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class notes - First Year BHMS

Physiology 1

1. HOMEOSTASIS

  • Means keeping body conditions almost the same all the time
  • Even if outside conditions change (heat, cold, hunger)
  • Body keeps temperature about 37°C
  • Blood sugar stays normal
  • Blood pH stays around 7.4

How it works

  1. Sensor

    • Detects the change in body

  2. Control centre (Brain)

    • Decides what action to take

  3. Effector (muscle or gland)

    • Corrects the problem

Types of control

Negative feedback

  • Most common control system
  • Change is corrected and body returns to normal

Examples

  • Body temperature increases → sweating → body cools
  • Blood sugar increases → insulin released → sugar decreases

Positive feedback

  • Change becomes stronger and stronger
  • Happens only in few situations

Example

  • During childbirth → contractions increase → baby is delivered faster

2. CELL JUNCTIONS

Cells connect with each other so tissues can work properly.

Types of cell junctions

Tight junctions

  • Cells are tightly sealed together
  • Prevent substances from leaking between cells
  • Found in intestine, kidney, and blood-brain barrier

Gap junctions

  • Small channels between neighboring cells
  • Allow ions and small molecules to pass directly
  • Important in heart muscle so heart beats together

Anchoring junctions

  • Provide strong attachment between cells

Types

Desmosomes

  • Strong connection like buttons
  • Found in skin and heart muscle

Hemidesmosomes

  • Attach cell to the basement membrane (floor)

Easy memory tip

  • Tight junction = no leak
  • Gap junction = cells communicate
  • Desmosome = strong attachment

3. PEROXISOMES

  • Small sacs inside the cell
  • Contain special enzymes that break harmful substances

Main functions

  • Break very long fatty acids
  • Produce hydrogen peroxide and then destroy it using catalase
  • Help in formation of bile acids
  • Help produce special fats needed for brain cells

Disease example

Zellweger syndrome

  • Peroxisomes do not function properly
  • Causes severe brain problems in babies

4. PHAGOCYTOSIS

  • Means “cell eating”
  • Cells engulf and destroy germs or dead cells

Steps of phagocytosis

  1. Chemotaxis

    • Cell moves toward the germ

  2. Attachment

    • Cell sticks to the germ
    • Easier if germ is coated with antibodies

  3. Engulfment

    • Germ is surrounded and enclosed in a vesicle (phagosome)

  4. Digestion

    • Phagosome joins lysosome
    • Germ is destroyed by enzymes and toxic chemicals

  5. Waste removal

    • Undigested material is removed from the cell

Main phagocytic cells

  • Neutrophils
  • Macrophages

5. LYSOSOME

  • Small sacs containing digestive enzymes
  • Interior of lysosome is acidic

Often called "suicide bags" because rupture can destroy the cell.

Functions

  • Digest foreign particles taken into the cell
  • Remove damaged cell parts (autophagy)
  • Break down the whole cell after cell death

Lysosomal storage diseases

If enzymes are missing, substances accumulate inside cells.

Examples

  • Tay-Sachs disease
  • Gaucher disease
  • Pompe disease

6. OSMOSIS

  • Movement of water across a semi-permeable membrane
  • Water moves from low salt concentration to high salt concentration

Effect on red blood cells

Isotonic solution (0.9% saline)

  • Cell remains normal

Hypotonic solution

  • Water enters cell
  • Cell swells and may burst

Hypertonic solution

  • Water leaves cell
  • Cell shrinks

Easy memory

Water follows salt.

7. DIFFUSION

  • Movement of molecules from higher concentration to lower concentration
  • Does not require energy
  • Happens naturally

Types of diffusion

Simple diffusion

  • Small molecules move directly through cell membrane
  • Examples: Oxygen (O₂) and Carbon dioxide (CO₂)

Facilitated diffusion

  • Uses special carrier or channel proteins
  • Still moves from high concentration to low concentration
  • Example: Glucose entering cells using GLUT transporters

Easy summary

Diffusion

  • Movement of molecules from high concentration to low concentration

Osmosis

  • Movement of water from low solute concentration to high solute concentration through a semi-permeable membrane

http://googleusercontent.com/image_generation_content/0

II. BODY FLUIDS AND IMMUNE MECHANISM

1. FUNCTION OF BLOOD

Blood is like body's super transport & guard system

Main jobs (easy list):

  • Carry oxygen from lungs to all body parts
  • Take carbon dioxide back to lungs to throw out
  • Carry food (glucose, vitamins, proteins) to cells
  • Carry waste (like urea) to kidneys & liver to remove
  • Carry hormones from glands to where needed
  • Help fight germs & infections (with white cells)
  • Stop bleeding by making clots (platelets)
  • Keep body temperature normal (spread heat)
  • Keep pH & water balance okay

Blood = plasma (liquid part) + cells (RBC, WBC, platelets)

2. ERYTHROPOIESIS & DIFFERENT STAGES

Erythropoiesis = making of red blood cells (RBCs or erythrocytes)

Where: Mostly in red bone marrow (flat bones like pelvis, ribs, spine)
Controlled by: Erythropoietin (EPO) hormone from kidneys (when low oxygen, kidneys send EPO to make more RBCs)

Stages (simple step by step – from stem cell to mature RBC):

  1. Hemocytoblast (stem cell in bone marrow) → starts the process
  2. Proerythroblast (early stage) – big cell, starts making hemoglobin
  3. Basophilic erythroblast – more hemoglobin, nucleus still big
  4. Polychromatophilic erythroblast – hemoglobin increases, cell smaller
  5. Normoblast / Orthochromatic erythroblast – almost full hemoglobin, nucleus shrinks
  6. Reticulocyte – loses nucleus, goes into blood (still young RBC, has some RNA bits)
  7. Mature Erythrocyte (RBC) – no nucleus, biconcave shape, lives ~120 days

Easy tip: Starts big with nucleus → gets smaller, makes hemoglobin → throws out nucleus → becomes RBC

Needs: Iron, vitamin B12, folic acid, protein

3. WBC AND ITS FUNCTION

WBC = white blood cells (leukocytes) – body's soldiers against infection

Main job: Fight germs, viruses, parasites, clean dead cells

Types (5 main – remember percentages approx):

  • Neutrophils (50-70%) – first to fight bacteria & fungi; eat them (phagocytosis); most common
  • Lymphocytes (20-40%) – make immunity strong;
    • B cells → make antibodies
    • T cells → kill virus-infected cells or help others
  • Monocytes (2-8%) – big eaters; become macrophages in tissues; eat big germs & dead stuff
  • Eosinophils (1-4%) – fight parasites (worms); help in allergies
  • Basophils (0-1%) – least; release histamine in allergies; help inflammation

Easy remember: Neutrophils = bacteria killers, Lymphocytes = smart immunity, Monocytes = big cleaners, Eosinophils = parasite hunters, Basophils = allergy helpers

4. SYNTHESIS OF HAEMOGLOBIN AND ABNORMAL HAEMOGLOBIN DERIVATIVES

Hemoglobin = red protein in RBC; carries oxygen

Synthesis (making): Happens inside RBC during erythropoiesis

Steps simple:

  • Starts in erythroblast stages
  • Made of: 4 globin chains (protein) + 4 heme groups (each heme has iron in centre)
  • Iron comes from food → stored as ferritin
  • Globin made from amino acids
  • Vitamin B12 & folic acid needed for DNA (to make cells fast)

Normal hemoglobin = HbA (adult), HbF (fetus)

Abnormal hemoglobin derivatives (changed forms – bad ones):

  • Carboxyhemoglobin – CO (carbon monoxide) binds instead of O₂ → no oxygen carry (poisoning)
  • Methemoglobin – iron in heme becomes Fe³⁺ (not Fe²⁺) → can't carry O₂ well (blue baby look)
  • Sulfhemoglobin – from some drugs/sulfur → green-black, can't carry O₂
  • Sickle cell Hb (HbS) – wrong shape, RBC sickle → blocks vessels
  • Thalassemia Hb – less globin made → small weak RBC

Easy: Normal Hb carries O₂; abnormal = can't carry or shape wrong → anemia or poisoning

5. DEFINE HAEMOSTASIS & MECHANISM OF BLOOD COAGULATION

Haemostasis = stop bleeding when blood vessel damaged

3 main steps:

  1. Vascular spasm – blood vessel squeezes tight (less blood flow)
  2. Platelet plug – platelets stick to damaged area → form temporary plug
  3. Blood coagulation (clotting) – makes strong fibrin clot

Blood coagulation mechanism (clotting cascade – simple):

  • Damage → tissue factor released
  • Starts extrinsic pathway (fast) or intrinsic pathway (inside blood)
  • Both end in common pathway
  • Makes thrombin from prothrombin
  • Thrombin changes fibrinogen → fibrin threads
  • Fibrin threads trap RBC & platelets → strong clot
  • Needs: Calcium, vitamin K, clotting factors (13 factors)

After healing: Clot dissolves by plasmin

6. DESCRIBE THE LYMPHATIC SYSTEM AND COMPOSITION OF LYMPH

Lymphatic system = extra cleaning & transport network

Parts:

  • Lymph vessels (like veins but thinner)
  • Lymph nodes (filters)
  • Lymph organs: spleen, thymus, tonsils
  • Lymph capillaries in tissues

Lymph = clear fluid in lymphatic vessels

Composition of lymph:

  • Mostly water (like plasma but less protein)
  • Some proteins (albumin, globulins)
  • Fats (from intestine – chyle)
  • White blood cells (mostly lymphocytes)
  • Waste, germs, dead cells

Job:

  • Collect extra tissue fluid → return to blood
  • Fight infection (lymph nodes trap germs)
  • Absorb fats from food

Easy: Lymph = filtered tissue water + immune cells; goes back to blood near heart

7. RE SYSTEM & FUNCTION OF RE SYSTEM

RE system = Reticuloendothelial system (now called mononuclear phagocyte system)

Main cells: Macrophages & monocytes

Where: Liver (Kupffer cells), spleen, lymph nodes, bone marrow, lungs

Functions:

  • Eat old/damaged RBC (spleen & liver destroy old RBC)
  • Eat germs, dead cells, foreign stuff (phagocytosis)
  • Clean blood & tissues
  • Help make antibodies (present antigens to lymphocytes)
  • Store iron from broken RBC

Easy: RE system = body's big cleaners & garbage removers

8. DEFINE IMMUNITY AND TYPES OF IMMUNITY

Immunity = body's protection against disease & germs

Two main types:

  1. Innate immunity (natural, fast, from birth)

    • First defense
    • Skin, mucus, tears, saliva, stomach acid
    • Fever, inflammation
    • Phagocytes (neutrophils, macrophages)
    • Natural killer cells
    • No memory – same every time

  2. Acquired / Adaptive immunity (learned, slow first time, has memory)

    • Gets stronger after infection
    • Two parts:
      • Humoral / Antibody-mediated – B cells make antibodies (fight outside germs)
      • Cell-mediated – T cells kill infected cells or help others
    • Has memory cells → next time fast & strong (vaccines work here)

Easy remember: Innate = born with, quick but general; Acquired = learns, specific & remembers

II. BODY FLUIDS AND IMMUNE MECHANISM (continued)

1. THROMBOCYTES (PLATELETS)

  • Smallest blood cells – no nucleus
  • Size: 2–4 μm
  • Normal count: 1.5–4.5 lakh per mm³ (150,000–450,000/μL)
  • Made in: Bone marrow (from megakaryocytes – big cells break into platelets)
  • Live: 8–10 days

Main jobs

  • Help stop bleeding (haemostasis)
  • Stick to damaged vessel wall → form plug
  • Release chemicals → help make clot
  • Help heal wounds

Problems

  • Low platelets (thrombocytopenia) → easy bleeding, bruises
  • High platelets → blood clots easily

Easy remember: Platelets = body's emergency band-aid team

2. COMPOSITION OF BLOOD

Blood = liquid tissue – about 7–8% of body weight

Two main parts
A. Plasma (55% of blood – liquid part)

  • Water – 90–92%
  • Proteins – 7% (albumin, globulins, fibrinogen)
  • Salts (electrolytes) – Na, K, Cl, Ca etc.
  • Food – glucose, amino acids, fats
  • Waste – urea, uric acid
  • Hormones, vitamins, gases

B. Formed elements (cells – 45%)

  • Red blood cells (RBC / erythrocytes) – 95% of cells
  • White blood cells (WBC / leukocytes) – few
  • Platelets (thrombocytes) – very few

Easy: Plasma = watery soup with proteins & stuff; Cells = RBC (oxygen), WBC (fight), platelets (clot)

3. BLOOD GROUP

Blood groups decided by antigens on RBC surface

Main systems

  1. ABO system (most important)
    • 4 groups: A, B, AB, O
    • Antigens:
      • A group – A antigen
      • B group – B antigen
      • AB – both A & B
      • O – no antigen
    • Antibodies in plasma:
      • A group – anti-B
      • B group – anti-A
      • AB – no antibodies
      • O – anti-A & anti-B

Universal donor → O (no antigen, safe to give to anyone)
Universal receiver → AB (no antibodies, can take any blood)

  1. Rh system
    • Rh positive – has D antigen
    • Rh negative – no D antigen

Easy table to remember:

Blood GroupAntigens on RBCAntibodies in PlasmaCan receive fromCan donate to
AAanti-BA, OA, AB
BBanti-AB, OB, AB
ABA & BNoneA, B, AB, OAB only
ONoneanti-A & anti-BO onlyA, B, AB, O

4. HAEMOPHILIA

  • Genetic disease – blood doesn’t clot properly
  • Mostly boys (X-linked recessive – mothers carry, sons get)

Cause

  • Missing or less clotting factors
    • Haemophilia A – factor VIII missing (most common)
    • Haemophilia B – factor IX missing

Symptoms

  • Long bleeding after cut/injury
  • Big bruises
  • Joint bleeding (painful, swollen joints)
  • Blood in urine/stool

Treatment

  • Give missing factor by injection
  • Avoid injury
  • Gene therapy coming now

Easy: Haemophilia = “bleeder’s disease” – clotting factors low → blood keeps flowing

5. Rh INCOMPATIBILITY

  • Problem when mother is Rh negative & baby is Rh positive

How happens

  • First pregnancy: Usually okay (no problem)
  • During delivery: Baby’s Rh+ blood mixes with mother’s blood
  • Mother makes anti-Rh antibodies
  • Next pregnancy: If baby Rh+ again → mother’s antibodies attack baby’s RBC → break them

Result in baby (erythroblastosis fetalis / HDN)

  • Baby’s RBC destroyed → severe anemia
  • Jaundice (yellow baby)
  • Big liver/spleen
  • Brain damage (kernicterus) if very bad

Prevention

  • Give mother Anti-D injection (RhoGAM) after first delivery or abortion
  • Stops mother making antibodies

Easy: Rh- mother + Rh+ baby = danger in 2nd pregnancy unless injection given

6. ESR (Erythrocyte Sedimentation Rate)

  • Simple blood test
  • Measures how fast RBC settle down in tube in 1 hour

Normal value

  • Men: 0–15 mm/hr
  • Women: 0–20 mm/hr
  • Children: lower

Why it increases (high ESR = problem)

  • Inflammation (infection, arthritis)
  • Anaemia
  • Cancer
  • Pregnancy (normal high)
  • Old age

Why low (rare)

  • Polycythemia (too many RBC)
  • Sickle cell

Easy: ESR = RBC falling speed; high = body has inflammation or disease

7. BLOOD VOLUME

  • Total blood in body: 7–8% of body weight

Normal values

  • Adult male: 5–6 litres
  • Adult female: 4–5 litres
  • Newborn baby: 300–400 mL

Parts

  • Plasma: ~55% (3–3.5 L)
  • Cells (mostly RBC): ~45% (2–2.5 L)

Regulation

  • Kidneys control water & salt → keep volume normal
  • Hormones: ADH (save water), aldosterone (save salt)
  • If low volume (bleeding, dehydration) → thirst + less urine + heart beats faster

Easy: Blood volume = 5 litres average adult; body keeps it steady like petrol in car tank

III. MUSCLE PHYSIOLOGY

1. NEUROMUSCULAR JUNCTION

  • Place where nerve meets skeletal muscle
  • Like a special connection (synapse) so nerve can tell muscle to contract

Simple parts

  • Motor neuron end (presynaptic) – has vesicles full of acetylcholine (ACh)
  • Synaptic cleft – small gap between nerve & muscle
  • Muscle end plate (postsynaptic) – has receptors for ACh

How it works (steps)

  1. Nerve impulse comes → calcium enters nerve end
  2. Vesicles release ACh into gap
  3. ACh binds to receptors on muscle → opens channels
  4. Sodium enters muscle → action potential starts
  5. Muscle contracts
  6. ACh broken by enzyme (acetylcholinesterase) → stops signal

Easy: Nerve shoots ACh → muscle gets excited → contracts
Problem example: Myasthenia gravis – antibodies block receptors → weak muscles

2. WHAT IS TISSUE AND CLASSIFICATION OF CONNECTIVE TISSUE

Tissue = group of similar cells working together

Connective tissue – supports, connects, protects body parts
Has: cells + fibers + ground substance (jelly-like matrix)

Main classification
A. Connective tissue proper

  • Loose connective tissue (more jelly, less fibers)

    • Areolar – soft packing under skin, around organs
    • Adipose (fat) – stores energy, keeps warm, cushions
    • Reticular – makes network in lymph nodes, spleen

  • Dense connective tissue (more fibers, less jelly)

    • Dense regular – strong parallel fibers (tendons, ligaments)
    • Dense irregular – fibers in all directions (dermis of skin)
    • Elastic – stretchy (arteries, lungs)

B. Specialized connective tissue

  • Cartilage – flexible support (nose, ear, joints)
  • Bone – hard support
  • Blood – liquid transport
  • Lymph – immune fluid

Easy remember: Loose = soft & flexible; Dense = strong ropes; Specialized = special jobs like bone or blood

3. PROPERTIES OF CARDIAC MUSCLE

Cardiac muscle = heart muscle

Main properties (compare to others)

  • Involuntary (works automatically)
  • Striated (has stripes like skeletal)
  • Branched cells, connected by intercalated discs (gap junctions + desmosomes)
  • Contracts as one unit (syncytium)
  • Has own rhythm (automatic pacemaker – SA node)
  • Does not get tired (fatigue resistant) – lots of mitochondria
  • Short contractions but long refractory period (no tetanus)
  • Needs oxygen always (aerobic)

Easy: Heart muscle – never stops, beats on its own, stripes + branches, no tiredness

4. PROPERTIES OF SMOOTH MUSCLE

Smooth muscle = in walls of organs (stomach, intestine, blood vessels, uterus)

Main properties

  • Involuntary (automatic)
  • No stripes (smooth look)
  • Spindle-shaped cells (pointed ends)
  • Slow & sustained contractions (can stay contracted long)
  • Can contract with little energy (latch state)
  • Controlled by nerves + hormones + stretch
  • No T-tubules, calcium from outside & inside
  • Can divide & grow (hyperplasia)

Easy: Smooth muscle – slow, steady, no stripes, in tubes & organs, works automatically

Quick comparison table (draw in book)

PropertySkeletalCardiacSmooth
ControlVoluntaryInvoluntaryInvoluntary
StripesYesYesNo
SpeedFastMediumSlow
FatigueTires easilyNo fatigueVery little fatigue
LocationAttached to boneHeartOrgans, vessels

5. MECHANISM OF MUSCLE CONTRACTION WITH DIAGRAM (SLIDING FILAMENT THEORY)

Happens in skeletal & cardiac muscle (sliding filament theory)

What happens

  • Thin filaments (actin) slide over thick filaments (myosin)
  • Sarcomere shortens → muscle shortens
  • Filaments don’t shorten – just overlap more

Steps simple

  1. Nerve signal → ACh → action potential in muscle
  2. Calcium released from sarcoplasmic reticulum
  3. Calcium binds to troponin → moves tropomyosin → exposes binding sites on actin
  4. Myosin heads bind to actin → cross-bridge forms
  5. Myosin head pulls actin (power stroke) using ATP → filaments slide
  6. New ATP binds → myosin releases actin
  7. Cycle repeats as long as calcium high
  8. Calcium pumped back → relaxation

Diagram description (draw this)

  • Relaxed sarcomere: Z-line — I-band — A-band (with H-zone in middle)
  • Contracted: Z-lines closer, I-band smaller, H-zone almost gone, A-band same
  • Show thick myosin (dark) in middle, thin actin from Z-lines overlapping

Easy: Actin slides on myosin like rope pulling – calcium starts it, ATP powers it

6. MUSCLE PROTEIN

Main proteins in skeletal muscle (in sarcomere)

Contractile proteins (do the pulling)

  • Actin – thin filaments
  • Myosin – thick filaments, has heads that bind & pull

Regulatory proteins (control when to contract)

  • Troponin – on actin, binds calcium → starts contraction
  • Tropomyosin – covers actin binding sites in rest, moves away when calcium comes

Other important

  • Titin – giant protein, like spring, keeps sarcomere in place
  • Nebulin – helps actin length

Easy: Actin + myosin = pull; Troponin + tropomyosin = on/off switch with calcium

7. SARCOMERE

  • Smallest unit of contraction in striated muscle (skeletal & cardiac)
  • Between two Z-lines

Parts (draw lines)

  • Z-line / Z-disc – anchors actin
  • I-band – only actin (light)
  • A-band – full length of myosin (dark)
  • H-zone – only myosin, no actin overlap (middle of A)
  • M-line – holds myosin in center

During contraction:

  • Z-lines come closer
  • I-band shortens
  • H-zone shortens or disappears
  • A-band stays same length

Easy: Sarcomere = from Z to Z; contracts by sliding → shorter I & H, same A

IV. CVS – CARDIOVASCULAR SYSTEM

1. CARDIAC CYCLE IN DETAIL

Cardiac cycle = one complete heartbeat (from start of one beat to next)
Time: ~0.8 seconds (at 75 beats per minute)

Two main phases
A. Systole (contraction) – heart pumps blood out
B. Diastole (relaxation) – heart fills with blood

Detailed events (simple steps)

  1. Atrial systole (last 0.1 sec)

    • Atria contract
    • Push extra blood into ventricles (atrial kick – 20-30% filling)
    • Ventricles already 70% full from passive filling

  2. Isovolumetric contraction (0.05 sec)

    • Ventricles start contracting
    • AV valves (tricuspid, mitral) close → “lub” sound
    • Pressure rises fast but no blood out yet (volume same)
    • Semilunar valves (aortic, pulmonary) still closed

  3. Ventricular ejection (0.25 sec)

    • Ventricle pressure > aorta/pulmonary pressure
    • Semilunar valves open
    • Blood ejected: stroke volume ~70 mL
    • Fast ejection first, then slow

  4. Isovolumetric relaxation (0.05 sec)

    • Ventricles relax
    • Semilunar valves close → “dub” sound
    • AV valves still closed
    • Pressure falls fast, volume same

  5. Ventricular filling (0.4 sec – longest)

    • AV valves open
    • Blood flows passively from atria to ventricles (70-80%)
    • Then atrial systole adds more

Heart sounds

  • 1st sound (S1) – “lub” – AV valves close
  • 2nd sound (S2) – “dub” – semilunar valves close

Diagram tip (draw this)

  • Time on bottom (0.8 sec)
  • Show pressure curves: aortic, left ventricle, left atrium
  • Volume curve: ventricular volume changes
  • Mark systole (contraction), diastole (relaxation), valves open/close

Easy: Heart squeezes (systole – push blood), relaxes (diastole – fill blood)

2. INITIATION AND SPREAD OF CARDIAC IMPULSE

Heart has its own electrical system – beats automatically

Main parts (conduction system)

  1. Sinoatrial node (SA node) – pacemaker

    • In right atrium wall
    • Starts impulse (60-100 beats/min)

  2. Internodal pathways – carry impulse to AV node

  3. Atrioventricular node (AV node) – in septum

    • Delays impulse ~0.1 sec (so atria finish contracting first)

  4. Bundle of His – splits into left & right bundle branches

  5. Purkinje fibers – spread fast to ventricle walls

    • Make ventricles contract from apex to base (squeeze blood up)

How impulse spreads

  • SA node fires → atria contract
  • Delay at AV node
  • Through bundle branches & Purkinje → ventricles contract bottom-up

ECG waves (related)

  • P wave – atrial depolarization
  • QRS – ventricular depolarization
  • T wave – ventricular repolarization

Easy: SA node = boss starts beat → AV node delays → Purkinje spreads fast to ventricles

3. DESCRIBE THE ARTERIAL BLOOD PRESSURE

Arterial BP = pressure of blood on artery walls

Two values

  • Systolic BP – higher number (during ventricular contraction) – normal 110-130 mmHg
  • Diastolic BP – lower number (during relaxation) – normal 70-80 mmHg

Written as 120/80 mmHg (systolic/diastolic)

How measured – sphygmomanometer (BP apparatus) + stethoscope

  • Sounds (Korotkoff): first sound = systolic, disappear = diastolic

Factors affecting BP

  • Cardiac output (heart pumps more → BP up)
  • Blood volume (more blood → BP up)
  • Artery elasticity (stiff arteries → high systolic)
  • Resistance in small arteries (vasoconstriction → BP up)

Mean arterial pressure (MAP) ≈ Diastolic + 1/3 (Systolic – Diastolic)

  • Normal ~93 mmHg
  • Important for organ blood flow

Easy: Systolic = heart squeeze pressure; Diastolic = heart rest pressure

4. WHAT IS ARRHYTHMIA AND ITS CLASSIFICATION

Arrhythmia = abnormal heart rhythm (too fast, too slow, irregular)

Classification (simple groups)

A. By rate

  • Bradycardia – slow (<60 beats/min)
  • Tachycardia – fast (>100 beats/min)

B. By site/origin

  1. Supraventricular (above ventricles)

    • Sinus tachycardia
    • Atrial fibrillation (AF) – irregular, no P waves
    • Atrial flutter
    • Supraventricular tachycardia (SVT)

  2. Ventricular (from ventricles)

    • Ventricular tachycardia (VT) – dangerous
    • Ventricular fibrillation (VF) – no effective beat, emergency
    • Premature ventricular contraction (PVC)

  3. Conduction blocks

    • AV block (1st, 2nd, 3rd degree) – delay or block between atria & ventricles
    • Bundle branch block

C. By regularity

  • Regular – like sinus rhythm
  • Irregular – like AF

Easy examples:

  • Too fast regular → tachycardia
  • Irregular no pattern → atrial fibrillation
  • Very dangerous shaking → ventricular fibrillation

5. CARDIAC OUTPUT

Cardiac output (CO) = amount of blood heart pumps in 1 minute

Formula
CO = Heart rate (HR) × Stroke volume (SV)

  • Normal HR: 70-75 beats/min
  • Normal SV: 70 mL/beat
  • Normal CO: ~5 litres/min (at rest)

During exercise

  • HR up to 180-200
  • SV up to 100-120 mL
  • CO up to 20-30 litres/min

How body controls CO

  • Heart rate – by SA node (nerves: sympathetic ↑, parasympathetic ↓)
  • Stroke volume – by
    • Preload (more filling → more stretch → more force – Frank-Starling law)
    • Contractility (stronger squeeze – sympathetic, adrenaline)
    • Afterload (easy to pump out – low resistance → more SV)

Easy: CO = how fast heart beats × how much blood per beat
Body changes it to match body need (rest low, exercise high)

IV. CVS (continued)
STROKE VOLUME
(Super simple notes – easy words)

Stroke volume (SV) = amount of blood pumped out by one ventricle in one beat

  • Normal value (adult at rest): 60–80 mL per beat (usually ~70 mL)

What decides stroke volume? (3 main factors)

  1. Preload – how much blood fills ventricle before contraction

    • More filling → more stretch → stronger squeeze (Frank-Starling law)
    • Like stretching rubber band more → shoots farther

  2. Contractility – strength of heart muscle squeeze

    • Sympathetic nerves + adrenaline → higher contractility → more SV
    • Calcium helps muscle contract stronger

  3. Afterload – resistance heart must push against

    • High BP or stiff aorta → harder to pump → lower SV
    • Low resistance → easier → higher SV

Easy formula reminder
Cardiac output = Heart rate × Stroke volume

Example:
Rest: HR 70 × SV 70 mL = 4.9 L/min
Exercise: HR 150 × SV 100 mL = 15 L/min

Easy remember: SV = preload (fill) + contractility (power) – afterload (resistance)

V. RESPIRATORY AND ENVIRONMENTAL PHYSIOLOGY

1. MECHANISM OF RESPIRATION (INSPIRATION AND EXPIRATION)

Inspiration (breathing in) – active process

  • Diaphragm contracts → moves down
  • External intercostal muscles contract → ribs up & out
  • Chest cavity bigger → pressure inside lungs falls (negative pressure)
  • Air rushes in from outside (higher pressure) to lungs
  • Normal quiet breathing: mostly diaphragm (75%), some ribs

Expiration (breathing out) – mostly passive at rest

  • Diaphragm relaxes → moves up
  • External intercostals relax → chest smaller
  • Elastic recoil of lungs + chest wall → air pushed out
  • No muscle work needed in quiet breathing

Forced breathing (exercise, cough)

  • Expiration becomes active: internal intercostals + abdominal muscles contract → push air out fast

Easy: Inspiration = suck air in (diaphragm down); Expiration = let air out (elastic bounce back)

2. LUNG VOLUMES AND CAPACITIES

Lung volumes (measured by spirometer)

  • Tidal volume (TV): normal breath in/out – ~500 mL
  • Inspiratory reserve volume (IRV): extra deep breath in after normal – ~3000 mL
  • Expiratory reserve volume (ERV): extra force out after normal – ~1100 mL
  • Residual volume (RV): air left after maximum exhale – ~1200 mL (can’t remove)

Lung capacities (sums of volumes)

  • Inspiratory capacity (IC) = TV + IRV (~3500 mL)
  • Expiratory capacity (EC) = TV + ERV (~1600 mL)
  • Functional residual capacity (FRC) = ERV + RV (~2300 mL) – air left after normal exhale
  • Vital capacity (VC) = TV + IRV + ERV (~4600 mL) – maximum you can breathe out after max in
  • Total lung capacity (TLC) = VC + RV (~5800 mL) – all air lungs can hold

Easy remember:
TV = normal breath
VC = max you can use
TLC = everything lungs hold
RV = air you can’t blow out

3. OXYGEN-HEMOGLOBIN DISSOCIATION CURVE AND FACTORS AFFECTING IT

Oxyhemoglobin dissociation curve – graph showing how hemoglobin holds or releases oxygen

  • S-shaped (sigmoid) curve
  • At high PO₂ (lungs ~100 mmHg) → Hb almost 100% saturated
  • At low PO₂ (tissues ~40 mmHg) → Hb releases O₂ (only ~75% saturated)

Factors that shift curve (easy to remember)

  • Right shift (easier O₂ release to tissues – good in exercise)

    • ↑ CO₂
    • ↓ pH (acidic – Bohr effect)
    • ↑ temperature
    • ↑ 2,3-DPG (in RBC when hypoxic)

  • Left shift (Hb holds O₂ tighter – less release)

    • ↓ CO₂
    • ↑ pH (alkaline)
    • ↓ temperature
    • ↓ 2,3-DPG
    • Fetal Hb (holds O₂ better for baby)

Easy: Right shift = release more O₂ (exercise, fever, acid)
Left shift = keep O₂ (cold, alkaline)

4. HYPOXIA

Hypoxia = low oxygen in tissues (cells suffer)

Types

  • Hypoxic hypoxia – low O₂ in blood (high altitude, lung disease)
  • Anemic hypoxia – low Hb or bad Hb (anemia, CO poisoning)
  • Stagnant hypoxia – slow blood flow (heart failure, shock)
  • Histotoxic hypoxia – cells can’t use O₂ (cyanide poisoning)

Symptoms: headache, fast breathing, blue lips, confusion

Easy: Hypoxia = body tissues starved of oxygen

5. ASPHYXIA

Asphyxia = no breathing + no oxygen + CO₂ buildup (suffocation)

Causes: drowning, choking, strangulation, gas

Stages

  1. Hyperpnea – fast deep breathing
  2. Cyanosis + convulsions
  3. Loss of consciousness
  4. Death if not relieved

Easy: Asphyxia = can’t breathe + CO₂ high + O₂ low

6. EMPHYSEMA

Emphysema = lung disease – alveoli walls destroyed

Cause (most common): long-term smoking

What happens

  • Alveoli merge → big air spaces
  • Less surface area for gas exchange
  • Loss of elastic recoil → air trapped
  • Hard to exhale → barrel chest

Symptoms: shortness of breath, wheezing, chronic cough

Easy: Emphysema = lungs lose spring → air stuck, hard to breathe out

7. ANOXIA

Anoxia = complete absence of oxygen in tissues (extreme hypoxia)

  • Same as severe hypoxia but zero O₂
  • Brain dies in 4–6 minutes
  • Causes: cardiac arrest, severe asphyxia, high CO

Easy: Anoxia = total no oxygen (worse than hypoxia)

8. DESCRIBE THE CHEMICAL REGULATION OF RESPIRATION

Breathing controlled mainly by chemicals in blood & brain

Main sensors

  1. Central chemoreceptors (in medulla) – most important

    • Sense ↑ CO₂ or ↓ pH in CSF (brain fluid)
    • CO₂ → makes acid (H⁺) → stimulates breathing

  2. Peripheral chemoreceptors (carotid & aortic bodies)

    • Sense ↓ O₂, ↑ CO₂, ↓ pH in blood
    • Fast response when O₂ very low

How it works

  • ↑ CO₂ (hypercapnia) → strongest drive to breathe faster & deeper
  • ↓ O₂ (hypoxia) → increases breathing (but only when PO₂ <60 mmHg)
  • ↓ pH (acidosis) → breathe more to blow out CO₂

Easy: CO₂ is boss – high CO₂ → breathe fast to remove it
Low O₂ helps when very low
Acid in blood/brain → breathe more

VI. RENAL PHYSIOLOGY AND SKIN (INTEGUMENTARY SYSTEM)

1. MECHANISM OF URINE FORMATION IN DETAIL

Urine formation = 3 main steps in nephron

  1. Glomerular filtration (first step – like coffee filter)

    • Blood in glomerulus (capillaries)
    • High pressure forces water + small molecules out into Bowman’s capsule
    • Forms glomerular filtrate (almost same as plasma but no proteins, cells)
    • Amount: ~180 L/day (GFR)

  2. Tubular reabsorption (body takes back useful things)

    • In proximal tubule (65–70% reabsorbed):
      • Glucose, amino acids, vitamins – 100% back
      • Water, Na⁺, Cl⁻ – most back
    • Loop of Henle:
      • Descending limb – water out (concentrates urine)
      • Ascending limb – Na⁺, Cl⁻ out (dilutes urine) – makes counter-current multiplier
    • Distal tubule & collecting duct:
      • Fine tuning – aldosterone (Na⁺ reabsorb), ADH (water reabsorb)

  3. Tubular secretion (body throws out extra waste)

    • H⁺, K⁺, drugs, ammonia, creatinine added into tubule
    • Mainly in distal tubule & collecting duct

Final urine = filtrate – reabsorbed + secreted
Normal volume: 1–2 L/day

Easy: Filter blood → take back good stuff → add bad stuff → urine out

2. COMPOSITION OF URINE

Urine = water + waste + some salts

Normal composition (approx %):

  • Water – 95%
  • Urea – 2% (main nitrogen waste from protein)
  • Sodium chloride – 1%
  • Other: potassium, creatinine, uric acid, phosphates, sulfates
  • Small amounts: hormones, vitamins, traces of glucose (none normally)

Color: Yellow (urochrome from Hb breakdown)
Odour: Slight ammonia smell
pH: 4.5–8 (average 6) – depends on diet
Specific gravity: 1.010–1.025 (shows concentration)

Abnormal:

  • Glucose → diabetes
  • Protein → kidney damage
  • Blood → stones/infection

Easy: Urine mostly water + urea (protein waste) + salts

3. DESCRIBE THE PROCESS OF GFR AND FACTORS AFFECTING IT

GFR = Glomerular Filtration Rate
= Amount of filtrate formed per minute
Normal: 125 mL/min (180 L/day)

How it happens

  • Glomerulus has fenestrated capillaries (holes)
  • Bowman’s capsule surrounds it
  • Filtration barrier: endothelium + basement membrane + podocytes (foot processes)
  • Allows water, ions, glucose, urea → but stops big proteins & RBC

Net filtration pressure (Starling forces)
Net pressure = glomerular hydrostatic pressure – (Bowman’s capsule pressure + oncotic pressure)
Normal net: ~10 mmHg

Factors affecting GFR

  1. Glomerular hydrostatic pressure ↑ → GFR ↑ (main factor)

    • Afferent arteriole dilation → ↑
    • Efferent arteriole constriction → ↑

  2. Blood pressure – low BP → GFR ↓ (shock)

  3. Sympathetic nerves – constrict afferent → GFR ↓ (stress, bleeding)

  4. Oncotic pressure (plasma proteins) – high proteins → GFR ↓

  5. Tubuloglomerular feedback – high NaCl in distal tubule → constrict afferent → GFR ↓

  6. Hormones

    • Angiotensin II → constrict efferent → GFR little change or slight ↑

Easy: GFR = kidney filter speed; depends mostly on blood pressure in glomerulus

4. DESCRIBE THE RAAS (Renin-Angiotensin-Aldosterone System)

RAAS = hormone system to control BP & blood volume

Steps simple

  1. Low BP / low Na⁺ / low volume → juxtaglomerular cells in kidney release renin

  2. Renin changes angiotensinogen (from liver) → angiotensin I

  3. ACE (in lungs) changes angiotensin I → angiotensin II (active)

  4. Angiotensin II does many things:

    • Constricts arterioles → ↑ BP
    • Constricts efferent arteriole → maintains GFR
    • Stimulates adrenal cortex → release aldosterone
    • Makes thirst + ADH release → more water

  5. Aldosterone → distal tubule & collecting duct

    • ↑ Na⁺ reabsorption → water follows → ↑ blood volume → ↑ BP
    • ↑ K⁺ secretion

Easy flow: Low BP → renin → angiotensin II → aldosterone → save Na⁺ & water → BP up

5. NEPHRON AND ITS STRUCTURE

Nephron = functional unit of kidney (~1 million per kidney)

Two main types

  • Cortical nephrons (85%) – short loop
  • Juxtamedullary nephrons (15%) – long loop into medulla (concentrate urine)

Parts of nephron (draw this)

  1. Renal corpuscle

    • Glomerulus (capillary tuft)
    • Bowman’s capsule (double layer cup)

  2. Proximal convoluted tubule (PCT) – in cortex, long & coiled

  3. Loop of Henle

    • Descending limb – thin, water permeable
    • Ascending limb – thick, Na⁺/Cl⁻ pump

  4. Distal convoluted tubule (DCT) – in cortex

  5. Collecting duct – many nephrons join, goes to medulla → renal pelvis

Important cells

  • Juxtaglomerular apparatus – renin release
  • Macula densa – senses NaCl

Easy: Nephron = filter (corpuscle) → reabsorb (PCT) → concentrate (loop) → fine tune (DCT) → collect

6. RENAL CIRCULATION

Kidneys get ~20–25% of cardiac output (~1–1.2 L/min)

Blood flow path

  • Renal artery → segmental → interlobar → arcuate → interlobular → afferent arteriole
  • Afferent → glomerulus (filtration)
  • Efferent arteriole → peritubular capillaries (cortical nephrons) or vasa recta (juxtamedullary)
  • Peritubular / vasa recta → veins → renal vein

Special features

  • Two capillary beds: glomerulus (high pressure for filtration) + peritubular (low pressure for reabsorption)
  • Vasa recta – long straight vessels in medulla, help maintain high osmolarity (counter-current)
  • Autoregulation – kidney keeps blood flow & GFR constant between BP 80–180 mmHg

Easy: High blood to glomerulus for filtering → low blood around tubules for taking back water & salts

VI. RENAL PHYSIOLOGY (continued)

1. BOWMAN’S CAPSULE

  • Cup-shaped structure in nephron
  • Surrounds the glomerulus like a bowl
  • Made of two layers:
    • Outer parietal layer (simple squamous cells)
    • Inner visceral layer (podocytes with foot processes)

Job

  • Collects the filtrate that comes out of glomerular capillaries
  • Filtration barrier: podocytes + basement membrane + endothelium
  • Lets water, salts, glucose, urea pass → stops big proteins & blood cells

Easy: Bowman’s capsule = collecting cup for first filtered fluid (glomerular filtrate)

2. RENIN

  • Enzyme (not hormone) released by kidney
  • Made by juxtaglomerular cells (in afferent arteriole wall)

When released

  • Low blood pressure
  • Low Na⁺ in distal tubule (macula densa senses)
  • Sympathetic stimulation

What it does

  • Starts RAAS:
    Renin → angiotensinogen → angiotensin I → (ACE) → angiotensin II
  • Angiotensin II → constricts vessels → ↑ BP
  • Stimulates aldosterone → save Na⁺ & water

Easy: Renin = kidney’s BP alarm button – low BP → renin out → BP goes up

3. RFT – RENAL FUNCTION TEST

RFT = blood & urine tests to check if kidneys are working well

Common tests

  • Serum creatinine – waste from muscle; normal 0.6–1.2 mg/dL
    • ↑ creatinine = kidneys not clearing waste
  • Blood urea / BUN (blood urea nitrogen) – normal 7–20 mg/dL
    • ↑ in dehydration, high protein diet, kidney failure
  • GFR estimation (eGFR) – best overall kidney function
    • Calculated from creatinine, age, sex (Cockcroft-Gault or MDRD formula)
    • Normal >90 mL/min
  • Urine analysis – protein, blood, glucose, casts
  • Electrolytes – Na⁺, K⁺, Ca²⁺, phosphate
  • Urine output – oliguria (<400 mL/day) = kidney problem

Easy: RFT = kidney health report card; high creatinine & urea = red flag

4. MICTURITION

Micturition = urination / passing urine

Two phases

  1. Storage phase (filling)

    • Bladder relaxes & fills
    • Internal urethral sphincter (smooth muscle) closed
    • External urethral sphincter (skeletal muscle) closed (voluntary)

  2. Voiding phase (emptying)

    • When bladder ~300–400 mL → stretch receptors send signal to spinal cord & brain
    • Parasympathetic nerves → detrusor muscle (bladder wall) contracts
    • Internal sphincter relaxes
    • Voluntary relaxation of external sphincter
    • Urine flows out

Nerves involved

  • Parasympathetic (pelvic nerve) – contract bladder
  • Sympathetic – relax bladder, close internal sphincter
  • Pudendal nerve – control external sphincter (voluntary)

Easy: Micturition reflex = full bladder → brain says “go” → bladder squeezes + sphincters open

5. FUNCTION OF KIDNEY

Kidneys = body’s main filter & balance controller

Main functions (easy list)

  • Filter blood & remove waste (urea, creatinine, uric acid)
  • Keep water balance (ADH controls)
  • Keep electrolyte balance (Na⁺, K⁺, Ca²⁺, phosphate)
  • Maintain acid-base balance (excrete H⁺, reabsorb HCO₃⁻)
  • Regulate blood pressure (RAAS, renin)
  • Make hormones:
    • Erythropoietin (EPO) – for RBC production
    • Renin – for BP
    • Active vitamin D (calcitriol) – for calcium absorption
  • Gluconeogenesis (make glucose in fasting)

Easy remember: Filter waste + balance water/salts/acid + make hormones + BP control

6. JGA – JUXTAGLOMERULAR APPARATUS

JGA = special area where afferent arteriole touches distal tubule

Three parts

  1. Juxtaglomerular cells (in afferent arteriole wall) – make & release renin
  2. Macula densa (in distal tubule wall) – senses NaCl in filtrate
  3. Extraglomerular mesangial cells (support cells)

Job

  • Tubuloglomerular feedback:
    • High NaCl at macula densa → signal to constrict afferent arteriole → ↓ GFR
    • Low NaCl → dilate afferent → ↑ GFR
  • Releases renin when BP low or low NaCl

Easy: JGA = kidney’s smart sensor for GFR & BP control

7. RENAL FAILURE

Renal failure = kidneys can’t do their jobs properly

Two types

  1. Acute kidney injury (AKI) – sudden, reversible if treated fast

    • Causes: dehydration, low BP, toxins, infection, obstruction
    • Symptoms: less urine, swelling, high creatinine

  2. Chronic kidney disease (CKD) – slow, long-term, mostly irreversible

    • Causes: diabetes, hypertension, glomerulonephritis
    • Stages 1–5 (based on GFR)
    • Stage 5 = end-stage renal disease (ESRD) → needs dialysis or transplant

Symptoms (uremia when bad)

  • Tiredness, nausea, itching
  • Swelling (edema)
  • High BP
  • Anemia (low EPO)
  • Bone pain (low vitamin D)

Treatment

  • Control cause (sugar/BP)
  • Diet (low protein, low salt)
  • Dialysis (haemodialysis or peritoneal)
  • Transplant

Easy: Acute = sudden stop; Chronic = slow damage; both → waste builds up in body

SKIN

1. STRUCTURE OF SKIN WITH DIAGRAM

Skin = largest organ, two main layers + some parts

Main layers

  1. Epidermis (outer layer – no blood vessels)

    • Made of stratified squamous epithelium
    • 5 sublayers (from deep to superficial):
      • Stratum basale (germinativum) – new cells made here (mitosis), has melanocytes (pigment)
      • Stratum spinosum – spiny cells, strength
      • Stratum granulosum – granules, waterproofing
      • Stratum lucidum – clear layer (only thick skin – palms, soles)
      • Stratum corneum – dead flattened cells, keratin, falls off

  2. Dermis (inner layer – has blood vessels, nerves)

    • Connective tissue (collagen + elastic fibers)
    • Two parts:
      • Papillary dermis – loose, has fingerprints
      • Reticular dermis – dense, strong
    • Contains: sweat glands, oil glands, hair follicles, blood vessels, nerves, sensory receptors

  3. Hypodermis / Subcutaneous tissue (below dermis – not true skin layer)

    • Loose connective + fat
    • Anchors skin to muscle/bone
    • Fat for insulation & energy

Other structures

  • Hair follicles + arrector pili muscle (goosebumps)
  • Sebaceous (oil) glands
  • Sweat glands
  • Sensory receptors (touch, pain, temperature)

Diagram tip (draw this in exam)

  • Top: Epidermis (thin, label 5 sublayers)
  • Middle: Dermis (thicker, show papillary & reticular)
  • Bottom: Hypodermis (fat cells)
  • Add: hair coming out, sweat gland coiled in dermis, sebaceous gland near hair, blood vessels in dermis

Easy remember: Epidermis = dead shield on top; Dermis = living part with everything; Hypodermis = fat cushion

2. FUNCTION OF SKIN IN DETAIL

Skin does many jobs – like body’s bodyguard & regulator

Main functions

  • Protection

    • Physical barrier against germs, water loss, UV rays (melanin)
    • Keratin makes it tough
    • Acid mantle (sweat + sebum) kills bacteria

  • Temperature regulation

    • Sweat → cooling by evaporation
    • Blood vessels dilate (hot) or constrict (cold)
    • Hair + goosebumps trap air (insulation)

  • Sensation

    • Touch, pressure, pain, temperature, itch
    • Receptors send signals to brain

  • Excretion

    • Small amount of waste (urea, salts) in sweat

  • Vitamin D synthesis

    • UV light on skin → makes vitamin D (for bones & calcium)

  • Absorption

    • Some medicines, oils, chemicals go through (thin in some areas)

  • Immunity

    • Langerhans cells in epidermis catch germs & show to immune system

Easy one-liner: Skin protects, feels, cools/heats body, makes vitamin D, removes tiny waste

3. SWEAT GLANDS & ITS TYPES

Sweat glands = coiled tubes in dermis that make sweat

Two main types

  1. Eccrine sweat glands (most common)

    • All over body (highest on palms, soles, forehead)
    • Open directly to skin surface
    • Make watery sweat (mostly water + NaCl + urea)
    • For cooling (thermoregulation) + some excretion
    • Controlled by sympathetic nerves (cholinergic)

  2. Apocrine sweat glands

    • In armpits, groin, around nipples
    • Open into hair follicles (not skin surface)
    • Thick, milky sweat (proteins, lipids)
    • Starts at puberty
    • Smell when bacteria break it down (body odour)
    • Emotion/stress triggered (not heat)

Easy: Eccrine = everywhere, watery, cooling; Apocrine = hairy areas, smelly when bacteria act

4. REGULATION OF BODY TEMPERATURE

Body keeps core temp ~37°C (homeostasis) – skin plays big role

When body is HOT

  • Hypothalamus senses ↑ temp
  • Sweat glands active → sweat evaporates → cooling
  • Blood vessels in skin dilate (vasodilation) → more heat loss to air
  • Less shivering, less goosebumps

When body is COLD

  • Hypothalamus senses ↓ temp
  • Blood vessels constrict (vasoconstriction) → less heat loss
  • Shivering (muscle contraction) → heat production
  • Arrector pili contract → goosebumps → trap air for insulation
  • Less/no sweating

Easy: Hot → sweat + open vessels (lose heat); Cold → close vessels + shiver (save/make heat)

5. HYPERTHERMIA

Hyperthermia = body temp too high (> normal control fails)

Causes

  • Heat stroke (very hot weather + no cooling)
  • Exercise in hot/humid place
  • Drugs (ecstasy), fever too high
  • Blocked sweating

Symptoms

  • High temp (>40–41°C)
  • No sweating (dry skin in heat stroke)
  • Confusion, seizure, coma
  • Fast heart rate, low BP

Danger

  • Brain & organ damage if not cooled fast

Easy: Hyperthermia = body overheats, can’t cool – emergency (cool fast, fluids)

6. HYPOTHERMIA

Hypothermia = body temp too low (<35°C)

Causes

  • Cold exposure (water, snow)
  • Wet clothes
  • Old age, babies, alcohol, drugs
  • Low metabolism

Stages

  • Mild (32–35°C): shivering, confusion
  • Moderate (28–32°C): no shivering, slow heart, sleepy
  • Severe (<28°C): coma, heart stop, death

Treatment

  • Warm slowly (blankets, warm fluids)
  • No fast heating (can cause shock)

Easy: Hypothermia = body too cold, shivering stops in bad cases – warm gently