minimum - MCI)
  • Informed consent forms
  • Discharge summaries
  • Death certificates (accurate cause of death mandatory)
  • Referral letters (ISBAR format):
      I - Identify
      S - Situation
      B - Background
      A - Assessment
      R - Recommendation

---

17. ADRENAL INSUFFICIENCY

Classification

┌─────────────────────────────────────────────────────────────┐
│              ADRENAL INSUFFICIENCY                          │
├──────────────┬───────────────────┬──────────────────────────┤
│   PRIMARY    │    SECONDARY      │      TERTIARY            │
│  (Addison's) │ (Pituitary)       │ (Hypothalamic)           │
├──────────────┼───────────────────┼──────────────────────────┤
│ Adrenal      │ ↓ ACTH from       │ ↓ CRH →                  │
│ gland        │ pituitary         │ ↓ ACTH →                 │
│ destroyed    │ damage            │ ↓ Cortisol               │
│              │                   │                          │
│ Autoimmune   │ Pituitary tumor   │ MOST COMMON CAUSE:       │
│ (most common)│ Sheehan's         │ Chronic exogenous        │
│ TB (India)   │ syndrome          │ corticosteroid therapy   │
│ Bilateral    │ Hypophysitis      │                          │
│ hemorrhage   │                   │                          │
│ Fungal       │                   │                          │
│ Metastasis   │                   │                          │
└──────────────┴───────────────────┴──────────────────────────┘

HPA Axis Diagram

HYPOTHALAMUS
  → CRH (Corticotropin Releasing Hormone)
       ↓
ANTERIOR PITUITARY
  → ACTH (Adrenocorticotropic Hormone)
       ↓
ADRENAL CORTEX
  → Cortisol (Zona fasciculata)
  → Aldosterone (Zona glomerulosa) ← Only primary AI affected
  → Androgens (Zona reticularis)
       ↓
NEGATIVE FEEDBACK → suppresses CRH + ACTH

Primary vs Secondary - Key Differences

Diagnosis Algorithm

Morning cortisol (8am)
        │
   <3 μg/dL → Adrenal insufficiency CONFIRMED
        │
   >18 μg/dL → Adrenal insufficiency EXCLUDED
        │
   3-18 μg/dL → BORDERLINE → DO SHORT SYNACTHEN TEST (SST)
                                  │
                     Give Synacthen (ACTH analog) 250mcg IV
                                  │
                         Cortisol at 30 min
                                  │
                   >18 μg/dL → NORMAL (rules out primary/most secondary)
                   <18 μg/dL → ADRENAL INSUFFICIENCY CONFIRMED
                                  │
                    Check ACTH: High → Primary; Low → Secondary

Treatment

MAINTENANCE:
  Hydrocortisone 15-25mg/day in divided doses
    Morning: 10-15mg (larger dose - mimics cortisol peak)
    Afternoon: 5-10mg
  Fludrocortisone 100 mcg/day (PRIMARY ONLY - for aldosterone)
  DHEA in women for libido/wellbeing (optional)

SICK DAY RULES:
  Mild illness / fever: DOUBLE the dose
  Vomiting / unable to take orally: IM hydrocortisone 100mg
  Surgery: Triple dose perioperatively

PATIENT EDUCATION:
  → Steroid emergency card / medic-alert bracelet
  → Never stop steroids abruptly
  → Teach self-injection of hydrocortisone 100mg IM

---

18. ANTITHYROID DRUGS

Thyroid Hormone Synthesis

Dietary Iodide → Iodide trapped in thyroid (NIS)
        │
        ↓
IODIDE OXIDIZED to IODINE  ← TPO (Thyroid Peroxidase)
        │
        ↓
ORGANIFICATION: Iodine + Tyrosine → MIT, DIT  ← TPO blocks here
        │
        ↓
COUPLING: MIT + DIT → T3; DIT + DIT → T4  ← TPO blocks here
        │
        ↓
T3/T4 released into bloodstream
        │
T4 → T3 (peripheral conversion via deiodinase) ← PTU blocks here

Carbimazole vs PTU

┌─────────────────────────────────────────────────────────────┐
│              CARBIMAZOLE / METHIMAZOLE                      │
├─────────────────────────────────────────────────────────────┤
│  Mechanism: Inhibits TPO                                    │
│  Dose: 10-40mg OD (once daily - better compliance)         │
│  More potent than PTU                                       │
│  PREFERRED: 2nd trimester pregnancy, most adults            │
│  Side effects:                                              │
│    AGRANULOCYTOSIS (0.3-0.5%) - most serious               │
│    Aplasia cutis (fetal scalp defect) if used in 1st tri   │
│    Cholestatic jaundice, arthralgia, rash                   │
├─────────────────────────────────────────────────────────────┤
│              PROPYLTHIOURACIL (PTU)                         │
├─────────────────────────────────────────────────────────────┤
│  Mechanism: Inhibits TPO + blocks T4→T3 conversion         │
│  Dose: 50-200mg TDS (3 times daily)                        │
│  Less potent                                               │
│  PREFERRED: 1st trimester pregnancy, thyroid storm         │
│  Side effects:                                              │
│    AGRANULOCYTOSIS (0.3-0.5%)                              │
│    HEPATOTOXICITY (severe, fulminant - rare but serious)   │
│    ANCA-positive vasculitis                                 │
└─────────────────────────────────────────────────────────────┘

Adjunct Therapy for Hyperthyroidism

Agranulocytosis - Emergency Protocol

Patient on ATD develops:
  FEVER + SORE THROAT + MOUTH ULCERS
            │
            ↓
    STOP ATD IMMEDIATELY
            │
            ↓
Urgent CBC with differential
            │
     WBC <1000/mm³ or Neutrophils <500
            │
            ↓
 Admit + Isolation + Broad-spectrum antibiotics
 G-CSF (Filgrastim) to stimulate recovery
            │
            ↓
   Do NOT rechallenge with same ATD class
   Consider radioiodine or surgery instead

Thyroid Storm (Thyrotoxic Crisis)

Precipitants: Surgery, infection, trauma, iodine load
Burch-Wartofsky Score >45 = Thyroid storm

Treatment:
  PTU 200mg q4h (blocks synthesis + conversion)
  + Lugol's iodine 5 drops q8h (1 hour AFTER PTU)
  + Propranolol 60-80mg q4h
  + Hydrocortisone 100mg q8h (↓ T4→T3; ↑ survival)
  + Cooling, IV fluids, treat precipitant

---

19. DKA AND HYPOGLYCEMIA

A. DKA

Pathophysiology

INSULIN DEFICIENCY + ↑ GLUCAGON/CORTISOL/CATECHOLAMINES
            │
     ┌──────┴──────────────────────┐
     │                             │
HYPERGLYCEMIA                LIPOLYSIS
(↑ gluconeogenesis,          (FFA → Ketogenesis in liver)
↑ glycogenolysis,                  │
↓ glucose uptake)            Acetoacetate
     │                       Beta-hydroxybutyrate
Osmotic diuresis             Acetone (fruity breath)
     │                             │
Water/electrolyte loss         KETOACIDOSIS
(Na, K, Mg, PO4)            (High AG Metabolic Acidosis)
     │
DEHYDRATION

DKA Diagnostic Criteria

┌────────────────────────────────────────────────────────┐
│                DKA TRIAD                               │
├───────────────┬────────────────────────────────────────┤
│  HYPERGLYCEMIA│  BG >250 mg/dL (euglycemic DKA exists)│
│  ACIDOSIS     │  pH <7.3 AND/OR HCO3 <15 mEq/L        │
│  KETONEMIA    │  Ketones >3 mmol/L; 2+ urine ketones  │
└───────────────┴────────────────────────────────────────┘

Severity:
  Mild:   pH 7.25-7.30; HCO3 15-18; Ketones >3; Alert
  Moderate: pH 7.00-7.24; HCO3 10-14; Drowsy
  Severe: pH <7.00; HCO3 <10; Stupor/Coma

DKA Management - 4 Pillars

PILLAR 1: FLUIDS
  1L 0.9% NaCl over 1st hour
  Then 500mL/hr × 2 hours
  Then 250mL/hr → guided by clinical state
  Switch to 5% dextrose when BG <250 mg/dL

PILLAR 2: INSULIN
  ⚠️ ONLY START INSULIN IF K+ >3.3 mEq/L ⚠️
  Fixed rate IV insulin: 0.1 unit/kg/hr
  (Variable rate acceptable)
  Target: BG falls 50-70 mg/dL/hour
  Continue until: pH >7.3, HCO3 >15, ketones <0.6 mmol/L

PILLAR 3: POTASSIUM
  K+ >5.0: No K+, insulin can start
  K+ 3.3-5.0: 20-40 mEq K+/hr in fluids
  K+ <3.3: HOLD insulin, replete K+ aggressively first

PILLAR 4: BICARBONATE
  Only if pH <6.9 (controversial)
  100mEq NaHCO3 over 2 hours

Monitoring Protocol

Hourly: Blood glucose, vital signs
2-Hourly: Venous blood gas (pH, bicarbonate, ketones)
4-Hourly: Urea, electrolytes, creatinine
Continuous: Cardiac monitor (K+ changes)

Resolution criteria (all 3 must be met):
  pH >7.3
  HCO3 >15 mEq/L
  Ketones <0.6 mmol/L (or 2-step reduction in urine ketones)

Then: Overlap SC insulin (give 30-60 min before stopping IV)

B. HYPOGLYCEMIA

Whipple's Triad

1. SYMPTOMS of hypoglycemia
         +
2. LOW blood glucose (<70 mg/dL = alert value)
         +
3. RELIEF of symptoms after glucose administration

Symptom Progression

BG 60-70 mg/dL → ADRENERGIC (autonomic warning symptoms):
  Sweating, tremor, palpitations, anxiety, pallor, hunger

BG 50-60 mg/dL → NEUROGLYCOPENIC symptoms begin:
  Confusion, slurred speech, blurred vision, headache

BG <40 mg/dL → SEVERE neuroglycopenia:
  Seizures, unconsciousness, coma, death

⚠️ HYPOGLYCEMIA UNAWARENESS:
  Long-standing DM → loss of adrenergic warning symptoms
  → Present directly with neuroglycopenic symptoms
  → Very dangerous; requires CGM + relaxed BG targets

Management

CONSCIOUS patient (can swallow):
  15-20g fast-acting carbohydrates:
    4-5 glucose tablets
    150-200mL fruit juice
    5-6 teaspoons of sugar
  Wait 15 minutes → recheck BG
  If still <70: Repeat (Rule of 15)

UNCONSCIOUS patient (cannot swallow):
  IV: 50mL of 50% dextrose (25g glucose) IV push
  IM: Glucagon 1mg IM or SC
  Recheck BG in 15 minutes
  
Then: Give long-acting carbohydrate (bread, rice)
And: Identify and treat CAUSE

---

20. ADRENAL CRISIS

Definition

Causes

PRECIPITANTS OF ADRENAL CRISIS:
                │
     ┌──────────┼──────────────────┐
     │          │                  │
Known AI    Acute bilateral    Pituitary
patient     adrenal            apoplexy
with        destruction:       (sudden ↓
  • Missed   • Waterhouse-      ACTH)
    dose       Friderichsen
  • Infection  syndrome
  • Surgery    (meningococcemia)
  • Trauma   • Bilateral
             • adrenal
               hemorrhage
               (anticoagulants)
     │
Steroid withdrawal
(most common in practice)

Clinical Features

SHOCK (vasodilatory, refractory to vasopressors without steroids)
ABDOMINAL PAIN (severe; can mimic acute abdomen)
FEVER
CONFUSION / ALTERED CONSCIOUSNESS
HYPOGLYCEMIA
HYPONATREMIA (if primary)
HYPERKALEMIA (if primary)
HYPERPIGMENTATION (if chronic primary AI - may be pre-existing)

Emergency Management Flowchart

SUSPECT ADRENAL CRISIS
  (hypotension + known AI OR bilateral adrenal hemorrhage
   OR steroid withdrawal + stress)
        │
        ↓
DO NOT DELAY TREATMENT WAITING FOR CORTISOL RESULTS
        │
        ↓
STEP 1: Take blood (cortisol, ACTH, glucose, electrolytes, cultures)
        │
        ↓
STEP 2: IV HYDROCORTISONE 100mg STAT
        (Then 50-100mg Q6h OR 200mg/24h continuous infusion)
        │
        ↓
STEP 3: IV FLUIDS
        0.9% NaCl 1L FAST + Dextrose saline (correct hypoglycemia)
        │
        ↓
STEP 4: TREAT PRECIPITANT
        Antibiotics if sepsis
        Correct electrolytes
        │
        ↓
STEP 5: Once stable → Taper back to oral maintenance
        Add Fludrocortisone 100mcg/day when fully oral (primary AI)
        
NOTE: High-dose hydrocortisone has sufficient mineralocorticoid
      activity - fludrocortisone NOT needed acutely

---

21. DRUG-INDUCED LIVER INJURY (DILI)

Definition

Patterns of Injury (R-Ratio)

R = (ALT/ULN) ÷ (ALP/ULN)

R ≥ 5         → HEPATOCELLULAR
                 (ALT predominantly elevated)
                 e.g., Paracetamol, INH, Statins, Halothane

R ≤ 2         → CHOLESTATIC
                 (ALP predominantly elevated)
                 e.g., Amoxicillin-clavulanate, Chlorpromazine,
                       Anabolic steroids, Erythromycin

R 2-5         → MIXED
                 (Both elevated)
                 e.g., Phenytoin, Carbamazepine

Types of DILI

INTRINSIC (Predictable, dose-dependent, short latency):
  Affects everyone if dose is high enough
  Examples:
    PARACETAMOL (most important):
      Normal dose: CYP2E1 → NAPQI → Detoxified by glutathione
      Overdose: Glutathione depleted → NAPQI accumulates
              → Centrilobular (Zone 3) necrosis
              → Treatment: N-acetylcysteine (NAC) ASAP
                            (replenishes glutathione)
              → Use Rumack-Matthew nomogram to guide treatment

IDIOSYNCRATIC (Unpredictable, immune/metabolic, variable latency):
  Affects susceptible individuals only
  Examples:
    INH: 10-20% mild transaminase rise; fulminant in 1%
    Amoxicillin-clavulanate: most common cause of cholestatic DILI
    Halothane: immune-mediated hepatitis (repeat exposure = worse)
    Diclofenac: idiosyncratic hepatocellular
    Valproate: mitochondrial toxicity; children at risk

High-Yield DILI Drug List

RUCAM / CIOMS Causality Assessment

RUCAM Scale considers:
  Time to onset, course of reaction after withdrawal,
  risk factors (age, alcohol), concomitant drugs,
  exclusion of other causes, known hepatotoxicity of drug
  
Score:  >8 = Highly probable
        6-8 = Probable
        3-5 = Possible
        1-2 = Unlikely
        ≤0 = Excluded

---

22. OBESITY

Definition & Classification

BMI (Body Mass Index) = Weight (kg) / Height (m)²

WHO Classification:          Asian Cutoffs (India):
Underweight  < 18.5          Underweight  < 18.5
Normal       18.5-24.9       Normal       18.5-22.9
Overweight   25-29.9         Overweight   23-24.9
Obese I      30-34.9         Obese I      25-29.9
Obese II     35-39.9         Obese II     ≥30
Obese III    ≥40 (Morbid)

CENTRAL OBESITY (Waist circumference):
  Men: >102 cm (WHO) / >90 cm (Asian)
  Women: >88 cm (WHO) / >80 cm (Asian)

Pathophysiology

CALORIC INTAKE > CALORIC EXPENDITURE
            │
Adipose tissue accumulation (especially VISCERAL fat)
            │
     ┌──────┴──────────────────────────────┐
     │                                      │
↑ Leptin (resistance develops)         ↑ TNF-α, IL-6
↓ Adiponectin                          ↑ Free fatty acids
            │                               │
            ↓                               ↓
       Hyperphagia                   INSULIN RESISTANCE
       continues                     (Metabolic Syndrome)

Complications Diagram

                    OBESITY
                       │
    ┌──────────────────┼──────────────────┐
    │                  │                  │
CARDIOVASCULAR    METABOLIC          MECHANICAL
Hypertension      Type 2 DM          OSA
CAD/MI            Dyslipidemia       OA (knee, hip)
Stroke            NAFLD/NASH         GERD
Heart failure     Metabolic syndrome Hiatus hernia
AF                PCOS               Pseudotumor cerebri
DVT/PE            Hyperuricemia      Back pain
    │
PSYCHOSOCIAL: Depression, anxiety, social stigma, discrimination

CANCER: Breast, endometrial, colon, kidney, oesophageal, pancreatic

Management Algorithm

ASSESS BMI + WAIST + COMORBIDITIES
          │
          ↓
STEP 1 - LIFESTYLE MODIFICATION (ALL patients):
  Diet: Caloric deficit 500-750 kcal/day
        Mediterranean / Low GI / low carb diet
  Exercise: ≥150 min/week moderate aerobic
            + resistance training 2×/week
  Behaviour therapy: Food diary, CBT, group support
          │
   <5% weight loss at 6 months?
          │
          ↓
STEP 2 - PHARMACOTHERAPY (BMI ≥30 OR ≥27 + comorbidity):
  ┌──────────────────────────────────────────────────────┐
  │ Semaglutide (Ozempic/Wegovy) - GLP-1 agonist         │
  │ Best efficacy: 15-20% weight loss                     │
  │                                                       │
  │ Tirzepatide (GLP-1/GIP dual agonist) - even better   │
  │                                                       │
  │ Orlistat - Lipase inhibitor, 30% fat malabsorption   │
  │ Phentermine/topiramate                               │
  │ Naltrexone/bupropion                                 │
  └──────────────────────────────────────────────────────┘
          │
   <5-10% weight loss?
          │
          ↓
STEP 3 - BARIATRIC SURGERY (BMI ≥40 OR ≥35 + comorbidity):
  Roux-en-Y Gastric Bypass (RYGB) - gold standard
  Sleeve Gastrectomy - most popular
  Adjustable Gastric Band - least invasive
  Biliopancreatic Diversion

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23. SNAKE POISONING (ENVENOMATION)

The "Big Four" Venomous Snakes of India

┌──────────────────────────────────────────────────────────────┐
│  SNAKE              VENOM TYPE    KEY FEATURES               │
├──────────────────────────────────────────────────────────────┤
│  Russell's Viper    Hemotoxic     Most common cause of death │
│  (Daboia russelli)  Cytotoxic     Coagulopathy + AKI + local │
│                     Neurotoxic    necrosis (highly dangerous) │
├──────────────────────────────────────────────────────────────┤
│  Common Krait       Neurotoxic    Nocturnal bites during     │
│  (Bungarus caeruleus)(pre-synaptic)sleep; painless bite;     │
│                                   ascending paralysis;       │
│                                   neostigmine LESS effective │
├──────────────────────────────────────────────────────────────┤
│  Indian Cobra       Neurotoxic    Ptosis early sign;         │
│  (Naja naja)        (post-synaptic)bulbar palsy; respiratory │
│                     Cytotoxic     paralysis; local necrosis; │
│                                   neostigmine EFFECTIVE      │
├──────────────────────────────────────────────────────────────┤
│  Saw-Scaled Viper   Hemotoxic     Most number of bites;     │
│  (Echis carinatus)               coagulopathy; less severe  │
│                                   than Russell's             │
└──────────────────────────────────────────────────────────────┘

Venom Effects and Clinical Syndromes

NEUROTOXIC SYNDROME:
  Pre-synaptic (krait): irreversible block of ACh release
    → Weakness, ptosis → bulbar palsy → respiratory failure
    → Neostigmine NOT effective (block is pre-synaptic)
  Post-synaptic (cobra): reversible competitive block of nAChR
    → Similar features
    → Neostigmine + Atropine MAY reverse

HEMOTOXIC/VASCULOTOXIC SYNDROME (viper):
  Phospholipases, procoagulants → consume clotting factors
    → DIC (Disseminated Intravascular Coagulation)
    → Spontaneous bleeding from gums, old wounds, IV sites
    → Hematuria, hemoptysis, hematemesis
    → Renal failure (bilateral cortical necrosis)

CYTOTOXIC (local effects):
  Pain, swelling, blistering → necrosis → gangrene
  Compartment syndrome
  Lymphadenopathy

20-Minute Whole Blood Clotting Test (20WBCT)

HOW TO PERFORM:
  Take 2mL blood in PLAIN GLASS tube (NOT plastic/siliconized)
  Leave undisturbed at room temperature for 20 minutes
  Tilt tube:
    Blood clots → Normal coagulation
    Blood remains LIQUID → COAGULOPATHY → hemotoxic envenomation
  
Sensitivity: ~95% for systemic hemotoxic envenomation
Perform: At admission and every 1-2 hours after ASV

Management Flowchart

SNAKE BITE PATIENT
        │
        ↓
FIRST AID (at scene):
  Immobilize limb, keep BELOW heart level
  Remove tight clothing/jewelry
  Reassure, transport rapidly to hospital
  DO NOT: Cut, suck, tourniquet, ice, traditional remedies
        │
        ↓
HOSPITAL ASSESSMENT:
  Vital signs, neurological exam, examine bite site
  Identify type of envenomation
  Baseline: 20WBCT, CBC, PT/APTT, LFTs, RFTs, urine (hematuria)
        │
        ↓
INDICATIONS FOR ANTIVENOM (ASV):
  SYSTEMIC: Any coagulopathy (20WBCT positive)
            Neurotoxicity (ptosis, paralysis)
            Hemodynamic instability
            AKI, dark urine (myoglobinuria/hemoglobinuria)
  LOCAL: Rapidly progressive swelling beyond knee/elbow
        │
        ↓
POLYVALENT ASV (covers all 4 species):
  Skin test NOT recommended (unreliable, may cause anaphylaxis)
  IV route preferred (IM only if no IV access)
  Initial dose: 8-10 vials IV in 100mL NS over 1 hour
  Have ADRENALINE (epinephrine) 0.5mg IM drawn up ready
        │
   No improvement at:
   1 hour (coagulopathy) → Repeat 8-10 vials
   2 hours (neurotoxicity) → Repeat 4-6 vials
        │
        ↓
SUPPORTIVE CARE:
  Neurotoxic → Neostigmine 0.05mg/kg IV + Atropine 0.6mg IV
               (test dose; repeat if effective; cobra > krait)
               Mechanical ventilation if respiratory failure
  Hemotoxic → FFP, platelet transfusion; treat DIC
              Monitor urine output; dialysis for AKI
  Cytotoxic → Wound care, antibiotics, tetanus
              Fasciotomy ONLY if confirmed compartment syndrome
              (NOT prophylactically)

Complications to Monitor

EARLY (0-24h):    Anaphylaxis to ASV, respiratory failure,
                  hemorrhagic shock, hypotension
INTERMEDIATE:     AKI (peak 3-5 days), DIC, wound necrosis
LATE:             Bilateral renal cortical necrosis (dialysis-dependent),
                  pituitary infarction (Sheehan's-like from Russell's viper)
                  Gangrene, chronic wound complications

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QUICK REVISION TABLE - ALL 23 TOPICS

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RGUHS 10-Marker Format Reminder: Each answer should have - Definition (1 mark), Classification/Types (2 marks), Pathophysiology/Diagram (2 marks), Clinical features (2 marks), Investigations (1 mark), Management/Flowchart (2 marks). Always end with a labeled diagram or table.