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These are the questions... Do not give very long answers... But every important point should be there for first year bds

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Here are concise but complete answers for all topics visible in your image, organized for 1st year BDS:

1st Year BDS Physiology - Complete Topic Notes

1. BROWN-SEQUARD SYNDROME

Hemisection of spinal cord. Ipsilateral side: UMN paralysis (below lesion), loss of proprioception/vibration/fine touch (dorsal column). Contralateral: loss of pain and temperature (spinothalamic - crosses 1-2 segments above entry). Touch is partially preserved bilaterally.

2. REFERRED PAIN

Pain felt at a site distant from the actual source. Mechanism: Convergence theory - visceral and somatic pain fibers converge on the same second-order neuron in dorsal horn; brain misinterprets as somatic pain.

Examples: MI → left arm/jaw; liver → right shoulder; appendix → umbilicus (initially); kidney stone → groin

3. ORS JUNCTION (Ostiomeatal/Oral Structures)

In context of 1st year BDS - likely refers to Oropharyngeal isthmus or Oesophageal junction. If it means ORS (Oral Rehydration Solution): Na⁺ 75 mmol/L, Cl⁻ 65 mmol/L, Glucose 75 mmol/L, K⁺ 20 mmol/L, Citrate 10 mmol/L - uses Na-glucose cotransport for absorption.

4. NEUROMUSCULAR JUNCTION (NMJ) - Diagram

Structure: Motor nerve terminal (presynaptic) → synaptic cleft → motor end plate (postsynaptic)

Steps of transmission:

AP reaches axon terminal
Voltage-gated Ca²⁺ channels open → Ca²⁺ influx
Acetylcholine (ACh) vesicles fuse → exocytosis into cleft
ACh binds nicotinic receptors on motor end plate
Na⁺/K⁺ influx → End Plate Potential (EPP) generated
EPP triggers muscle AP → contraction
ACh broken down by acetylcholinesterase → choline recycled

Static & Dynamic aspects:

Static: structural components (AZ = active zone, junctional folds)
Dynamic: quantal release, facilitation, fatigue

5. MYASTHENIA GRAVIS

Autoimmune: antibodies against nicotinic ACh receptors (postsynaptic)
Results in reduced EPP → fatigable weakness, worsens with activity
Features: ptosis, diplopia, dysphagia, proximal limb weakness
Edrophonium (Tensilon) test: improves symptoms transiently
Treatment: anticholinesterases (neostigmine), immunosuppressants, thymectomy

6. LUNG CAPACITIES & VOLUMES (Diagram)

Volume/Capacity	Value	Definition
TV (Tidal Volume)	500 mL	Normal breath
IRV	3000 mL	Extra air after normal inspiration
ERV	1100 mL	Extra air after normal expiration
RV	1200 mL	Air remaining after max expiration
IC	3500 mL	TV + IRV
FRC	2300 mL	ERV + RV
VC	4600 mL	TV + IRV + ERV
TLC	5800 mL	All volumes

Vital Capacity significance: Reflects respiratory muscle strength, lung compliance. Reduced in restrictive disease, useful to monitor respiratory failure (e.g., Guillain-Barre).

7. ERYTHROPOIESIS

Stages (in bone marrow): Proerythroblast → Basophilic erythroblast → Polychromatic erythroblast → Orthochromatic erythroblast → Reticulocyte → Mature RBC

Factors affecting:

Erythropoietin (EPO) - from kidney, chief regulator
Iron, Vitamin B12, Folic acid, Vitamin C
Androgens (stimulate), estrogens (inhibit)
Hypoxia stimulates EPO release

Normal RBC values: Male 5-5.5 million/mm³; Female 4.5-5 million/mm³

+ve Feedback: Hypoxia → EPO ↑ → RBC ↑ → O₂ delivery ↑ -ve Feedback: O₂ normalizes → EPO ↓

Derivatives of Hb: Oxyhaemoglobin, Carbaminohaemoglobin, Carboxy-Hb (CO poisoning), Methaemoglobin (Fe²⁺→Fe³⁺)

8. CARDIAC OUTPUT (CO)

CO = HR × Stroke Volume (Normal: 5 L/min)

Factors affecting CO:

Preload (Frank-Starling law): ↑ venous return → ↑ SV
Afterload: Aortic resistance - ↑ afterload → ↓ SV
Contractility: Sympathetics, Ca²⁺, catecholamines increase it
Heart Rate: Sympathetics ↑ HR; Parasympathetics ↓ HR

9. CARDIAC CYCLE

Duration: 0.8 sec (at 75 bpm)

Atrial systole: 0.1 sec
Ventricular systole: 0.3 sec (isovolumetric contraction + ejection)
Diastole: 0.4 sec (isovolumetric relaxation + filling)

Phases: Atrial systole → Isovolumetric contraction → Rapid ejection → Reduced ejection → Isovolumetric relaxation → Rapid filling → Slow filling

10. HEART SOUNDS

S1 (lub): Closure of mitral + tricuspid valves; beginning of systole; best heard at apex
S2 (dub): Closure of aortic + pulmonary valves; beginning of diastole
S3: Rapid ventricular filling (pathological in adults - heart failure)
S4: Atrial contraction against stiff ventricle (hypertension, LVH)

11. PACEMAKER POTENTIAL (Action Potential)

SA node - no stable resting membrane potential. Funny current (If): Na⁺ influx during phase 4 causes slow depolarization.

Phase 4: Spontaneous slow depolarization (pacemaker potential) - If (Na⁺ in), IK decay (K⁺ out decreases), ICa-T (Ca²⁺ in)
Phase 0: Rapid upstroke by L-type Ca²⁺ channels (not Na⁺!)
Phase 3: Repolarization by K⁺ efflux

Sympathetics: ↑ slope of phase 4 → ↑ HR Parasympathetics: ↓ slope of phase 4, ↑ K⁺ conductance → ↓ HR

12. JUXTAGLOMERULAR APPARATUS (JGA)

Components:

Macula densa (modified DCT cells)
Juxtaglomerular cells (JG cells - modified smooth muscle of afferent arteriole) - secrete renin
Extraglomerular mesangial cells (Lacis cells)

Functions: Renin secretion (→ Angiotensin → Aldosterone), autoregulation of GFR via tubuloglomerular feedback.

13. COUNTER-CURRENT MECHANISM (Kidney)

Multiplier: Loop of Henle - ascending limb actively pumps NaCl out (impermeable to water) creating hyperosmotic medullary interstitium Exchanger: Vasa recta - preserves medullary gradient by passive equilibration Result: Concentrated urine (up to 1200 mOsm/kg) ADH acts on collecting duct (aquaporin-2) to reabsorb water

14. NEPHRON (Structure & Function)

Parts:

Glomerulus: Filtration (GFR = 125 mL/min, ~180 L/day)
PCT: Reabsorbs 65% Na⁺, glucose (all), amino acids, HCO₃⁻, water
Loop of Henle: Concentrating mechanism
DCT: Aldosterone-mediated Na⁺ reabsorption, K⁺ secretion
Collecting duct: ADH-mediated water reabsorption, final urine concentration

15. PAIN PATHWAY (Diagram)

Fast pain (Aδ fibers): Neospinothalamic tract → VPL of thalamus → somatosensory cortex Slow pain (C fibers): Paleospinothalamic tract → reticular formation → thalamus → diffuse cortex

First-order neuron: Peripheral receptor → dorsal horn (synapse at substantia gelatinosa) Second-order neuron: Crosses midline → ascends in lateral spinothalamic tract Third-order neuron: Thalamus → cortex

16. OVARIAN CYCLE (Secretory Phase)

Follicular phase (days 1-14): FSH → follicle development → estrogen ↑ Ovulation (day 14): LH surge → ovulation Luteal/Secretory phase (days 15-28): LH → corpus luteum → progesterone + estrogen

Progesterone: makes endometrium secretory (glands coil, glycogen rich)
If no fertilization: corpus luteum degenerates → progesterone falls → menstruation

17. HAEMOSTASIS

Steps:

Vascular spasm - vasoconstriction
Primary haemostasis - platelet plug formation (adhesion via vWF→GPIb, activation, aggregation via fibrinogen→GPIIb/IIIa)
Secondary haemostasis - coagulation cascade → fibrin mesh
Fibrinolysis - plasmin dissolves clot

18. BLOOD CLOTTING

Intrinsic pathway: XII → XI → IX → VIII → X Extrinsic pathway: Tissue factor + VII → X Common pathway: X + V → prothrombin → thrombin → fibrinogen → fibrin → XIII stabilizes

Vitamin K dependent factors: II, VII, IX, X (+ Protein C, S)

19. BLOOD GROUPING & RH INCOMPATIBILITY

ABO System:

Group	Antigen	Antibody	Can receive
A	A	Anti-B	A, O
B	B	Anti-A	B, O
AB	A+B	None	Universal recipient
O	None	Anti-A + Anti-B	O only; Universal donor

Rh Incompatibility: Rh-ve mother + Rh+ve fetus → mother forms Anti-D antibodies in 1st pregnancy → 2nd pregnancy: antibodies cross placenta → hemolytic disease of newborn (HDN) Prevention: Anti-D immunoglobulin (Rho-GAM) within 72 hrs of delivery

20. SALIVA (Types, Composition, Function, Regulation)

Types: Parotid (serous, 25%), Submandibular (mixed, 70%), Sublingual (mucous, 5%) Composition: Water (99%), amylase (ptyalin), mucin, lysozyme, IgA, lingual lipase, electrolytes (Na⁺, K⁺, Cl⁻, HCO₃⁻) Functions: Digestion (starch), lubrication, antimicrobial, taste, speech, dental protection, buffering Regulation: Entirely neural (no hormonal). Both sympathetic (small viscid) and parasympathetic (large watery) stimulate. Parasympathetics dominate. Conditioned and unconditioned reflexes.

21. BLOOD PRESSURE (BP) & REGULATION

Normal: 120/80 mmHg

MAP = Diastolic + 1/3 Pulse pressure (~93 mmHg)

Short-term regulation:

Baroreceptor reflex (most important)
Chemoreceptor reflex
CNS ischemic response

Long-term regulation:

RAAS (Renin-Angiotensin-Aldosterone)
ADH
Atrial natriuretic peptide (ANP)

22. BARORECEPTOR REFLEX

Receptors: Carotid sinus (CN IX) + Aortic arch (CN X)

↑ BP → baroreceptors fire more → NTS → ↓ sympathetic, ↑ parasympathetic → ↓ HR, ↓ vasoconstriction → BP normalizes
↓ BP: opposite response

Role of baroreceptors in BP regulation: They are rapid, short-term regulators (reset with chronic hypertension - hence NOT for long-term)

23. OXY-Hb DISSOCIATION CURVE & HALDANE EFFECT

Shifts right (↓ affinity, ↑ O₂ release): ↑ CO₂, ↑ temp, ↑ 2,3-DPG, ↑ H⁺ (Bohr effect) Shifts left (↑ affinity): ↓ CO₂, ↓ temp, ↓ 2,3-DPG, fetal Hb, CO

O₂ transport: 97% as oxyhaemoglobin, 3% dissolved CO₂ transport: 70% as bicarbonate, 23% carbamino, 7% dissolved

Haldane Effect: Oxygenation of Hb reduces its ability to carry CO₂; deoxygenated Hb carries more CO₂. Important in lungs (O₂ loading → CO₂ release) and tissues (O₂ unloading → CO₂ uptake).

24. PLASMA PROTEINS

Protein	Site of synthesis	Function
Albumin	Liver	Oncotic pressure (main), transport
Globulins (α,β,γ)	Liver (α,β); Plasma cells (γ)	Transport, immunity
Fibrinogen	Liver	Clotting

Normal total: 7.2 g/dL (Albumin 4.5, Globulin 2.5, Fibrinogen 0.3) A/G ratio: 1.5-2.5:1 (reversed in cirrhosis, nephrotic syndrome)

25. MOLECULAR MECHANISM OF MUSCLE CONTRACTION (Sliding Filament Theory)

AP → T-tubule → SR releases Ca²⁺
Ca²⁺ binds troponin C → tropomyosin shifts → actin active site exposed
Myosin head (ATPase) binds actin → cross-bridge forms
Power stroke: ADP+Pi released → myosin head pivots → thin filament slides
ATP binds myosin → cross-bridge detaches
ATP hydrolysis → myosin re-cocked
Ca²⁺ pumped back into SR → relaxation

H zone and I band shorten; A band remains constant.

26. JAUNDICE

Excess bilirubin in blood (>2 mg/dL causes visible jaundice)

Type	Pre-hepatic	Hepatic	Post-hepatic
Cause	Hemolysis	Hepatitis, cirrhosis	Bile duct obstruction
Bilirubin	Unconjugated ↑	Both ↑	Conjugated ↑
Urine bilirubin	Absent	Present	Present (dark)
Urine urobilinogen	↑↑	↑	Absent
Stool color	Normal/dark	Pale	Clay-colored (acholic)

27. CALCIUM REGULATION; PTH, CALCITONIN & VITAMIN D

Normal serum Ca²⁺: 8.5-10.5 mg/dL (4.5 mEq/L ionized)

PTH (parathyroid glands): ↑ by low Ca²⁺

Bone: ↑ resorption → Ca²⁺ + PO₄ release
Kidney: ↑ Ca²⁺ reabsorption, ↓ PO₄ reabsorption, ↑ 1,25-(OH)₂D₃ synthesis
Gut: indirect (via Vit D) → ↑ absorption

Vitamin D (1,25-dihydroxycholecalciferol):

Skin (UV) → Liver (25-OH) → Kidney (1,25-OH) - active form
↑ Ca²⁺ & PO₄ absorption from gut; ↑ bone mineralization

Calcitonin (parafollicular C cells of thyroid): ↑ by high Ca²⁺

↓ bone resorption (inhibits osteoclasts)
↓ renal Ca²⁺ reabsorption
Overall: ↓ serum Ca²⁺

28. HCl SECRETION (STOMACH)

Secreted by parietal cells (oxyntic cells) Mechanism: Carbonic anhydrase → H₂CO₃ → H⁺ + HCO₃⁻

H⁺/K⁺ ATPase (proton pump) pumps H⁺ into lumen
Cl⁻ enters via Cl⁻/HCO₃⁻ exchanger (chloride shift)
HCO₃⁻ goes to blood → "alkaline tide"

Stimulation: Gastrin (G cells), ACh (vagus), Histamine (ECL cells via H2 receptors) Inhibition: Somatostatin, secretin, GIP, low pH

29. PEPTIC ULCER

Imbalance between aggressive factors (HCl, pepsin, H. pylori) and defensive factors (mucus, HCO₃⁻, prostaglandins, blood flow)

Duodenal ulcer: more common, excess acid, H. pylori (90%)
Gastric ulcer: H. pylori (70%), NSAIDs
Treatment: PPIs, H. pylori eradication (triple therapy)

30. DIGESTION OF PROTEINS IN STOMACH

HCl activates pepsinogen → pepsin
Pepsin (endopeptidase): cleaves peptide bonds → proteoses, peptones, polypeptides
Optimal pH: 1.5-2.5
Denaturation of proteins by HCl (unfolds tertiary structure)

31. TRANSPORT MECHANISMS ACROSS CELL MEMBRANE

Type	Energy	Examples
Simple diffusion	None	O₂, CO₂, lipids
Facilitated diffusion	None	Glucose (GLUT), urea
Primary active transport	ATP directly	Na⁺/K⁺ ATPase, Ca²⁺ pump
Secondary active transport	Na⁺ gradient (indirect ATP)	Na-glucose cotransport (SGLT1)
Endocytosis/Exocytosis	ATP	Large molecules
Osmosis	None	Water via aquaporins

32. ACTION POTENTIAL OF VENTRICULAR CARDIAC MUSCLE

Phases:

Phase 0: Rapid depolarization - voltage-gated Na⁺ channels open (fast Na⁺ in)
Phase 1: Early repolarization - Na⁺ channels close, transient K⁺ out (Ito)
Phase 2: Plateau - L-type Ca²⁺ channels open (Ca²⁺ in) balanced by K⁺ out; unique to cardiac muscle; allows excitation-contraction coupling and prevents tetanus
Phase 3: Repolarization - K⁺ efflux (IKr, IKs), Ca²⁺ channels close
Phase 4: Resting membrane potential (-90 mV), stable (unlike SA node)

Duration: ~300 ms (long refractory period prevents tetanus)

33. DISEASE STATES (Short Notes)

Acromegaly: Excess GH in adults (after epiphyseal fusion). Enlarged hands, feet, jaw (prognathism), coarse features. Cause: pituitary adenoma. IGF-1 elevated.

Hypoxia types:

Hypoxic: Low PaO₂ (altitude, lung disease)
Anaemic: Low Hb
Stagnant (ischemic): Low blood flow
Histotoxic: Cells can't use O₂ (cyanide poisoning)

Rickets/Osteomalacia: Vit D deficiency → ↓ Ca²⁺ absorption → ↑ PTH → bone demineralization. In children: rickets (bowed legs, rachitic rosary); adults: osteomalacia.

Goitre: Enlarged thyroid. Simple (iodine deficiency), toxic (Graves' disease - TSH receptor antibodies), non-toxic nodular.

Haemophilia:

A: Factor VIII deficiency (X-linked recessive)
B: Factor IX deficiency (Christmas disease)
Prolonged aPTT, normal PT. Hemarthrosis, easy bruising. Treatment: factor replacement.

Cushing Syndrome: Excess cortisol. Moon face, buffalo hump, central obesity, striae, hypertension, hyperglycemia, osteoporosis. Cause: pituitary (Cushing disease), adrenal adenoma, ectopic ACTH, iatrogenic.

Addison Disease: Adrenocortical insufficiency. ↓ cortisol + ↓ aldosterone. Weakness, hyperpigmentation (↑ ACTH/MSH), hypotension, hyponatremia, hyperkalemia, hypoglycemia. Crisis is life-threatening.

Diabetes Mellitus (Insipidus mentioned):

DM Type 1: Insulin deficiency (autoimmune β-cell destruction)
DM Type 2: Insulin resistance
Diabetes Insipidus: ADH deficiency (central) or resistance (nephrogenic) → polyuria of dilute urine

34. STRETCH REFLEX

Monosynaptic reflex. Muscle stretch → Ia afferent from muscle spindle → directly synapses on alpha motor neuron → muscle contraction.

Example: knee jerk (patellar reflex)
Gamma motor neurons maintain spindle sensitivity during contraction
Reciprocal inhibition: antagonist relaxes via Ia inhibitory interneuron

35. REFLEX ARC

Components: Receptor → Afferent neuron → Integration center (spinal cord/brain) → Efferent neuron → Effector

36. THALAMIC SYNDROME

Damage to VPL nucleus of thalamus (usually by vascular event). Contralateral loss of all sensation initially, then recovery with severe burning/dysesthetic pain (hyperpathia) on the affected side. Called Dejerine-Roussy syndrome. Even light touch causes pain.

37. GATE CONTROL THEORY OF PAIN (Melzack & Wall, 1965)

Substantia gelatinosa (SG) in dorsal horn acts as a "gate"
Large Aβ fibers (touch, pressure) → activate SG interneurons → CLOSE gate → inhibit pain transmission
Small C/Aδ fibers (pain) → OPEN gate
Descending control (brain) can also close gate (endorphins, enkephalins)
Explains: rubbing an injury helps; TENS therapy; psychological modulation of pain
T cells (transmission cells) are the final output neurons

38. PITUITARY GLAND HORMONES

Anterior pituitary (adenohypophysis):

GH (growth hormone)
TSH (thyroid stimulating)
ACTH (adrenocorticotrophic)
FSH, LH (gonadotrophins)
Prolactin
MSH

Posterior pituitary (neurohypophysis) - stores, doesn't synthesize:

ADH (vasopressin) - from supraoptic nucleus
Oxytocin - from paraventricular nucleus

Hyposecretion: Hypopituitarism, GH deficiency (dwarfism), DI (ADH) Hypersecretion: Acromegaly/gigantism (GH), Cushing disease (ACTH), hyperprolactinemia

39. HYPOTHALAMUS (Functions)

Temperature regulation (thermostat)
Hunger & satiety (lateral = hunger center; ventromedial = satiety center)
Thirst center
Sleep-wake cycle
Autonomic regulation (sympathetic/parasympathetic)
Endocrine control via releasing/inhibiting hormones (TRH, CRH, GHRH, GnRH, Somatostatin, Dopamine)
Emotional behavior (rage, fear via limbic connections)
Circadian rhythms (suprachiasmatic nucleus)
Cardiovascular regulation

40. FACTORS AFFECTING DIFFUSION ACROSS RESPIRATORY MEMBRANE

Fick's Law: Rate ∝ (Surface area × Pressure gradient × Solubility) / (Thickness × √Molecular weight)

Factors:

Surface area (↓ in emphysema, pneumonia)
Thickness of membrane (↑ in pulmonary fibrosis, edema)
Partial pressure gradient (O₂: 100 vs 40 mmHg; CO₂: 45 vs 40 mmHg)
Solubility (CO₂ is 20× more soluble than O₂)
Molecular weight

41. DIFFERENCE BETWEEN AP AND CNS (Diff b/w APs)

Likely: Difference between nerve AP and cardiac muscle AP, or between nerve and skeletal muscle AP.

Nerve AP vs Cardiac AP:

Feature	Nerve AP	Cardiac AP
Duration	1-2 ms	200-400 ms
Plateau phase	Absent	Present (Phase 2)
Refractory period	Short (1-2 ms)	Long (200 ms)
Can tetanus occur	Yes	No
Upstroke	Na⁺	Na⁺ (ventricular) / Ca²⁺ (nodal)

42. ACTION POTENTIAL IN NERVE (with Ionic Changes - Diagram)

Resting: -70 mV. Na⁺ outside, K⁺ inside (maintained by Na⁺/K⁺ ATPase)

Steps:

Threshold (-55 mV): Stimulus reaches threshold
Depolarization (Phase 0): Voltage-gated Na⁺ channels open → Na⁺ rushes in → reaches +30 to +40 mV
Repolarization: Na⁺ channels inactivate; K⁺ channels open → K⁺ rushes out → membrane repolarizes
Afterhyperpolarization: K⁺ channels slow to close → membrane overshoots to -80 mV
Return to resting: Na⁺/K⁺ ATPase restores gradients (3Na⁺ out, 2K⁺ in)

Absolute refractory period: Na⁺ channels inactivated - no stimulus possible Relative refractory period: Some K⁺ still open - suprathreshold stimulus needed

43. IRON DEFICIENCY ANAEMIA & ANAEMIA

Anaemia definition: Hb < 13 g/dL (males), < 12 g/dL (females), < 11 g/dL (pregnancy)

Iron Deficiency Anaemia:

Most common anaemia worldwide
Microcytic hypochromic RBCs (low MCV, MCH, MCHC)
↓ serum iron, ↓ ferritin, ↑ TIBC
Causes: poor intake, malabsorption, chronic blood loss
Features: pallor, fatigue, koilonychia (spoon nails), glossitis, angular stomatitis, Plummer-Vinson syndrome
Treatment: oral iron (ferrous sulfate), treat cause

44. VISUAL PATHWAY (Diagram) & EFFECTS OF LESIONS

Pathway: Retina → Optic nerve → Optic chiasma → Optic tract → Lateral geniculate body (thalamus) → Optic radiation → Primary visual cortex (occipital lobe, area 17)

Lesions:

Site	Effect
Optic nerve (right)	Right monocular blindness
Optic chiasma (central)	Bitemporal hemianopia (pituitary tumor)
Optic tract (right)	Left homonymous hemianopia
Optic radiation (right)	Left homonymous hemianopia
Occipital cortex (right)	Left homonymous hemianopia (with macular sparing)

45. LUNG SURFACTANT

Secreted by Type II pneumocytes
Composition: Dipalmitoyl phosphatidylcholine (DPPC) - main component; also phospholipids, surfactant proteins (SP-A, B, C, D)
Function: Reduces surface tension in alveoli, prevents collapse (atelectasis), allows smaller alveoli to remain open (Laplace law: P = 2T/r - surfactant reduces T)
Deficiency: Respiratory distress syndrome (RDS) of newborn (premature infants)
Appears at 24 weeks, matures at 34-36 weeks
Treatment of RDS: exogenous surfactant, corticosteroids to mother

46. THYROID HORMONES (Actions)

Hormones: T3 (triiodothyronine - active) and T4 (thyroxine - prohormone; converted to T3 in periphery) Synthesized using: Iodine + Tyrosine residues on thyroglobulin

Actions:

↑ BMR (calorigenic effect)
↑ protein synthesis, growth (essential for brain development)
↑ carbohydrate absorption, gluconeogenesis
↑ lipid mobilization
Cardiac: ↑ HR, ↑ contractility, ↑ CO
↑ Sensitivity to catecholamines
Essential for CNS maturation (deficiency in fetus/newborn → cretinism)

Hypersecretion: Grave's disease - heat intolerance, weight loss, tachycardia, exophthalmos, goitre, tremor Hyposecretion: Hypothyroidism - cold intolerance, weight gain, bradycardia, myxedema, goitre

47. SHOCK

Inadequate tissue perfusion → cellular hypoxia

Types:

Type	Mechanism	Example
Hypovolemic	↓ blood volume	Haemorrhage, burns, dehydration
Cardiogenic	↓ cardiac output	MI, heart failure
Distributive	Vasodilation → ↓ SVR	Septic, anaphylactic, neurogenic
Obstructive	Outflow obstruction	PE, cardiac tamponade

Features: Hypotension, tachycardia, cold clammy skin (except distributive), oliguria, altered consciousness

Stages:

Compensated (reversible): SNS activated, vasoconstriction, tachycardia
Decompensated: Acidosis, cell injury
Irreversible: Organ failure, death

These notes cover all topics listed in your image for 1st year BDS Physiology. Let me know if you want any topic expanded further or need diagrams described in more detail.

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