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cd /home/daytona/workspace/attachments/f3a7b748-4398-4603-810f-87b6f8d7a170/ && python3 -c " import subprocess result = subprocess.run(['antiword', 'practical skills 2026.doc'], capture_output=True, text=True) print(result.stdout[:5000]) print('STDERR:', result.stderr[:500]) "

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cd "/home/daytona/workspace/attachments/f3a7b748-4398-4603-810f-87b6f8d7a170/" && python3 -c " import subprocess # Try libreoffice conversion result = subprocess.run(['libreoffice', '--headless', '--convert-to', 'txt', 'practical skills 2026.doc', '--outdir', '/home/daytona/workspace/'], capture_output=True, text=True, timeout=60) print('STDOUT:', result.stdout) print('STDERR:', result.stderr[:500]) print('Return code:', result.returncode) "

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cd "/home/daytona/workspace/attachments/f3a7b748-4398-4603-810f-87b6f8d7a170/" && python3 -c " import subprocess # Try docx conversion result = subprocess.run(['libreoffice', '--headless', '--convert-to', 'docx', 'practical skills 2026.doc', '--outdir', '/home/daytona/workspace/'], capture_output=True, text=True, timeout=60) print('STDOUT:', result.stdout) print('STDERR:', result.stderr[:500]) print('Return code:', result.returncode) "

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# Try extracting text directly from the binary doc file with python-docx or olefile python3 -c " import olefile import os path = '/home/daytona/workspace/attachments/f3a7b748-4398-4603-810f-87b6f8d7a170/practical skills 2026.doc' ole = olefile.OleFileIO(path) # Word document streams if ole.exists('WordDocument'): stream = ole.openstream('WordDocument') data = stream.read() print('WordDocument stream size:', len(data)) # Try to get text from the 0Table or 1Table stream if ole.exists('1Table'): stream = ole.openstream('1Table') data1 = stream.read() print('1Table stream size:', len(data1)) # decode stream = ole.openstream('WordDocument') raw = stream.read() # Extract ASCII text import re text = raw.decode('latin-1', errors='replace') # Find readable text - look for sequences of printable chars readable = re.findall(r'[ -~\n\r\t]{4,}', text) for r in readable[:100]: if len(r) > 8: print(repr(r)) "

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python3 -c " import re, struct path = '/home/daytona/workspace/attachments/f3a7b748-4398-4603-810f-87b6f8d7a170/practical skills 2026.doc' with open(path, 'rb') as f: data = f.read() # Extract readable text sequences (latin-1 encoded) text = data.decode('latin-1', errors='replace') readable = re.findall(r'[A-Za-z0-9 .,;:!?()\-\'\"]{10,}', text) for r in readable: if any(c.isalpha() for c in r): print(r) " 2>/dev/null | head -200

I now have all the questions. These are physiology practical skills questions. Let me answer them all comprehensively using the medical library.Now let me search the medical library for relevant content to answer these physiology questions:

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I now have comprehensive content to answer all questions. Let me write the full answers:Here are comprehensive answers to all 30 practical skills questions:

Practical Skills 2026 - Complete Answers

Q1. Draw the graph of action potential. Indicate its phases and explain ionic mechanism of its generation.

Graph:

+40 mV ─────────────────────────────── peak (overshoot)
         /\
        /  \
       /    \
0 mV ─/──────\──────────────────────────────
             \     /‾‾‾‾‾‾‾‾‾‾‾‾ resting
-55 mV ───────\   / (undershoot/AHP)
  (threshold)  \ /
-70 mV ─────────V─────────────────────────── resting

         Phase: 0  1  2  3   4
         (nerve: upstroke → repolarization → undershoot)

Phases (nerve/skeletal muscle):

Phase	Event	Ion(s)
Resting (-70 mV)	K⁺ channels open, K⁺ leaks out	K⁺
Upstroke (depolarization)	Depolarization to threshold (~-55 mV) → voltage-gated Na⁺ channels open rapidly (activation gates open) → massive Na⁺ influx → membrane reaches ~+40 mV	Na⁺ in
Repolarization	Na⁺ channel inactivation gates close (slow); voltage-gated K⁺ channels open → K⁺ efflux	K⁺ out
Undershoot (hyperpolarizing afterpotential)	K⁺ conductance remains transiently elevated → membrane driven closer to E_K (~-90 mV)	K⁺ out
Return to resting potential	K⁺ conductance falls back to resting level	K⁺

Ionic mechanism summary:

Resting state: activation gate closed, inactivation gate open (channel available)
Upstroke: depolarization → activation gate opens quickly → both gates open → Na⁺ flows in
Repolarization: inactivation gate closes (slowly) + K⁺ channels open → K⁺ flows out
Undershoot: excess K⁺ conductance persists briefly
Recovery: Na⁺/K⁺-ATPase restores ion gradients

(Costanzo Physiology 7e, p.27-29)

Q2. Draw the graph of changes in excitability during AP: refractory periods and their phases

Graph:

Membrane potential:
+40 ──── /\
         /  \
-70 ─────    ────────────────────── (resting)

Excitability:
 Normal ─────────────────────────── restored
                              /
 Supranormal ─────────────── (relative refractory → slightly above normal)
                      /
 Subnormal ──────────  
 ZERO (ARP) ─────
        |      |              |
       AP      ARP ends      RRP ends

Phases:

Absolute Refractory Period (ARP): Coincides with the upstroke and most of repolarization. Na⁺ channels are inactivated (inactivation gates closed) - no stimulus of any strength can elicit a new AP. Ensures unidirectional propagation and limits firing frequency.
Relative Refractory Period (RRP): Follows ARP. Membrane is still somewhat hyperpolarized; Na⁺ channels partially recovered. A stronger-than-normal stimulus can elicit an AP, but it will be smaller and slower.
Supranormal period: Membrane has slightly recovered past resting potential in some cell types - threshold is easier to reach transiently.
Subnormal period (undershoot): Membrane is hyperpolarized during AHP - threshold is harder to reach, so excitability is reduced below normal.

Q3. Draw a scheme explaining mechanism of AP propagation along myelinated and non-myelinated nerve fibers

Non-myelinated (continuous conduction):

   Active site        Adjacent sites (brought to threshold)
   ─────────────────────────────────────────────────────────
   [Na⁺ in → +]  →→→→ current spreads to neighbor → depolarizes
   ←←←←←←←←←←←← (inside current loop)
   ─────────────────────────────────────────────────────────
   Direction: →→→→→→→→→→→→

Local current flows from active (+) to inactive (-) segment
Each adjacent membrane is brought to threshold sequentially
Slow (0.5-2 m/s), energy-expensive

Myelinated (saltatory conduction):

   Node of        Node of        Node of
   Ranvier 1      Ranvier 2      Ranvier 3
      |              |              |
  ────[AP]───────────[AP]───────────[AP]────
      ↑              ↑              ↑
   myelin sheath (insulator - no ion flow between nodes)
   
   Current jumps: Node 1 → Node 2 → Node 3 (saltatory = "jumping")

Myelin sheath insulates internodal segments; ion exchange only at nodes of Ranvier
Current "jumps" from node to node
Fast (70-120 m/s), energy-efficient
Multiple sclerosis damages myelin → slows/blocks conduction

Q4. Draw a scheme of the neuromuscular junction and explain mechanism of synaptic transmission

Scheme:

Motor neuron axon terminal (presynaptic)
┌─────────────────────────────────────────┐
│  Mitochondria  ●●●●  Vesicles (ACh)     │
│                ↓ Ca²⁺ influx            │
└─────────────────────────────────────────┘
           Synaptic cleft
           (AChE present)
┌─────────────────────────────────────────┐
│  Muscle fiber (postsynaptic)            │
│  Nicotinic ACh receptors                │
│  Motor end plate                        │
└─────────────────────────────────────────┘

Steps of transmission:

AP arrives at axon terminal
Voltage-gated Ca²⁺ channels open → Ca²⁺ enters terminal
Ca²⁺ triggers vesicle fusion (exocytosis) → acetylcholine (ACh) released into cleft
ACh diffuses across cleft and binds nicotinic ACh receptors (ligand-gated Na⁺/K⁺ channels) on motor end plate
Channels open → Na⁺ influx > K⁺ efflux → end-plate potential (EPP) generated
EPP depolarizes surrounding muscle membrane to threshold → AP in muscle fiber
Acetylcholinesterase (AChE) in cleft rapidly hydrolyzes ACh → choline recycled back into terminal

Blockers: curare/tubocurarine blocks nicotinic receptors (flaccid paralysis); neostigmine inhibits AChE (prolongs EPP)

Q5. Draw curves of single twitch and tetanic contractions

Graph:

Force
  │         ___
  │        /   \          _____________________  Complete tetanus
  │       /     \        /
  │      /       \      /  /\/\/\/\/\/\          Incomplete tetanus
  │     /         \    /
  │    / Single    \  /
  │   /   twitch    \/
  │──────────────────────────────────────────── Time
  
  Latent  Contraction  Relaxation
  period  phase        phase

Single twitch: One stimulus → one AP → brief Ca²⁺ release from SR → cross-bridge cycling → force rises then falls (refractory period ends, Ca²⁺ pumped back)

Incomplete tetanus: Stimuli before full relaxation → summation of twitches → wave-like force

Complete tetanus: High-frequency stimuli → Ca²⁺ remains elevated continuously → maximal sustained force (~3-4x single twitch)

Q6. Draw a scheme illustrating mechanism of muscular contraction and relaxation

Mechanism:

AP in muscle fiber
        ↓
T-tubule depolarization
        ↓
Voltage-sensor (DHPR/dihydropyridine receptor) activated
        ↓
RyR (ryanodine receptor) on SR opens → Ca²⁺ released into cytoplasm
        ↓
Ca²⁺ binds Troponin C → conformational change in Troponin-Tropomyosin complex
        ↓
Tropomyosin moves → exposes actin binding sites for myosin
        ↓
Myosin S1 head (with ADP+Pi) binds actin → POWER STROKE
        ↓
ADP + Pi released → cross-bridge formed (rigor state)
        ↓
New ATP binds myosin → cross-bridge detaches
        ↓
ATP hydrolyzed → myosin re-cocked → cycle repeats → SHORTENING

RELAXATION:
AP stops → Ca²⁺ pumped back into SR by SERCA (SR Ca²⁺-ATPase)
→ Ca²⁺ off Troponin C → Tropomyosin covers actin sites → no more cross-bridges

Q7. Draw a scheme of the spinal cord reflex arch

     Stimulus (e.g., muscle stretch)
           ↓
   [RECEPTOR] (muscle spindle / skin receptor)
           ↓
   [AFFERENT NEURON] (sensory/dorsal root)
           ↓
   ┌──────────────────────────────────┐
   │      SPINAL CORD (CNS)          │
   │   [INTERNEURON] (association)   │ ← may be absent in monosynaptic reflex
   └──────────────────────────────────┘
           ↓
   [EFFERENT NEURON] (motor/ventral root)
           ↓
     [EFFECTOR] (muscle)
           ↓
      RESPONSE (contraction)

5 components: receptor → afferent neuron → nerve center (interneuron) → efferent neuron → effector

Monosynaptic reflex (knee-jerk): no interneuron - afferent Ia fiber synapses directly on alpha motor neuron

Q8. Draw schemes of pre- and postsynaptic inhibition in the CNS

Presynaptic inhibition:

Excitatory neuron A ────→ [Terminal A]
                               ↓ (reduced neurotransmitter release)
Inhibitory neuron B → [Terminal B]──┤[Terminal A]
                     (GABA acts on A's terminal → reduces Ca²⁺ → ↓ACh/Glu release)
                               ↓
                         Postsynaptic cell (less EPSP)

Mechanism: GABA-B receptors on presynaptic terminal → ↑K⁺ conductance or ↓Ca²⁺ → less transmitter released from A → weaker EPSP

Postsynaptic inhibition:

Excitatory neuron A ────────────────→ [Postsynaptic cell]
                                             ↑
Inhibitory neuron B ───────── IPSP ──────────┤
              (opens Cl⁻ or K⁺ channels → hyperpolarizes postsynaptic membrane)

Mechanism: Inhibitory interneuron releases GABA or glycine → opens Cl⁻ channels (IPSP) → membrane hyperpolarizes → harder to reach threshold

Renshaw cell inhibition (recurrent inhibition) = postsynaptic inhibition of motor neurons

Q9. Draw a scheme of autonomic reflex arch (sympathetic and parasympathetic)

Sympathetic:

[Higher centers / Hypothalamus]
         ↓
[Preganglionic neuron] - short fiber, ACh, nicotinic receptor
Lateral horn T1-L2 (spinal cord)
         ↓  (synapse in paravertebral or prevertebral ganglia)
[Postganglionic neuron] - long fiber, Norepinephrine (NE), α/β receptors
         ↓
[Target organ] → "Fight or flight": ↑HR, vasoconstriction, pupil dilation

Parasympathetic:

[Brainstem (CN III, VII, IX, X) + Sacral S2-S4]
         ↓
[Preganglionic neuron] - long fiber, ACh, nicotinic receptor
         ↓ (synapse in ganglion near/within target organ)
[Postganglionic neuron] - short fiber, ACh, muscarinic receptor
         ↓
[Target organ] → "Rest and digest": ↓HR, ↑GI motility, pupil constriction

Q10. Draw a scheme showing mechanism of protein hormone action on target cells

Protein hormone (e.g., insulin, glucagon, TSH, LH)
  │  (hydrophilic - cannot cross membrane)
  ↓
[Cell surface receptor] (GPCR or receptor tyrosine kinase)
  │
  ├─── GPCR pathway:
  │     Hormone + GPCR → G protein (Gs/Gi) activated
  │     Gs → adenylyl cyclase → ↑cAMP → activates PKA
  │     PKA phosphorylates proteins → cellular response
  │     (e.g., glucagon → glycogenolysis in liver)
  │
  └─── RTK pathway:
        Hormone + RTK → receptor dimerizes → autophosphorylation (Tyr)
        → adaptor proteins → RAS/MAPK or PI3K/Akt cascade
        → gene expression, cell growth, glucose uptake
        (e.g., insulin → GLUT4 translocation)

Key: protein hormones act via second messengers (cAMP, IP₃/DAG, Ca²⁺) - response is fast but does NOT require entry into nucleus

Q11. Draw a scheme showing mechanism of steroid hormone action on target cells

Steroid hormone (e.g., cortisol, aldosterone, estrogen, testosterone)
  │  (lipophilic - crosses plasma membrane freely)
  ↓
[Cytoplasmic or nuclear receptor]
  │
  Hormone + receptor → receptor activated (releases heat-shock proteins)
  │
  Receptor-hormone complex dimerizes
  │
  Translocates to nucleus
  │
  Binds Hormone Response Elements (HRE) on DNA
  │
  Alters gene transcription (↑ or ↓ mRNA synthesis)
  │
  ↓ protein synthesis (new enzymes, structural proteins)
  │
  CELLULAR RESPONSE (hours to days)

Key differences from protein hormones: slow onset (hours), prolonged effect, directly modifies gene expression

Q12. Draw the hypothalamic-pituitary axis for any peripheral endocrine gland

Example: Hypothalamic-Pituitary-Thyroid (HPT) Axis:

HYPOTHALAMUS
     ↓ TRH (Thyrotropin-Releasing Hormone)  [+]
ANTERIOR PITUITARY
     ↓ TSH (Thyroid-Stimulating Hormone)    [+]
THYROID GLAND
     ↓ T3, T4 (thyroid hormones)
     
NEGATIVE FEEDBACK:
T3/T4 ──────────────→ HYPOTHALAMUS [−]
T3/T4 ──────────────→ ANTERIOR PITUITARY [−]

General principle (applies to HPA, HPG axes too):

Hypothalamus releases releasing hormone → stimulates pituitary
Pituitary releases tropic hormone → stimulates peripheral gland
Peripheral gland releases end hormone → negative feedback on both hypothalamus and pituitary
This maintains homeostatic set-point

HPG axis: GnRH → LH/FSH → sex steroids (testosterone/estrogen) HPA axis: CRH → ACTH → cortisol

Q13. Interpret blood test results

Normal reference ranges and interpretation framework:

Parameter	Normal Range	Low suggests	High suggests
Hb (male)	130-170 g/L	Anemia	Polycythemia
Hb (female)	120-150 g/L	Anemia	Polycythemia
RBC (male)	4.5-5.5 ×10¹²/L	Anemia	Polycythemia
WBC	4.0-9.0 ×10⁹/L	Leukopenia (viral, aplastic)	Leukocytosis (infection, leukemia)
Platelets	150-400 ×10⁹/L	Thrombocytopenia (bleeding risk)	Thrombocytosis
Hct (PCV)	36-48%	Anemia	Dehydration, polycythemia
MCV	80-100 fL	Microcytic (Fe deficiency, thalassemia)	Macrocytic (B12/folate deficiency)
MCH	27-33 pg	Hypochromic	Hyperchromic
ESR	<15 mm/hr (M), <20 (F)	-	Inflammation, infection
Neutrophils	50-70% of WBC	Neutropenia	Bacterial infection
Lymphocytes	20-40%	Lymphopenia	Viral infection, CLL
Eosinophils	1-4%	-	Allergy, parasites

Approach: Check each value against reference range → categorize (normal/low/high) → correlate with clinical picture → form differential diagnosis

Q14. Outline principles of blood typing by ABO and Rh systems

ABO System:

Blood Group	Antigens on RBC	Antibodies in plasma	Can receive	Can donate to
A	A antigen	Anti-B	A, O	A, AB
B	B antigen	Anti-A	B, O	B, AB
AB	A + B antigens	None	A, B, AB, O	AB only
O	None	Anti-A and Anti-B	O only	A, B, AB, O

Principles:

Agglutination occurs when antibody meets corresponding antigen
ABO antibodies are naturally occurring (no prior sensitization needed)
Standard typing: add Anti-A and Anti-B sera to patient RBCs → observe agglutination

Rh System:

Rh+ (D antigen present): ~85% of population
Rh- (D antigen absent): ~15% of population
Anti-D antibodies are immune (formed only after exposure to Rh+ blood)
Danger: Rh- mother with Rh+ fetus → hemolytic disease of the newborn (HDN) in subsequent pregnancies
Prevention: Anti-D immunoglobulin (RhoGAM) given to Rh- mothers

Procedure:

Mix patient RBCs with anti-A, anti-B, anti-D sera
Observe for agglutination (clumping = positive reaction)
Cross-match: donor cells + recipient serum and vice versa before transfusion

Q15. Draw a graph of action potential of a typical cardiomyocyte and explain mechanism of its formation

Graph (ventricular cardiomyocyte):

mV
+20 ──── Phase 0 (upstroke)
         /|
        / |  Phase 1 (early repolarization)
       /  |\_____________________________
      /   |     Phase 2 (plateau)        |
-40 ─/    |                              |
          |                              |\ Phase 3
-85 ──────|──────────────────────────────── Phase 4 (resting)

Phases:

Phase	Name	Ion current
0	Rapid depolarization	Voltage-gated Na⁺ channels open → fast inward Na⁺
1	Early repolarization	Na⁺ channels inactivate + transient outward K⁺ (Ito)
2	Plateau (unique to heart!)	L-type Ca²⁺ channels open (slow inward Ca²⁺) balanced by K⁺ efflux; maintains ~0 mV for 200-300 ms
3	Rapid repolarization	Ca²⁺ channels inactivate; K⁺ channels (IKr, IKs) open → K⁺ out
4	Resting potential	Resting at -85 mV; IK1 (inward rectifier K⁺) maintains

Key differences from nerve AP: long plateau (Phase 2) due to Ca²⁺ influx → extended ARP → cannot be tetanized (essential for pumping function). Ca²⁺ from Phase 2 triggers Ca²⁺-induced Ca²⁺ release (CICR) from SR → contraction.

Q16. Draw a graph of action potential of a pacemaker cell and explain mechanism of its formation

Graph (SA node pacemaker cell):

mV
-40 ─────────────────────────────── threshold
      /\        /\        /\
     /  \      /  \      /  \
    /    \    /    \    /    \
-60 \    /──/ \    /──/ \    /──→
  ↑  \  /      \  /      \  /
  |   \/        \/        \/
  |
  Pacemaker potential (If - "funny current")
  (slow spontaneous depolarization to threshold)

Mechanism of pacemaker potential (spontaneous depolarization):

Phase 4 - Pacemaker potential (slow, spontaneous depolarization):
- Starts at ~-60 mV (not at -85 mV like ventricular cells)
- If ("funny" current / HCN channels): activated by hyperpolarization → slow Na⁺ (and some K⁺) inward current → gradual depolarization
- ICaT (T-type Ca²⁺ channels): activate as membrane reaches ~-50 mV → additional inward Ca²⁺ current
- IK decay: K⁺ channels gradually close → less outward K⁺ current → further depolarization
Upstroke (Phase 0): NO fast Na⁺ channels! Upstroke carried by L-type Ca²⁺ channels → slow upstroke, slower conduction
Repolarization (Phase 3): K⁺ channels (IK) open → K⁺ efflux → repolarization back to ~-60 mV → cycle repeats

Rate modulation:

Sympathetic (NE): ↑If, ↑ICa → faster pacemaker potential → ↑HR
Parasympathetic (ACh): ↓If, ↑IKACh (hyperpolarizes) → slower pacemaker potential → ↓HR

Q17. Draw a scheme of the conduction system of the heart; define frequency of generation and velocity of excitation spread

Scheme:

SA NODE (sinoatrial node)
  Right atrium, crista terminalis
  Rate: 60-100 bpm (dominant pacemaker)
  Velocity: 0.05 m/s
       ↓ spreads through both atria (0.3-0.5 m/s) → ATRIAL CONTRACTION
       ↓
AV NODE (atrioventricular node)
  Interatrial septum, Koch's triangle
  Rate: 40-60 bpm (latent pacemaker)
  Velocity: 0.02-0.05 m/s ← SLOW (AV delay 0.1 s - allows atria to fill ventricles)
       ↓
BUNDLE OF HIS
  Velocity: 0.1-0.2 m/s
       ↓
RIGHT & LEFT BUNDLE BRANCHES
  Velocity: 2-4 m/s (fast! for synchronous ventricular contraction)
       ↓
PURKINJE FIBERS
  Rate: 20-40 bpm (latent pacemaker)
  Velocity: 2-4 m/s (fastest in heart)
       ↓
VENTRICULAR MYOCARDIUM
  Rate: 20-40 bpm (idioventricular)
  Velocity: 0.3-0.5 m/s → VENTRICULAR CONTRACTION

Summary of rates:

SA node: 60-100/min (dominant)
AV node: 40-60/min
Purkinje/ventricle: 20-40/min

Principle of dominance: highest frequency pacemaker drives the whole heart. SA node suppresses lower pacemakers via overdrive suppression.

Q18. Based on ECG analysis - determine the pacemaker and explain the answer

Criteria for identifying pacemaker from ECG:

SA node (normal sinus rhythm):
- P wave present before every QRS complex
- P wave is positive in leads II, III, aVF; negative in aVR
- PR interval: 0.12-0.20 s (constant)
- Rate 60-100 bpm
AV node (junctional rhythm):
- P waves absent, inverted, or after QRS
- Narrow QRS (normal ventricular conduction)
- Rate 40-60 bpm
Ventricular (idioventricular rhythm):
- No P waves
- Wide, bizarre QRS (>0.12 s) - abnormal ventricular conduction
- Rate 20-40 bpm

Rule: Find P waves first. If present and before QRS → SA node. If P absent/inverted → junctional. If wide QRS with no P → ventricular.

Q19. Based on ECG analysis - determine heart rate and cardiac cycle duration

Method 1 (regular rhythm):

Count the number of large squares (each = 0.2 s) between two consecutive R peaks (R-R interval)
HR = 300 ÷ (number of large squares between R-R)
e.g., 3 large squares → HR = 300/3 = 100 bpm

Method 2 (precise):

Measure R-R interval in seconds
HR = 60 ÷ R-R interval (in seconds)
e.g., R-R = 0.8 s → HR = 60/0.8 = 75 bpm

Method 3 (count in 6-second strip):

Count QRS complexes in 6-second strip × 10 = HR (good for irregular rhythms)

Cardiac cycle duration:

= R-R interval in seconds
e.g., HR = 75 bpm → cycle duration = 60/75 = 0.8 s
HR = 60 bpm → 1.0 s; HR = 80 bpm → 0.75 s

ECG paper speed = 25 mm/s:

1 small square = 1 mm = 0.04 s
1 large square = 5 mm = 0.2 s

Q20. Based on ECG analysis - determine position of heart electrical axis in frontal plane

Normal axis: -30° to +90°

Quick method using leads I and aVF:

Lead I	aVF	Axis
+	+	Normal (0° to +90°)
+	-	Left axis deviation (LAD)
-	+	Right axis deviation (RAD)
-	-	Extreme axis (no man's land)

Precise method:

Find the most isoelectric (equiphasic) lead in frontal plane
The axis is perpendicular to that lead
Look at the perpendicular lead to determine positive or negative direction

Causes:

LAD: left ventricular hypertrophy, left bundle branch block, inferior MI
RAD: right ventricular hypertrophy, right bundle branch block, pulmonary hypertension

Q21. Draw a curve of sphygmogram, label and explain its phases

Sphygmogram (arterial pulse wave):

        Anacrotic          Catacrotic
        limb               limb
  ─────────────────────────────────────────
  Pressure
         /\
        /  \  Dicrotic notch (aortic valve closure)
       /    \/\
      /        \  Dicrotic wave
     /           \____
  ──────────────────────── Time
  ↑               ↑
 Percussion      Dicrotic
 wave            wave

Phases:

Anacrotic (ascending) limb: Rapid pressure rise during systole (ventricular ejection); steep upstroke
Peak (percussion wave): Maximum systolic pressure
Dicrotic notch (incisura): Transient pressure dip when aortic valve closes; marks end of systole
Dicrotic wave: Small secondary wave caused by elastic recoil of aorta wall after valve closure
Catacrotic (descending) limb: Gradual pressure fall during diastole as blood flows into periphery

Clinical significance: Shape reflects arterial compliance, cardiac output, and peripheral resistance. Water-hammer pulse (Corrigan's) in aortic regurgitation; pulsus paradoxus in cardiac tamponade.

Q22. Draw a curve of phlebogram, label and explain its phases

Phlebogram (jugular venous pulse):

   a     c   x   v    y
   wave  wave     wave
    /\   /\ /\    /\
   /  \ /  X  \  /  \
──/    X    \  \/    \────
            ↓  ↓
            x  y
          descent descent

Waves and descents:

Component	Cause	Timing
a wave	Atrial contraction (presystolic)	Before QRS on ECG
c wave	Tricuspid valve bulging into atrium at onset of ventricular systole	After QRS
x descent	Atrial relaxation + downward displacement of tricuspid valve during systole	During systole
v wave	Passive venous filling of atrium (tricuspid valve closed during systole)	End systole
y descent	Tricuspid valve opens → blood flows into ventricle	Early diastole

Absent a wave: Atrial fibrillation Large a wave: Tricuspid stenosis, pulmonary hypertension Large v wave: Tricuspid regurgitation

Q23. List and analyze methods of external respiration examination

Methods:

Spirometry - measures lung volumes and capacities:
- TV (Tidal Volume): ~500 mL - volume per normal breath
- IRV (Inspiratory Reserve Volume): ~3000 mL
- ERV (Expiratory Reserve Volume): ~1100 mL
- VC (Vital Capacity) = TV + IRV + ERV: ~4600 mL
- FVC (Forced Vital Capacity): vital capacity with maximal forced effort
- FEV₁ (Forced Expiratory Volume in 1 sec): volume exhaled in first second of FVC
- FEV₁/FVC ratio: normal >70-80%; reduced in obstructive disease
- RV (Residual Volume): ~1200 mL - cannot be measured by simple spirometry
- TLC = VC + RV: ~5800 mL
Peak Flow Meter (PEFR): measures peak expiratory flow rate; used to monitor asthma
Pneumotachography: measures airflow rates; generates flow-volume loops
Body Plethysmography: measures FRC and RV (which spirometry cannot)
Diffusion capacity (DLCO): measures ability of lungs to transfer gas (CO used as test gas); reduced in emphysema, pulmonary fibrosis, pulmonary hypertension
Arterial Blood Gas (ABG): measures PaO₂, PaCO₂, pH, HCO₃⁻ - assesses gas exchange and acid-base status

Pattern recognition:

Obstructive (asthma, COPD): ↓FEV₁/FVC, ↑TLC (hyperinflation)
Restrictive (fibrosis, neuromuscular): ↓TLC, ↓VC, FEV₁/FVC normal or ↑

Q24. Draw a scheme of renin-angiotensin-aldosterone system and explain kidney's role in maintenance of arterial blood pressure

↓BP / ↓Na⁺ / ↑sympathetic
          ↓
    JUXTAGLOMERULAR CELLS (kidney)
          ↓ RENIN secretion
          ↓
    ANGIOTENSINOGEN (liver) → ANGIOTENSIN I
          ↓ ACE (Angiotensin Converting Enzyme - in lungs)
          ↓
    ANGIOTENSIN II
     ↙        ↘         ↘            ↘
Vasoconstriction  Aldosterone    ADH release  Thirst (hypothalamus)
(↑BP directly)    (adrenal cortex) (↑water retention)
     ↓
Kidney: ↑Na⁺ & H₂O reabsorption
(collecting duct, DCT)
     ↓
↑Blood volume → ↑BP → negative feedback on renin release

Kidney's role:

Renin production (granular cells of JGA): responds to ↓renal perfusion pressure, ↓NaCl at macula densa, sympathetic activation
Aldosterone effect: ↑Na⁺ reabsorption in collecting duct → ↑ECF volume → ↑BP
Long-term BP control via volume regulation (Guyton's theory: only the kidney can provide sustained BP regulation)

ACE inhibitors (ramipril) and ARBs (losartan) target this system therapeutically

Q25. Draw a scheme of feedback loop of blood osmotic pressure regulation by kidneys

↑Plasma osmolality (e.g., dehydration, Na⁺ excess)
          ↓
    OSMORECEPTORS (hypothalamus - supraoptic nucleus)
          ↓ stimulated
    ┌─────────────────────┐
    │ 1. ADH (vasopressin) │
    │    secretion ↑       │──→ Kidney collecting duct → ↑H₂O reabsorption
    └─────────────────────┘        (aquaporin-2 insertion)
    ┌─────────────────────┐
    │ 2. THIRST           │──→ ↑Water intake
    └─────────────────────┘
          ↓
    ↑Water retention / intake
          ↓
    ↓Plasma osmolality → back to ~290 mOsm/kg
          ↓
    NEGATIVE FEEDBACK → ↓ADH secretion

INVERSE:
↓Osmolality → ↓ADH → kidney excretes dilute urine (aquaporin-2 removed)

Key mechanisms:

ADH acts on V2 receptors in collecting duct principal cells
Inserts aquaporin-2 (AQP2) water channels
Water follows osmotic gradient into hyperosmotic medullary interstitium
Normal plasma osmolality: ~285-295 mOsm/kg H₂O

Q26. Draw the scheme of structural and functional organization of a sensory system

STIMULUS (external/internal)
          ↓
    [RECEPTOR] (transduction: stimulus → generator potential → AP)
    Types: extero-, intero-, proprioceptors; mechanoreceptors, thermoreceptors, nociceptors
          ↓ (1st order neuron - afferent)
    [SPINAL CORD / BRAINSTEM]
    (processing, reflex arcs, crossover - decussation)
          ↓ (2nd order neuron)
    [THALAMUS] (relay station, filtering)
          ↓ (3rd order neuron)
    [PRIMARY SENSORY CORTEX] (conscious perception)
          ↓
    [ASSOCIATION AREAS] (integration, interpretation, memory)

Properties of sensory systems:

Adequate stimulus: each receptor responds best to one type of stimulus
Receptor potential: graded, proportional to stimulus intensity; if reaches threshold → AP
Adaptation: fast-adapting (Meissner, Pacinian) vs. slow-adapting (Merkel, Ruffini)
Labeled line code: specific pathway encodes specific modality
Dermatome: area of skin served by one spinal nerve
Receptive field: area of body monitored by one receptor/neuron

Q27. Write down the rules and stages of conditioned reflex development

Rules (Pavlov's conditions) for conditioned reflex (CR) development:

Conditioned stimulus (CS) must precede the unconditioned stimulus (UCS) by a short interval (optimal 0.5-5 seconds)
CS must be repeated together with UCS multiple times (reinforcement)
UCS must be stronger (biologically more significant) than CS
Animal/person must be healthy and in a state of attention; no distracting stimuli
CS must be initially neutral (not cause a strong reaction by itself before conditioning)

Stages of CR development (using salivary reflex example):

Stage	Description
1. Generalization	Initial conditioning: similar stimuli also elicit CR (broad response)
2. Concentration/Specialization	With repeated reinforcement: CR becomes specific to exact CS
3. Stabilization	CR becomes reliable and consistent

Extinction: CS presented repeatedly without UCS → CR gradually disappears (not destroyed, but inhibited)

Types of inhibition:

External inhibition: Novel stimulus interrupts CR temporarily
Internal inhibition: Unreinforced repetition → extinction, differentiation, conditioned inhibition

Q28. Draw scheme illustrating reflex regulation of constant body temperature under HIGH environmental temperature

HIGH ENVIRONMENTAL TEMPERATURE
          ↓
    THERMORECEPTORS (skin + hypothalamic)
    → ↑warm receptor firing
          ↓
    HYPOTHALAMUS (thermoregulatory center - preoptic area)
    Activates HEAT DISSIPATION mechanisms:
          ↓
    ┌─────────────────────────────────────────────────────┐
    │ 1. SWEATING (↑evaporative heat loss)               │
    │    Sympathetic cholinergic fibers → sweat glands   │
    │    (1 L sweat = ~580 kcal heat loss)               │
    │ 2. VASODILATION of skin vessels                    │
    │    → ↑blood flow to skin → ↑radiation/convection  │
    │ 3. ↓Muscle tone (↓heat production)                 │
    │ 4. ↑Respiratory rate (↑evaporation - panting)      │
    └─────────────────────────────────────────────────────┘
          ↓
    Body temperature maintained at ~37°C
    (NEGATIVE FEEDBACK: T↑ → heat loss ↑ → T returns to normal)

Q29. Draw scheme illustrating reflex regulation of constant body temperature under LOW environmental temperature

LOW ENVIRONMENTAL TEMPERATURE
          ↓
    THERMORECEPTORS (skin + hypothalamic)
    → ↑cold receptor firing
          ↓
    HYPOTHALAMUS (thermoregulatory center - posterior area)
    Activates HEAT CONSERVATION & PRODUCTION mechanisms:
          ↓
    ┌─────────────────────────────────────────────────────┐
    │ HEAT CONSERVATION:                                  │
    │ 1. VASOCONSTRICTION of skin vessels                │
    │    → ↓blood flow to skin → ↓heat loss              │
    │ 2. PILOERECTION (↑insulation layer - less in humans)│
    │ 3. Behavioral: curling up, seeking warmth          │
    │                                                     │
    │ HEAT PRODUCTION:                                    │
    │ 4. SHIVERING (involuntary muscle contractions)     │
    │    → ↑metabolic heat production up to 5x           │
    │ 5. NON-SHIVERING THERMOGENESIS                     │
    │    ↑Sympathetic → ↑NE → ↑brown adipose tissue      │
    │    (uncoupling protein - UCP1/thermogenin)         │
    │ 6. ↑Thyroid hormone (long-term cold adaptation)    │
    └─────────────────────────────────────────────────────┘
          ↓
    Body temperature maintained at ~37°C
    (NEGATIVE FEEDBACK)

Q30. Draw the schemes of conditioned and unconditioned salivary reflexes

Unconditioned Salivary Reflex:

FOOD IN MOUTH (UCS - unconditioned stimulus)
          ↓
Mechanoreceptors/chemoreceptors in oral cavity
          ↓ (afferent: CN V, VII, IX)
SALIVARY CENTERS (medulla oblongata - superior & inferior salivatory nuclei)
          ↓ (efferent: CN VII to submandibular/sublingual glands;
              CN IX to parotid gland via otic ganglion)
SALIVARY GLANDS
          ↓
SALIVATION (UCR - unconditioned response)

Inborn, innate; does not require learning; consistent and reliable

Conditioned Salivary Reflex (Pavlov's experiment):

BELL (CS - conditioned stimulus) [was neutral]
  +
FOOD (UCS) ─────────────────────────→ SALIVATION (UCR)
(paired repeatedly)
          ↓ After conditioning:
BELL (CS) ALONE
          ↓
CEREBRAL CORTEX (temporal lobe auditory area)
          ↓ (conditioned pathway established through learning)
SUBCORTICAL CENTERS → SALIVATORY CENTERS (medulla)
          ↓
SALIVARY GLANDS
          ↓
SALIVATION (CR - conditioned response)

Acquired, learned; requires repeated pairing of CS + UCS; can be extinguished; depends on intact cerebral cortex

Q31. Draw a scheme of the gamma loop and give functional characteristics of alpha- and gamma motoneurons

Gamma Loop Scheme:

MOTOR CORTEX / BRAINSTEM
     ↓ (upper motor neurons)
     ├─── ALPHA (α) MOTOR NEURON ──────────────────────────→ Extrafusal muscle fibers
     │    (large, Aα fibers, fast)                            (main contractile force)
     │
     └─── GAMMA (γ) MOTOR NEURON ──────────────→ Intrafusal fibers (muscle spindle)
               ↓ (sets spindle sensitivity)
          MUSCLE SPINDLE (intrafusal fibers)
          ─────────────────────────────────
          When γ fires → intrafusal fibers contract → spindle is stretched
               ↓
          Ia AFFERENT (annulospiral ending) → fires
               ↓
          α MOTOR NEURON in spinal cord activated
               ↓
          EXTRAFUSAL FIBER CONTRACTS

Alpha-Gamma coactivation: Both α and γ neurons fire simultaneously during voluntary movement → extrafusal fibers contract (via α) while spindle tension maintained (via γ) → continuous proprioceptive feedback during movement

Characteristics:

Property	Alpha (α) motoneuron	Gamma (γ) motoneuron
Target	Extrafusal muscle fibers	Intrafusal fibers of muscle spindle
Function	Generates muscle force/contraction	Adjusts spindle sensitivity
Size	Large soma, fast conduction (Aα, 70-120 m/s)	Smaller, slower (Aγ, 15-30 m/s)
Proportion	~70% of ventral horn motoneurons	~30%
Reflex	Stretch reflex effector	Modulates stretch reflex sensitivity
Upper motor neuron control	Direct cortical control	Via brainstem (reticulospinal, vestibulospinal)

Q32. Draw a scheme of the stages of Hans Selye's General Adaptation Syndrome (GAS) and note the role of hormones in each stage

Scheme:

STRESSOR (physical, psychological, chemical)
          ↓
┌─────────────────────────────────────────────────────────────────────┐
│ STAGE 1: ALARM REACTION                                             │
│  (mobilization of body defenses)                                    │
│                                                                     │
│  a) Shock phase:  ↓BP, ↓temperature, ↑capillary permeability       │
│                   ↓resistance (initial disorganization)             │
│                                                                     │
│  b) Counter-shock: Hypothalamus → CRH → ACTH → CORTISOL ↑↑        │
│     + Sympathetic activation → Epinephrine/NE from adrenal medulla  │
│     Effects: ↑HR, ↑BP, ↑glucose, ↑O₂ delivery, ↑alertness        │
└─────────────────────────────────────────────────────────────────────┘
          ↓ (if stress continues)
┌─────────────────────────────────────────────────────────────────────┐
│ STAGE 2: STAGE OF RESISTANCE (adaptation)                           │
│  Body adapts; resistance to current stressor reaches maximum        │
│                                                                     │
│  Hormones:                                                          │
│  - CORTISOL (sustained) → ↑gluconeogenesis, anti-inflammatory      │
│  - ALDOSTERONE → ↑Na⁺ retention → maintains BP/volume              │
│  - GH, Glucagon → protein catabolism, fat mobilization             │
│  - ↓Reproductive hormones (GnRH, sex hormones suppressed)          │
│  Resources mobilized; normal function maintained                    │
└─────────────────────────────────────────────────────────────────────┘
          ↓ (if stress is severe/prolonged)
┌─────────────────────────────────────────────────────────────────────┐
│ STAGE 3: STAGE OF EXHAUSTION                                        │
│  Adaptive capacity depleted; resistance breaks down                 │
│                                                                     │
│  - Adrenal cortex exhausted → ↓cortisol, ↓aldosterone              │
│  - ↓Glucose, ↓immunity, ↓Na⁺ retention                             │
│  - Multi-organ failure, disease, death if untreated                 │
│  - Similar to initial alarm reaction but without adaptive capacity  │
└─────────────────────────────────────────────────────────────────────┘

Key hormones summary:

Stage	Key Hormones	Role
Alarm	Epinephrine, NE, Cortisol	"Fight-or-flight"; mobilize energy, ↑BP
Resistance	Cortisol, Aldosterone, GH	Sustained adaptation, anti-inflammation, volume maintenance
Exhaustion	↓All adaptive hormones	Failure of adaptation; tissue damage

Sources: Costanzo Physiology 7th Edition; Guyton & Hall Medical Physiology; Kandel Principles of Neural Science; Pavlov's classical conditioning theoryAll 30 questions from your practical skills document have been answered. Here is a summary of what was covered:

Questions covered:

#	Topic
1	Action potential graph + phases + ionic mechanism
2	Excitability changes during AP + refractory periods (ARP, RRP)
3	AP propagation - myelinated (saltatory) vs. non-myelinated (continuous)
4	Neuromuscular junction scheme + synaptic transmission steps
5	Single twitch vs. tetanic contraction curves
6	Mechanism of muscular contraction and relaxation (Ca²⁺, troponin, cross-bridge cycling)
7	Spinal cord reflex arch (5 components)
8	Pre- and postsynaptic inhibition in CNS
9	Autonomic reflex arch - sympathetic and parasympathetic
10	Protein hormone action (GPCR/RTK, cAMP, second messengers)
11	Steroid hormone action (nuclear receptor, gene expression)
12	Hypothalamic-pituitary axis (HPT axis example + negative feedback)
13	Blood test interpretation (CBC reference ranges)
14	ABO and Rh blood typing principles
15	Ventricular cardiomyocyte AP - phases 0-4 + ionic basis
16	Pacemaker cell AP - If current, T-type Ca²⁺, spontaneous depolarization
17	Cardiac conduction system + frequencies + conduction velocities
18	ECG pacemaker identification criteria
19	ECG heart rate calculation + cardiac cycle duration
20	Electrical axis determination in frontal plane
21	Sphygmogram curve + phases (anacrotic, dicrotic notch, catacrotic)
22	Phlebogram curve + a, c, x, v, y waves
23	External respiration methods (spirometry, FEV₁, plethysmography, DLCO, ABG)
24	RAAS scheme + kidney's role in BP maintenance
25	Osmotic pressure regulation feedback loop (ADH, osmoreceptors)
26	Sensory system structural and functional organization
27	Conditioned reflex rules (Pavlov) + stages of development
28	Thermoregulation at HIGH temperature (sweating, vasodilation)
29	Thermoregulation at LOW temperature (shivering, vasoconstriction, thermogenesis)
30	Conditioned vs. unconditioned salivary reflexes
31	Gamma loop scheme + alpha vs. gamma motoneuron characteristics
32	Hans Selye's GAS - 3 stages + hormonal roles

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Q1 & Q2 — Nerve Action Potential + Ionic Conductances + Refractory Periods

(Costanzo Physiology 7th Ed., Fig. 1.13)

$Nerve action potential with Na+ and K+ conductance curves and refractory periods labeled$

Shows the AP waveform (purple), Na⁺ conductance spike (green dashed), K⁺ conductance curve (orange dashed), equilibrium potentials, resting potential (-70 mV), undershoot, and both the absolute and relative refractory periods marked above.

Q1 (continued) — Na⁺ Channel Gate States

(Costanzo Physiology 7th Ed., Fig. 1.14)

Na+ channel activation and inactivation gate states - closed available, open, inactivated

The three states of the voltage-gated Na⁺ channel: (1) Closed but available (resting) - activation gate closed, inactivation gate open; (2) Open (upstroke) - both gates open, Na⁺ flows in; (3) Inactivated (repolarization) - inactivation gate closed, channel non-conducting. This directly explains the ARP.

Q4 — Neuromuscular Junction Structure

(Kandel, Principles of Neural Science 6th Ed., Fig. 57-9)

Normal neuromuscular junction showing axon terminal, mitochondria, synaptic vesicles, ACh receptors, junctional folds

The normal NMJ (left): axon terminal contains mitochondria and synaptic vesicles (ACh); active zones release ACh into the cleft; nicotinic ACh receptors cluster at the peaks of junctional folds on the muscle fiber membrane. AChE in the cleft hydrolyzes ACh.

Q6 — Mechanism of Muscular Contraction (Cross-Bridge Cycle)

(Harrison's Principles of Internal Medicine 22nd Ed., Fig. 244-6)

Four-step cross-bridge cycle: relaxed, energized, active complex, rigor complex with ATP/ADP/actin/myosin

The 4-step cross-bridge cycle:

Relaxed → ATP on myosin head dissociates thick/thin filaments

Step 1 (ATP hydrolysis): Myosin head "re-cocked", energized (ADP + Pi)

Step 2 (Active complex): Ca²⁺ exposes actin sites; myosin binds actin, Pi released

Step 3 (Power stroke): ADP released; myosin head pivots → filaments slide → force

Step 4 (Rigor): New ATP binds → cross-bridge detaches → cycle repeats

Q15 — Cardiac Ventricular Action Potential (Phases 0-4 + Ionic Currents)

(Guyton & Hall Medical Physiology, Fig. 9.5)

Cardiac ventricular AP phases 0-4 with Na+, Ca2+, K+ ionic currents below

Phase 0: Fast Na⁺ influx (iNa) → rapid upstroke to +20 mV Phase 1: Na⁺ channels inactivate → brief early repolarization Phase 2 (Plateau): L-type Ca²⁺ influx (iCa²⁺) balanced by K⁺ efflux → flat plateau ~200 ms Phase 3: Ca²⁺ channels close; K⁺ channels (iK⁺) fully open → rapid repolarization Phase 4: Resting at -85 to -90 mV; iK⁺ (inward rectifier) maintains

Q16 — Pacemaker AP (SA Node) vs. Ventricular AP - Side by Side

(Ganong's Review of Medical Physiology 26th Ed., Fig. 29-2)

Side-by-side: ventricular myocyte AP phases 0-4 (left) and SA node pacemaker spontaneous depolarization with If, IcaT, IcaL currents (right)

Panel A (ventricular): Phases 0-4 with ion current labels (↑INa = upstroke; ↑ICa + ↑IK = plateau; ↓IK = resting at -90 mV)

Panel B (pacemaker - SA node): No stable resting potential - instead a slow spontaneous depolarization (pacemaker potential) from -60 mV to threshold:

↑Ih (HCN "funny" current): inward Na⁺ current activated by hyperpolarization → initial slow drift upward

↓IK: K⁺ channels gradually close → less outward current → further depolarization

↑ICaT (T-type Ca²⁺): activates near -50 mV → accelerates depolarization to threshold

↑ICaL (L-type Ca²⁺): carries the upstroke (no fast Na⁺ channels in nodal cells!)

Q17 — Cardiac Conduction System

(Costanzo Physiology 7th Ed., Fig. 4.11)

Heart cross-section showing SA node, AV node, Bundle of His, right and left bundle branches, Purkinje fibers with activation sequence arrows

Activation sequence: SA node (right atrium) → spreads through both atria via internodal tracts → AV node (slow conduction - delay allows ventricular filling) → Bundle of His → Right & Left bundle branches → Purkinje fibers → ventricular myocardium (endocardium to epicardium)

Summary of diagrams provided:

Diagram	Source
Q1/Q2: Nerve AP + conductances + refractory periods	Costanzo Physiology 7e
Q1: Na⁺ channel gate states	Costanzo Physiology 7e
Q4: Neuromuscular junction	Kandel - Principles of Neural Science 6e
Q6: Cross-bridge contraction cycle	Harrison's Internal Medicine 22e
Q15: Cardiac ventricular AP + ionic currents	Guyton & Hall Medical Physiology
Q16: Ventricular vs. pacemaker AP comparison	Ganong's Medical Physiology 26e
Q17: Cardiac conduction system	Costanzo Physiology 7e

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Textbook Diagrams for All 32 Practical Skills Questions

Q1 — Action Potential Graph + Ionic Conductances

(Costanzo Physiology 7th Ed., Fig. 1.13)

$Nerve action potential: AP waveform with Na+ conductance spike, K+ conductance, resting potential -70mV, Na+ equilibrium +65mV, K+ equilibrium -85mV, absolute and relative refractory periods$

Key points from graph:

AP rises from -70 mV → peak near +40 mV → repolarizes → undershoot to ~-80 mV
Na⁺ conductance peaks first (upstroke), then falls
K⁺ conductance rises later, causing repolarization and undershoot
Absolute refractory period (ARP): Na⁺ channels inactivated - no new AP possible
Relative refractory period (RRP): partial recovery - suprathreshold stimulus needed

Q1 (continued) — Na⁺ Channel Gate States (Ionic Mechanism)

(Costanzo Physiology 7th Ed., Fig. 1.14)

Na+ channel: 3 states - (1) Closed but available at rest, (2) Open during upstroke with Na+ influx, (3) Inactivated at peak of AP

State 1 - Closed/available (resting): Activation gate CLOSED, inactivation gate OPEN. Channel ready to fire. State 2 - Open (upstroke): Both gates open. Na⁺ rushes in → depolarization. State 3 - Inactivated (repolarization): Inactivation gate CLOSED (slow). Na⁺ current stops → ARP corresponds to this state.

Q2 — Refractory Periods

The graph above (Fig. 1.13) shows both refractory periods labeled directly:

ARP = during upstroke + most of repolarization (Na⁺ channels in state 3/inactivated)
RRP = after return to resting potential, while K⁺ conductance still slightly elevated (hyperpolarized undershoot)
During ARP: zero excitability, no AP possible at any stimulus strength
During RRP: reduced excitability, supranormal stimulus required; AP will be smaller

Q3 — AP Propagation: Myelinated (Saltatory) vs. Non-myelinated

Saltatory conduction in myelinated axon (Kaplan & Sadock's, Fig. 1.5-4)

Neuron with soma, dendrites, axon initial segment, myelin sheaths, nodes of Ranvier - AP waveform jumps from node to node (active) while internodal segments conduct passively

Underlying cable properties (Medical Physiology - equivalent circuit model)

Axon cable model: equivalent circuit with membrane resistance rm, capacitance cm, internal resistance ri; current distribution spreading from injection site; voltage decay exponentially with length constant λ

Key explanation:

Non-myelinated: Current leaks continuously across membrane at every point → slow, energy-costly (0.3-2 m/s). Decremental passive spread is regenerated at each point.
Myelinated (saltatory): Myelin ↑membrane resistance + ↓membrane capacitance → current forced to flow along axoplasm and "jump" node to node. AP regenerated only at nodes of Ranvier → fast (up to 130 m/s), energy-efficient.

Q4 — Neuromuscular Junction

(Kandel, Principles of Neural Science 6th Ed., Fig. 57-9)

Normal NMJ (left): axon terminal with mitochondria and ACh synaptic vesicles, active zones, synaptic cleft, ACh receptors clustered at peaks of junctional folds on muscle fiber

Transmission steps:

AP reaches terminal → voltage-gated Ca²⁺ channels open → Ca²⁺ influx
Ca²⁺ triggers exocytosis of ACh vesicles into synaptic cleft
ACh binds nicotinic receptors on junctional folds → Na⁺/K⁺ channels open → EPP
EPP spreads → AP in muscle → contraction
AChE in cleft rapidly hydrolyzes ACh → signal terminated

Q5 — Single Twitch and Tetanus

(Ganong's Review of Medical Physiology, Fig. 5-9)

Isometric tension recording of single muscle fiber showing discrete single twitches at low frequency progressing through incomplete tetanus to complete tetanus at high frequency, then return as frequency decreases

Explanation:

Single twitch: one stimulus → brief Ca²⁺ release → force rises and falls completely
Incomplete tetanus: stimuli before full relaxation → summation → undulating elevated force
Complete tetanus: high-frequency stimuli → Ca²⁺ continuously elevated → maximal smooth force (~4x single twitch)

Q6 — Mechanism of Muscular Contraction (Cross-Bridge Cycle)

(Harrison's Internal Medicine 22nd Ed., Fig. 244-6)

4-panel cross-bridge cycle: Relaxed (ATP on myosin, tropomyosin blocks actin) → Relaxed energized (ATP hydrolyzed, myosin re-cocked) → Active complex (Ca2+ exposes actin sites, myosin-actin bind, Pi released) → Rigor (power stroke, ADP released, filaments slide) → new ATP detaches cross-bridge

Steps:

ATP hydrolysis: Myosin re-cocked, energized with ADP + Pi
Active complex: Ca²⁺ binds troponin C → tropomyosin shifts → actin binding sites exposed → myosin head attaches to actin; Pi released
Power stroke: ADP released → myosin head pivots → thin filament pulled → force/shortening (rigor complex)
Detachment: New ATP binds → cross-bridge detaches → cycle repeats

Relaxation: Ca²⁺ pumped back into SR by SERCA → troponin-tropomyosin complex covers actin → no more cross-bridges

Q7 — Spinal Cord Reflex Arc (Knee-Jerk / Stretch Reflex)

(Medical Physiology - Boron & Boulpaep, Fig. 16-3)

Knee-jerk reflex: patellar tendon tap → muscle spindle stretched → Ia afferent → dorsal root ganglion → spinal cord: (1) monosynaptic excitatory synapse on α motor neuron → ventral root → extensor (quadriceps) contracts; (2) inhibitory interneuron → inhibitory synapse on flexor α motor neuron → flexor (semitendinosus) relaxes

5 components of reflex arc shown:

Receptor - muscle spindle (stretch detector)
Afferent neuron - Ia axon (primary sensory, fast)
Nerve center - spinal cord (monosynaptic + inhibitory interneuron)
Efferent neuron - α motor neuron (ventral root)
Effector - quadriceps muscle (contracts); antagonist flexor (relaxed via reciprocal inhibition)

Q8 — Pre- and Postsynaptic Inhibition in CNS

(No single textbook image available from library for both simultaneously — described below based on principles from Costanzo Physiology)

Presynaptic inhibition: An inhibitory neuron (releasing GABA) synapses onto the terminal of an excitatory neuron. GABA-B receptors → ↑K⁺ conductance / ↓Ca²⁺ entry → less neurotransmitter released from excitatory terminal → weaker EPSP in postsynaptic cell.

Postsynaptic inhibition (Renshaw cell): Inhibitory interneuron synapses directly onto the postsynaptic cell body → opens Cl⁻ channels (GABA-A or glycine receptors) → IPSP → membrane hyperpolarizes → harder to reach threshold.

Q9 — Autonomic Nervous System Organization (Sympathetic + Parasympathetic + Somatic)

(Costanzo Physiology 7th Ed., Fig. 2.1)

Full autonomic scheme: Somatic (single motoneuron → ACh → N1 receptor → skeletal muscle); Sympathetic (preganglionic ACh → N2 → postganglionic NE → α1/α2/β1/β2 receptors → smooth muscle/glands; also ACh → M → sweat glands); Parasympathetic (long preganglionic ACh → N2 → short postganglionic ACh → M receptor → smooth muscle/glands); Adrenal medulla (preganglionic ACh → N2 → epinephrine 80% + NE 20% → circulation)

Key differences:

Sympathetic: short preganglionic (T1-L2), long postganglionic, NE transmitter, α/β receptors
Parasympathetic: long preganglionic (CN III/VII/IX/X + S2-4), short postganglionic, ACh transmitter, muscarinic receptors
Both divisions use ACh at preganglionic synapse (nicotinic N2 receptors)

Q10 — Protein Hormone Mechanism (Cell Surface Receptors)

Described from Cecil Medicine text: Protein hormones bind cell surface receptors (G protein-coupled or receptor tyrosine kinases). They generate second messengers (cAMP, IP₃/DAG, Ca²⁺) that activate kinase cascades → rapid effects (exocytosis, channel opening) and longer-term gene regulation. They do NOT enter the nucleus directly.

Q11 — Steroid Hormone Mechanism (Nuclear Receptors)

Steroid hormones are lipophilic → cross plasma membrane freely → bind cytoplasmic or nuclear receptors → receptor-hormone complex dimerizes → binds Hormone Response Elements (HRE) on DNA → acts as a ligand-regulated transcription factor → alters gene expression → new protein synthesis → biological effect (hours to days onset).

Q12 — Hypothalamic-Pituitary Axis (Feedback Regulation)

(Harrison's Internal Medicine 22nd Ed., Fig. 389-4)

Hypothalamic-pituitary-peripheral gland axis: CNS influences hypothalamus → releasing factors (+) → pituitary → trophic hormones (+) → adrenal/thyroid/gonads → target hormones feed back negatively (-) on both hypothalamus and pituitary

Three axes shown:

HPA: CRH → ACTH → Cortisol (−feedback)
HPT: TRH → TSH → T3/T4 (−feedback)
HPG: GnRH → LH/FSH → sex steroids (−feedback)

A small drop in thyroid hormone → rapid ↑TRH + ↑TSH → ↑thyroid hormone → negative feedback suppresses TRH/TSH → new steady state. This "exquisite control" operates for all axes.

Q13 — Blood Test Interpretation

Normal reference values (from Harrison's / Tietz Laboratory Medicine):

Parameter	Reference Range	Low =	High =
Hb ♂	130-170 g/L	Anemia	Polycythemia
Hb ♀	120-150 g/L	Anemia	Polycythemia
WBC	4.0-9.0 ×10⁹/L	Leukopenia	Leukocytosis
Platelets	150-400 ×10⁹/L	Thrombocytopenia	Thrombocytosis
MCV	80-100 fL	Microcytic anemia	Macrocytic anemia
Neutrophils	50-70%	Neutropenia	Bacterial infection
ESR	<15 mm/h (♂), <20 (♀)	—	Inflammation

Q14 — ABO and Rh Blood Typing

ABO system principle:

Group	RBC Antigen	Plasma Antibody
A	A	Anti-B
B	B	Anti-A
AB	A + B	None (universal recipient)
O	None	Anti-A + Anti-B (universal donor)

Typing: Add anti-A and anti-B sera to patient's RBCs → agglutination = antigen present. Rh system: D antigen. Rh+ (~85%). Anti-D is immune (needs prior sensitization). Critical in pregnancy - Rh− mother + Rh+ fetus → HDN risk in 2nd pregnancy. Prevented by RhoGAM.

Q15 — Cardiac Ventricular AP (Phases 0-4) + Ionic Currents

(Guyton & Hall Medical Physiology, Fig. 9.5)

Cardiac ventricular muscle AP: phase 0 fast upstroke to +20mV, phases 1-2 plateau (~200ms), phase 3 rapid repolarization, phase 4 resting -85mV; below: iNa (orange, large inward peak), iCa2+ (blue, sustained inward during plateau), iK+ (red, outward throughout)

Purkinje fiber vs. ventricular muscle comparison (Guyton & Hall, Fig. 9.4)

Purkinje fiber (red, top): resting -95mV, tall upstroke, distinct plateau, longer duration; Ventricular muscle (blue, bottom): resting -85mV, shorter, both showing characteristic plateau; both firing rhythmically over 4 seconds

Q16 — Pacemaker Cell AP vs. Ventricular AP

(Ganong's Review of Medical Physiology, Fig. 29-2)

Panel A: Ventricular myocyte AP phases 0-4 labelled with ion current changes (↑INa upstroke, ↑ICa plateau, ↓IK resting); Panel B: Pacemaker (SA node) spontaneous depolarization from -60mV showing ↑Ih (funny current, HCN), ↓IK decay, ↑ICaT (T-type), then ↑ICaL (L-type) for upstroke - no fast Na+ channels

Critical distinction: SA node has NO stable resting potential and NO fast Na⁺ channels. Its upstroke is carried by L-type Ca²⁺ channels (slow) - this is why AV conduction is slow and why Ca²⁺ channel blockers (verapamil) slow heart rate.

Q17 — Cardiac Conduction System

(Costanzo Physiology 7th Ed., Fig. 4.11)

Heart cross-section: SA node (green, right atrium) → arrows spread across both atria → AV node (purple, interatrial septum) → Bundle of His → right and left bundle branches along interventricular septum → Purkinje fiber network spreading to ventricular myocardium (arrows show endocardium-to-epicardium spread)

Structure	Rate (bpm)	Conduction Velocity
SA node	60-100	0.05 m/s
AV node	40-60	0.02-0.05 m/s (slowest - AV delay)
Bundle of His	—	0.1-0.2 m/s
Bundle branches / Purkinje	20-40	2-4 m/s (fastest)
Ventricular muscle	20-40	0.3-0.5 m/s

Q18 — ECG: Determine Pacemaker

P wave before every QRS, upright in II → SA node (normal sinus rhythm)
No P waves, narrow QRS → AV node (junctional rhythm, 40-60 bpm)
No P waves, wide bizarre QRS (>0.12s) → ventricular pacemaker (idioventricular, 20-40 bpm)

Q19 — ECG: Heart Rate + Cardiac Cycle Duration

HR = 300 ÷ (number of large squares between R-R peaks)
e.g., 4 large squares → HR = 300/4 = 75 bpm
Cardiac cycle duration = 60 ÷ HR (in seconds)
e.g., 75 bpm → 0.8 s; 60 bpm → 1.0 s; 100 bpm → 0.6 s
Paper speed 25 mm/s: 1 small square = 0.04 s; 1 large square = 0.2 s

Q20 — ECG: Electrical Axis in Frontal Plane

Lead I	aVF	Axis
+	+	Normal (0° to +90°)
+	−	Left axis deviation (<−30°)
−	+	Right axis deviation (>+90°)
−	−	Extreme axis (±180°)

Precise method: Find the most isoelectric (biphasic) limb lead → axis is perpendicular to it → confirm direction with perpendicular lead.

Q21 — Sphygmogram (Arterial Pulse Curve)

(Described from Costanzo + Guyton — no isolated sphygmogram figure found in library)

Pressure
↑          Peak (systolic)
     /‾‾\   /\ ← dicrotic wave
    /    \_/ \___  → diastolic baseline
   /  ↑  ↑
  ↑  dicrotic notch
anacrotic
limb

Anacrotic limb: Rapid systolic pressure rise (ventricular ejection)
Dicrotic notch: Aortic valve closure (end systole)
Dicrotic wave: Aortic wall elastic recoil after valve closure
Catacrotic limb: Gradual diastolic pressure fall

Q22 — Phlebogram (Venous/JVP Waveform)

Pressure
↑   a  c  v
   /\ /|/\
  /  X  \ /\
─/  / \  V  \─
     x    y
   descent

a wave: Atrial contraction (just before QRS)
c wave: Tricuspid valve bulging into atrium
x descent: Atrial relaxation + tricuspid descent
v wave: Passive venous filling (tricuspid closed during systole)
y descent: Tricuspid opens → blood empties into ventricle

Q23 — External Respiration: Spirometry (Lung Volumes + FEV₁)

(Harriet Lane Handbook / Johns Hopkins, Fig. 25.2)

Spirometry trace: left side shows normal breathing (resting tidal volume, functional residual capacity, total lung capacity labeled with double arrows); right side shows forced maneuver with FVC labeled, FEV1 measured at 1 second, FEF25-75 (mid-expiratory flow) labeled between 25% and 75% of FVC; residual volume at baseline

Pattern	FEV₁/FVC	TLC	Example
Normal	>70%	Normal	—
Obstructive	↓ (<70%)	↑ or normal	Asthma, COPD
Restrictive	Normal or ↑	↓	Fibrosis, NM disease

Q24 — RAAS Scheme (Renin-Angiotensin-Aldosterone)

(Ganong's Review of Medical Physiology, Fig. 19-22)

RAAS feedback loop: Juxtaglomerular apparatus secretes renin → cleaves angiotensinogen → Angiotensin I → ACE → Angiotensin II → adrenal cortex → aldosterone → decreased Na+/water excretion → increased ECF volume → increased renal arterial pressure → inhibits renin (dashed negative feedback arrow)

Kidney's role:

Renin release (JGA): triggered by ↓renal perfusion pressure, ↓NaCl at macula densa, ↑sympathetic discharge
Aldosterone effect on kidney: ↑Na⁺ + H₂O reabsorption in collecting duct → ↑ECF volume → ↑BP
Negative feedback: restored BP/volume shuts off renin release

Q25 — Osmotic Pressure Regulation by Kidneys (ADH Feedback)

Hypothalamic osmoreceptors detect ↑plasma osmolality → ADH (vasopressin) secreted from posterior pituitary → acts on V2 receptors in collecting duct → inserts aquaporin-2 channels → ↑water reabsorption → dilutes plasma → osmolality falls → ADH suppressed (negative feedback). Simultaneously: thirst center activated → water intake. Inverse: ↓osmolality → ↓ADH → dilute urine excreted.

Q26 — Sensory System Structure and Function

Three-neuron relay:

1st order (peripheral receptor): Transduces adequate stimulus → generator potential → AP in afferent fiber
2nd order (spinal cord / brainstem): Crosses midline (decussates), ascends to thalamus
3rd order (thalamus → cortex): Projects to primary somatosensory cortex (postcentral gyrus) → conscious perception
Association cortex: Integration, interpretation, memory

Q27 — Conditioned Reflex Development Rules (Pavlov)

5 rules:

CS must precede UCS by short interval (0.5-5 s)
Repeated pairing required (reinforcement)
UCS must be biologically stronger/more significant than CS
Subject must be healthy and attentive
CS must be initially neutral (no strong pre-existing response)

Stages: Generalization → Specialization → Stabilization → (Extinction without reinforcement)

Q28 — Thermoregulation at High Environmental Temperature

High temp → skin + hypothalamic thermoreceptors activated → preoptic area of hypothalamus → effector responses:

↑Sweating (sympathetic cholinergic to sweat glands → evaporative cooling)
Cutaneous vasodilation → ↑blood to skin surface → ↑radiation + convection
↓Muscle tone → ↓metabolic heat production
↑Respiratory rate → ↑evaporative loss

Negative feedback: body temp returns to 37°C → thermoreceptors less stimulated → responses reduce.

Q29 — Thermoregulation at Low Environmental Temperature

Low temp → cold receptors activated → posterior hypothalamus → effector responses:

Cutaneous vasoconstriction → ↓blood to skin → ↓heat loss
Shivering (involuntary skeletal muscle contractions) → ↑heat up to 5x resting
Non-shivering thermogenesis (sympathetic → NE → brown adipose tissue → UCP1/thermogenin → uncoupled oxidative phosphorylation → heat)
Piloerection → traps air layer (minimal in humans)
Long-term: ↑thyroid hormone → ↑basal metabolic rate

Q30 — Conditioned vs. Unconditioned Salivary Reflexes

Unconditioned: Food → oral receptors → CN VII/IX → salivatory nuclei (medulla) → CN VII/IX → salivary glands. Innate, reliable, does not require learning.

Conditioned (Pavlov): Bell (CS) paired repeatedly with food (UCS) → after conditioning: Bell alone → cortex (auditory area) → subcortical pathway to salivatory nuclei → salivation (CR). Requires intact cerebral cortex. Can be extinguished by presenting CS without UCS.

Q31 — Gamma Loop + Alpha vs. Gamma Motoneurons

The spinal reflex arc diagram (Q7 above) directly shows α motor neurons and Ia afferents. The gamma loop adds:

α Motor neuron ──────────────────→ Extrafusal fibers (force)
                                    ↑
γ Motor neuron ──→ Intrafusal fibers (spindle tension set)
                   ↓
              Ia afferent fires ────→ α Motor neuron
              (if muscle too long)        (stretch reflex)

Feature	α Motoneuron	γ Motoneuron
Target	Extrafusal fibers	Intrafusal (spindle) fibers
Function	Force generation	Spindle sensitivity adjustment
Fiber type	Large, Aα (70-120 m/s)	Smaller, Aγ (15-30 m/s)
Proportion	~70% ventral horn	~30% ventral horn

Alpha-gamma coactivation: During voluntary movement both fire simultaneously → muscle shortens (via α) while spindle remains taut and sensitive (via γ) → continuous proprioceptive feedback.

Q32 — Hans Selye's General Adaptation Syndrome (GAS)

STRESSOR
   ↓
STAGE 1: ALARM
  Shock phase (↓BP, ↑capillary permeability)
  Counter-shock:
  • Epinephrine/NE (adrenal medulla) → ↑HR, ↑BP, ↑glucose
  • Cortisol ↑↑ (HPA: CRH → ACTH → cortisol)
   ↓ (if stress continues)
STAGE 2: RESISTANCE (Adaptation)
  • Cortisol (sustained): ↑gluconeogenesis, anti-inflammatory
  • Aldosterone: ↑Na⁺ retention → ↑volume → ↑BP
  • GH + Glucagon: fat/protein mobilization
  • Reproductive hormones suppressed
  Maximum resistance to stressor; normal function maintained
   ↓ (if severe/prolonged)
STAGE 3: EXHAUSTION
  • Adrenal cortex depleted: ↓cortisol, ↓aldosterone
  • ↓Immunity, ↓glucose, organ failure
  • Resembles alarm but without adaptive capacity
  • Death possible if untreated

Stage	Key Hormones	Effect
Alarm	Epinephrine, NE, Cortisol	Fight-or-flight mobilization
Resistance	Cortisol, Aldosterone, GH	Sustained adaptation
Exhaustion	All ↓	Failure, organ damage

All diagrams sourced from: Costanzo Physiology 7e · Guyton & Hall Medical Physiology · Ganong's Review of Medical Physiology 26e · Kandel Principles of Neural Science 6e · Harrison's Internal Medicine 22e · Boron & Boulpaep Medical Physiology · Kaplan & Sadock's Textbook of Psychiatry · Harriet Lane Handbook 23e

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