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eMRCS questions > Basic Science MRCS Physiology > Flashcards

Basic Science MRCS Physiology Flashcards

1
Q

Which body parts have higher temperatures on measurements

A

Rectal 0.5 higher than Mouth and axilla

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2
Q

When is temperature highest in menstrual cycle

A

0.5 higher in latter half

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3
Q

Sx of hypothermia

A

Bradycardia
Hypotension
Resp depression
Muscle stiffness
VF

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4
Q

Vessel Reflex to hot/cold stimulus

A

Cold- vasoconstriction on ispilateral and contralateral side
Afferent- cutaneous nerve
Centre- hypothalamus and spinal
Eff- symp

Hot- vasodilation
Centre- above c5
Reduced symp activity

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5
Q

Water composition of human

A

Of 70kg man -2/3 is water - 44kg

2/3 intracellular- 25kg
1/3 extracellular- 19kg

Of that 2/3 interstitial - 15L
intravascular 3L
Transcellular 1L

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6
Q

Water loss compostion

A

Resp 500
Urine -500
Skin- 400
Faeces-100

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7
Q

Which is triggered first ADH or thirst

A

ADH- low osmolality threshold of around 10
So triggered before getting thirsty

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8
Q

Triggers for thirst and ADH

A

Osmolality receptors
Baroreceptors- carotid and aortic
Reduced CVP- atrial
Angiotensin 2 in brain

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9
Q

ANP action

A

Increasing GFR
Inhibiting Na reabsorption in CD
Reducing secretion of renin and aldosterone

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10
Q

Water excess clinical manifestation

A

Primary- low osmolality- water intoxication
Secondary due to high sodium- oedema

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11
Q

Water depletion clinical manifestation

A

Primary- loss of water- high osmo- thirst
Secondary- loss of Na- circulatory collapse

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12
Q

ECG of hyperkalaemia and hypo

A

Hyper- broad QRS, flat p, tinted T

Hypo- Peaked P, flat/inverted T

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13
Q

Important buffer systems in body

A

Proteins- helps with pH ICF and ECF
Hb
Phopshate- of ICF and urine
Bicarbonate- most important in ECF

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14
Q

Cause of resp acidosis

A

CNS depression
Neuromuscular dise3ase
Skeletal disease
Impaired gas exchange- obstructive airway, alveolar disease- pneumonia, ARDS

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15
Q

Cause of resp alkalosis

A

High altitude
Pneumonia
Pul Oedema
PE

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16
Q

When is BE -/+

A

BE + in metabolic alkalosis
-in metabolic acidosis

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17
Q

24 hours maintainence fluids for uncomplicated patient

A

2L dextrose
1L NaCl
60mmol of KCL

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18
Q

Physiological response to surgery

A

Released catecholamines
Increased cortisol and aldosterone

Retention of Na- reduced urine
RAS activated
ADH released
K usually doesnt fall but might rise do to tissue damage

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19
Q

When is HAS used

A

Severe hypoproteinaemia in renal or liver disease
Large volume paracentesis
Massive liver resection

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20
Q

Problems with plasma expanders

A

Dilution coagulopathy
Allergic
Dextran intereferes with cross matching

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21
Q

Where does IV fluids go after administration

A

2/3- ECF
1/3- ICF

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22
Q

Tidal volume amount and changes in exercise

A

500ml

Goes up to 2-3L in exercise

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23
Q

Normal intrapleural pressure and during exercise

A

Beginning of inspiration-4
End -9

Exercise -30 in inspiration
+20 on expiration

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24
Q

Expanding lungs with air vs saline

A

Lack of surface tension with saline- greater compliance
Only opposing force is elastic tension

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25
Q

Surfactant functions

A

Lower surface tension- increase compliance- reduce work of breathing
Prevent fluid accumulation
Reduce tendency to collapse

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26
Q

Law of laplace in alveoli

A

Laplace
Alveolar pressure= 2 Tension/R

So smaller alveoli more prone to collapse - since generate larger pressure causing air to travel to larger alveoli

Therefore smaller alveoli have more surfactant to lower their Tension more

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27
Q

Compliance calculation

A

change in volume/change in pressure

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28
Q

Cause of increase/decrease in compliance

A

Increase- emphysema due to destruction of elastic tissue

Decrease- fibrosis, oedema, reduced surfactant, supine, mechanical ventilation due to reduced blood flow

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29
Q

Main resistance of air flow

A

1/3 nose, pharynx, larynx

2/3-tracheobronchial tree
little distally

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30
Q

Elastance equation

A

Change in pressure/change in volume

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31
Q

How to calculate FRV/RV

A

Helium dilution method

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32
Q

How to calculate anatomical dead space

A

Fowler method- breath of pure O2
nitrogen components measured - as alveolar has nitrogen from old breathing

Calculated from Bohr equation

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33
Q

Factors increasing anatomical vs physiological dead space

A

Anatomical- increase size of patient
Standing
Bronchodilation

Physiological
Hypotension
Hypoventilation
Emphysema and PE
PPV

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34
Q

Measuring closing capacity

A

Volume at which small airways at base start to close
Usually 10% of VC

Breathes out to FRC- takes 100% O2

Point between phase 3+4 on curve- there is an increase in 4 as only the poorly ventilated upper lobes are open

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35
Q

Flow volume curve characteristics with diseases

A

Obstructive- concave expiration phase

Restrictive- normal shape, volume lower

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36
Q

Which part of the lung has the lowest ventilation

A

Apex
Due to weight- causing pleural fluid - more negative intrapleural pressure and compliance differences

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37
Q

Determinates of pulmonary blood flow

A

Hydrostatic pressure in PA
Pressure in PV
Pressure of air in alveoli

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38
Q

Blood flow in zones of lungs

A

1- apex- alveolar pressure similar to PA- smaller vessels compressed- low flow
2-PA is higher- increased flow
3- PA greatly exceeds

These are only true with standing up

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39
Q

Change in pressure in Pul arterioles in excerise

A

Changes very little

Due to increase in CO
Causes Recruitment of additional vessels- many caps at rest closed
Vessels getting distended

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40
Q

V/Q ratio throughout lung

A

3 at apex- ventilated more than perfused
2/3 up chest-1
Base- 0.6- better perfused than ventilated

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41
Q

Stages of pulmonary oedema development

A

Interstitial oedema- doesnt affect ventilation at first- but once large enough to affect lymph to cause alveolar oedema

Alveolar oedema- fill with fluid- increasing surface tension and shrinking alveoli
leading to vasoconstiction due to hypoxia

Airway oedema- causing blood tinged frothy sputum

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42
Q

Diagnosis of ARDS

A

Known cause
Acute
Fluffy infiltrates
PWP- <18

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43
Q

Stages of ARDS

A

1- Intially active exudate- inflammtory mediators, proteases
Damage lung and Increase cap perm
Thrombosis and haemorrhage in alveolar capillaries- alveolar collapse - decreased lung compliance

2-Regeneration of type 2 pneumocytes- organisation with fibrosis, and obliteration of alveolar space

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44
Q

Factors affecting gas diffusion

A

Pressure gradient - partial pressure
Diffusion coefficient- how well it can diffuse- determined by solubility and molecular weight
Tissue factors- large SA, short diffusion distance -

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45
Q

Diffusion distance constituents

A

Pulmonary surfactant
Alveolar epithelium
BM
Pulmonary endothelium

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46
Q

Examples of pulmonary shunting

A

Travel through lungs without contact with ventilated alveoli
Bronchial veins
Pneumonia

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47
Q

Fetal and myoglobin oxygenation curve

A

Fetal comprimised of 2a 2y- shift to left

Myoglobin- even further left to provide additional O2 in anaerobic

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48
Q

Transportation methods of CO2

A

HCO3- 60-70% formed in red cell and diffuses out- Cl- replaces it in red cell- reversed in alveoli
Carbamino- between proteins mostly globin- 20-30%
Dissolved 10%

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49
Q

Difference between O2 and CO2 dissociation curve

A

Co2 solubility greater
Normal range of PaCo2 smaller
Blood cannot be saturated with CO2- so no plateau

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50
Q

Haldane effect

A

CO2 carried increases as O2 levels fall

At given partial pressure Co2 carried increases

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51
Q

Chemoreceptors of respiratory regulation

A

Central- close to medulla
Change relative to pH
Increase resp rate if CO2 increases

Peripheral
Carotid bifurcation and aortic arch
pH and PO2
Only PO2 when abnormally low- <8

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52
Q

Hering Bruer reflex

A

Strech receptors in lung - prevent over inflation via vagus

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53
Q

Carotid bodies CV response to hypoxia

A

Increased HR
Increased CO
Vasoconstriction in skin and splanchnic

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54
Q

Physiological alterations with chronic hypoxia

A

Increased minute volume
RBC
CO
Vascularity of organs

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55
Q

Complications of mechanical ventilation

A

*ventilator-induced injury
*volutrauma
*barotrauma
*hypotension and decreased cardiac output: decreased venous return due to positive intrathoracic pressure
*respiratory muscle atrophy
*nosocomial infections
*technical complications, e.g. disconnection
*increase in intracranial pressure (ICP) due to the increase in intrathoracic pressure.

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56
Q

Modes of ventilation

A

Controlled mandatory ventilation- no resp effort- set volume

Synchronised intermittent MV- less sedation- some breath initiated by patient

Pressure controlled ventilation- reduces risk of barotrauma

Pressure support ventilation- used in combo- allows weaning by triggering breath

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57
Q

Calcium in cardiac contraction

A

In the absence of calcium the troponin/tropomysin complex inhibits cross-bridging between actin and myosin filaments.

*When calcium binds to troponin, formation of cross-bridging occurs between the filaments. The filaments then slide over one another to cause contraction

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58
Q

Mechanism of contraction in cardiac cells

A

Arrival of the action potential allows Ca2+ to move from the sarcoplasmic reticulum into the cytoplasm.

*Ca2+ binds to troponin C, eventually activating the actin–myosin complex, resulting in contraction.

*The plateau phase, the result of further calcium influx, prolongs and enhances contraction.

*The cardiac action potential is very long (200–300 ms). After the contraction there is a refractory period when no further action potentials can be initiated and therefore no contraction occurs. The long action potential and refractory periods ensure contraction and relaxation of the heart, allowing the chambers to fill during relaxation and empty during contraction.
*Intracellular Ca2+ is the most important factor controlling myocardial contractility:
*increased intracellular Ca2+ increases force of myocardial contraction
*decreased intracellular Ca2+ decreases the force of myocardial contraction

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59
Q

Location of SA and AV node

A

SA- right atrium near SVC entrance

AV_ fibrous ring on right side of atrial septum

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60
Q

Properties of SA, AV node and purkinje

A

Ability to depolarise at regular intervals- self excitation
Long refractory period- so cells with highest frequency (SA node) control HR

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61
Q

Normal pressure in heart

A

RA- 0-4
RV- 25/0-4
PA- 25/15

LA-5-10
LV- 120/0-10

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62
Q

EF calculation

A

EF= SV/LVEDV

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63
Q

Which JVP wave is synchronous with carotid pulse

A

C wave

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64
Q

Factors affecting coronary blood flow

A

Coronary flow occurs mainly during diastole.

*Conditions resulting in low diastolic BP or increased intramyocardial tension during diastole (e.g. an increased end diastolic pressure) may compromise coronary blood flow.

*Subendocardial muscle, where the tension is highest, is particularly vulnerable.

*Diastolic time is important. At fast rates, inadequate myocardial perfusion occurs.

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65
Q

Factors affecting pre load

A

*venous return
*atrial systole (fibrillation)
*myocardial distensibility

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66
Q

How to measure pre load

A

central venous pressure (CVP)
*pulmonary artery occlusion pressure (PAOP).

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67
Q

What increases after load

A

*raised aortic pressure
*aortic valve resistance (aortic stenosis)
*ventricular cavity size; increased ventricular volume; requires greater tension to contract (Laplace’s law)
*raised systemic vascular resistance (SVR), e.g. shock

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68
Q

Ficks law

A

Amount of substance taken up by an organ per unit time is equal to the blood flow multiplied by the difference in concentration of that substance between arterial and mixed venous blood.

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69
Q

Factors affecting systolic and diastolic

A

Systolic pressure increases when there is an increase in:
*stroke volume
*ejection velocity (without an increase in stroke volume)
*diastolic pressure of the preceding pulse
*arterial rigidity (arteriosclerosis).

Diastolic pressure increases when there is an increase in:
*total peripheral resistance
*arterial compliance (distensibility)
*heart rate.

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70
Q

When would CVP not reflect filling pressure of left heart

A

If disparity between right and left ventricles

Right infarction
PE
LV disease

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71
Q

PAOP

A

Estimates LA pressure
Can estimate CO from catheter

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72
Q

Problems with pulse oximetry

A

*irregular pulse: atrial fibrillation
*venous pulsation (tricuspid incompetence)
*hypotension
*vasoconstriction
*abnormal Hb (carboxy-), and methaemoglobin
*bilirubin
*methylene blue dye

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73
Q

Isoprenaline effects

A

B effects only

Vasodilation in skeletal muscle- reduce SVR
Tachycardia

Use in HB while awaiting pacemaker

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74
Q

Dobutamine effects

A

B1 and 2
Increased HR and contraction
Mild vasodilation

Cariogenic shock- with low dose dopamine

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75
Q

Dopamine effects

A

Low dose- dilates renal, cerebral, coronary, splanchnic - via D1+2
and B1 increases contractility and HR

High dose- a-vasoconstriciton

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76
Q

Dopexamine effects

A

B2 and D

mild-Inotrope, chronotrope
Peripheral vasodilator

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77
Q

Phosphodiesterase inhibitor

A

Decrease the rate of breakdown of cAMP by phosphodiesterase III.
Increased contractility with reduced PAOP and SVR

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78
Q

Auerbach and Meissners plexus location and function

A

Myenteric (auer) lies between circular and longitudinal - motor

Meissner- submucosa- sensory

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79
Q

Para vs symp effect on enteric system

A

Symp- vasoconstriction
Inhibit glandular secretion
Contract sphincters
Inhibits muscle- motility

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80
Q

What types of saliva is excreted from each gland

A

Parotid- watery- amylase and IgA
Submandibular- 70%, mucous
Sublingual- mucoproteins 5%

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81
Q

Formation of saliva

A

Isotonic fluid secreted by acinar component

As moves along duct- NaCl removed
K HCO3 added

During high rates of secretion- Na Cl HCO3 more concentrated

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82
Q

Factors preventing reflux

A

the right crus of the diaphragm compresses the oeso­phagus as it passes through the oesophageal hiatus
*the acute angle at which the oesophagus enters the stomach acts as a valve
*mucosal folds in the lower oesophagus act as a valve
*closure of the sphincter is under vagal control- physiological sphincter

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83
Q

Where cells are located in stomach

A

fundus and body: peptic and parietal cells predominate
*antrum and pylorus: parietal cells are less common; mucus and neuroendocrine (secreting gastrin) cells predominate
*cardia: gastric glands are composed almost completely of mucus cell

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84
Q

How HCl is pumped in/out of parietal cells

A

H+ ions are pumped from the cell by the H+/K+ ATPase system.
*Cl− ions are pumped from the cell by two routes: one is a chloride channel, the other is a Cl−/K+ co-transport system (K+ is thus cycled into the cell via the H+/K+ ATPase system and out via the Cl−/K+ system).

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85
Q

What protects gastric cells from digestion

A

Mucus secretion barrier over gastric epithelium
Alkaline

Tight epithelial junctions
prostaglandin E secretion has a protective role by increasing the thickness of the mucus layer, stimulating HCO3− production and increasing blood flow in the mucosa (bringing nutrients to any damaged areas).

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86
Q

Phases of gastric secretion

A

Cepahlic- 30%- sight and smell
VIa- Ach from Vagus
Gastrin from G cells
Histamine from mast cells- stimulate H2

Gastric- 60%- food entering
Ach

Intestinal- presence in duodenum-5%
Releases Gastrin

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87
Q

Other factors influencing gastric sectretion

A

*the secretion of gastrin is inhibited when the pH falls to around 2–3
*somatostatin secreted from neuroendocrine cells (D-cells) inhibits gastrin secretion
*secretin from the duodenal mucosa is released in response to acid in the duodenum; it inhibits gastrin release
*fatty food in the duodenum leads to the release of CCK and GIP; both inhibit gastrin secretion.

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88
Q

Factors determining food allowed into duodenum

A

-gastric volume:↑volume then more rapid emptying

*fatty food: CCK and GIP are released by the small intestine in response to fatty foods; they increase contractility of the pyloric sphincter

*proteins: proteins and amino acids stimulate gastrin release; gastrin increases contractility of the pyloric sphincter

*acid: acid entering the duodenum results in a vagally mediated delay in gastric emptying and also leads to secretin release. Secretin inhibits antral contractions and increases contractility in the pyloric sphincter. Secretin also stimulates HCO3− release from the pancreas to neutralize the acid

*hypertonic chyme: delays gastric emptying.

89
Q

Drugs that reduce acid secretion

A

H2 receptors- cimetidine- block H2 on parietal

PPI- block H/K
Activated in acidic pH

90
Q

3 types of mucosal protectants

A

*sucralfate: formed from sulphated sucrose and aluminium hydroxide, it polymerizes at pH < 4 to form a sticky layer that adheres to the base of the ulcer

*bismuth chelate: acts in a similar manner to sucralfate; in addition it has been shown to eradicate Helicobacter pylori

*misoprostol: a synthetic analogue of prostaglandin E2. This prostaglandin is thought to protect gastric mucosa by stimulating the secretion of mucus and bicarbonate, and increasing the mucosal blood flow.

91
Q

Examples of antacids

A

*sodium bicarbonate
*magnesium hydroxide and magnesium trisilicate
*aluminium hydroxide.

92
Q

Post gastrectomy syndrome

A

Iron- wrong state for absorption
B12

Billious vomittng
Dumping
Diarrhoea
Infection- reduced ability to destroy bacteria
Carcinoma

93
Q

Effects of vagotomy

A

*Reduced gastric acid secretion.
*Delayed gastric emptying.
*Failure of the pylorus to relax prior to gastric peristaltic wave.
*Reduced pancreatic exocrine secretions.
*Diarrhoea secondary to loss of vagal control of the small bowel.
*Increased risk of large bowel cancer due to excessive bile salts reaching the colon.

94
Q

What is contained in the crypts of Lieber­kuhn

A

*undifferentiated cells that constantly replace entero­cytes
*Goblet
*Paneth
*D-cells: produce somatostatin
*S-cells: produce secretin
*N-cells: produce neurotensin
*Enterochromaffin cells: produce 5-hydroxytryptamine.- serotonin

95
Q

Brunners gland

A

Only in duodenum

Secrete bicarbonate rich mucus

96
Q

Brush borders enzymes

A

*disaccharidases: maltase, sucrase
*peptidases
*phosphatases
*enteropeptidase or enterokinase (activates pancreatic trypsinogen)
*lactase (under 4 years).

97
Q

Absoption of monosaccharides

A

Glucose and galactose via Na dependent

Fructose independent

98
Q

Fat absorption

A

Coated in bile salts in duodenum - smaller droplets
Lipases- monoglycerides and FFA
These combine with bile salts to form micelles

Diffused into enterocyte- bile salts stay in lumen

SER- reforms Triglycerides- formed into chylomicrons- diffuse into lacteals - then return to venous

99
Q

How vitamins are absorbed

A

C- by Na dependent in jejunum
B12- IF- ileum
Remaining B diffuse freely

ADEK- micelles

100
Q

How is iron absorbed

A

Duodenum and jejenum in Fe2+ not 3+
Gastric acid responsible for converting
Absorbed by transferrin
Into by endocytosis then to plasma

101
Q

Movement in small bowel

A

Segmentation- circular muscle- circular movement of chyme

Peristalsis- propulsion triggered by distention- longitundinal muse

MMC- contraction across full length of small bowel, lasts several hours- move remaining food to colon

102
Q

Reflexes affecting intestinal contractility

A

*ileogastric reflex: distension of the ileum decreases gastric motility
*gastroileal reflex: increase in gastric secretion or contractility increases ileal motility.

103
Q

Effect of duodenal resection

A

Ulceration of small bowel- no Brunner gland
Malasorption- Fe, Ca, P
Dumping

104
Q

Effects of Terminal ileal resection

A

Decreased Bile salt reabsorption- more gallstones
Bile salts in colon- malignancy

B12 def
reduced water reabs- diarrhoea

105
Q

Fluid secretions of pancreas

A

Epithelial cells- HCO3 secreted in exchange for Cl
Na K exchanged for H formed by carbonic anhydrase

106
Q

What activates trypinogen

A

Enterokinase- secreted by duodenum

107
Q

What dose trypsin do

A

Activates other enzymes

*chymotrypsinogen: chymotrypsin (cleaves peptide bonds)
*proelastase: elastase (cleaves peptide bonds)
*trypsinogen: trypsin (cleaves peptide bonds)
*procarboxypeptidase: carboxypeptidase (cleaves peptides at the C-terminus).

108
Q

Action of amylase

A

starch digestion; it splits α-1,4-glycosidic bond

109
Q

Lipolytic enzymes examples and what activates them

A

Tyson actviates

Lipase- TG- to FFA and glycerol
Co lipase- binds lipase to lipids
Phospolipase- FFA from PL
Cholesterol esterase

110
Q

Regulation of pancreatic secretions

A

Cephalic- vagal
Gastric- vagal
Intestinal- CCK and secretin
CCk- release of fluid rich in enzymes from acing cells
Secretin- bicarb rich

Lipid and peptides- increase CCK
Acid- secretin

111
Q

% of bile acids reabsorbed and location

A

> 90% of secreted bile is absorbed in distal ileum

112
Q

Livers role in protein metabolism

A

gluconeogenesis- produce glucose form amino acids
Synthesises albumin, clotting factors
Handles degradation products such as ammonia- converted to urea

113
Q

Liver role in fat metabolism

A

Glucose is converted to FFAs; this is then transported to adipose tissue. It is then combined with glycerol and stored as triglycerides. During starvation these stores are released, providing fatty acids (provides energy as ATP for gluconeogenesis) and glycerol (acts as a non-carbohydrate substrate for gluconeogenesis)

*synthesizes lipoproteins and cholesterol

114
Q

Which substances does liver detoxify

A

*peptide hormones: insulin, Anti-Diuretic Hormone (ADH), growth hormone
*steroid hormones: testosterone, oestrogen, adrenal cortex hormones
*catecholamines
*drugs
*toxins.

Via-1- increasing water solubility via p450
2- reducing biological activity

115
Q

What does the liver store

A

Iron
Copper
Vit ADEK, B12
Glycogen
Fats

116
Q

Cells in hepatic sinusoids that phagocytose

A

Kupffer cells

117
Q

Biochem findings of prehepatic jaundice

A

*no bilirubin in the urine (unconjugated bilirubin is not water-soluble)
*↑urobilinogen in the urine (as a result of more bilirubin being broken down in the intestine)
*reticulocytosis: in response to the need to replace destroyed blood cells
*anaemia
*↑lactate dehydrogenase (LDH)
*↓haptoglobin: protein that binds free haemoglobin and transfers it to the liver.

118
Q

Cause of congenital hyperbilirubinaemia

A

unconjugated hyperbilirubinaemia:
*Gilbert’s syndrome: due to an abnormality in bilirubin uptake
*Crigler–Najjar syndrome: due to the absence of glucuronyl-transferase

conjugated hyperbilirubinaemia:
*Dubin–Johnson and Rotor’s syndrome: defects in the handling of bilirubin.

119
Q

Lab findings of hepatocellular jaundice

A

*liver enzymes, i.e. ↑ aspartate amino transferase (AST) and ↑ alanine amino transferase (ALT); this reflects liver damage and thus release of these enzy­mes from hepatocytes
*↑alkaline phosphatase: reflects the partial cholestasis
*abnormal clotting tests reflect the impaired hepatocyte function.

120
Q

Lab findings form cholestatic jaundice

A

*bilirubin in the urine (characteristic dark colouration); this occurs as the bilirubin is conjugated and thus water-soluble
*no urobilinogen in the urine; due to the obstruction, no bilirubin enters the bowel to be converted to urobilinogen
*↑canalicular enzymes: alkaline phosphatase and γ-Glutamyl Transferase (GT)
*↑liver enzymes ALT and AST;

121
Q

Control of bile release into duodenum

A

Sphincter of oddi

CCK- gallbladder to contract, reduce tone of oddi and pancreatic secretions

CCK release stimulated bu fats and acid in duodenum

Small amount of contraction due to vagus

122
Q

Aldosterone effect in colon

A

Na absorbed
Causing water absorption

123
Q

Use of colonic flora

A

Fermentation of indigestible carbs- producing fatty acids used by mucosa
Degredation fo blurbing to uro and sterco

Synthesis of vit K, B12, thiamin and riboflavin

124
Q

Enteroglucagon- released by and function

A

Released in response to glucose and dat in ileum and colon
Inhibits gastric and small bowel motility

125
Q

Use of copper and zinc

A

Copper- Synthesis of Hb and coenzyme in electron transport chain

Zinc- cofactor, synthesis of RNA, DNA

126
Q

Vitamin deficiencies

A

A- night blindness
D- rickets, osteomalacia
E- haemorrhage anaemia
K- clotting
B1-thiamine- beriberi
2- riboflavin- dermatitis
3- pellagra- dermatitis, diarrhoea, dementia
6- convulsions, anaemia, skin lesions- pyridoxine
9- folate- anaemia
B12- cobalamin- anaemia
C- scurvy

127
Q

Renal circulation

A

Renal artery- branches to interlobar artery between pyramids- form acuate- form interlobular - form afferent arterioles

Efferent arterioles -either form peritubular capillaries to renal tubules
Or descend as vasa recta- to medulla

128
Q

When does auto regulation of kidneys fail

A

Systolic <80

129
Q

Which hormones cause vasodilation of renal blood flow

A

Prostaglandin
NO

130
Q

Which hormones cause vasoconstriction of renal blood flow

A

Angiotenin 1+2
Noradrenaline
Adrenaline

131
Q

Features of endothelium and epithelium of Bowmans capsule allowing filtraitin

A

Ednothelium- fenestrated
Glycoproteins negative charge in BM- greater permeability of positive/neutral more than negative
Podocytes- do not form continuous layer

132
Q

Forces in Bowman capsule generating urine

A

Hydrostatic pressure- greater than normal capillaries of 50mmg
Since proteins not filtered- opposing osmotic pressure of 10

Net 40

133
Q

Area in kidney most prone to ischaemia

A

PCT as many ATP dependent pumps

134
Q

Descending loop is permeable to

A

NaCl and water
But due to high osmolality surrounding- water moves out

135
Q

Juxtaglomerular apparatus constituents and functions

A

JXG cells- specialised smooth muscle cells in afferent arteriole- secrete renin
- responds to decrease afferent pressure, stimulation by sympathetic nerves and macula densa

Macula densa- DCT- responded to reduction of Na

136
Q

Where is Ca and P absorbed and regulated in kidneys

A

Actively absorbed in PCT
Remaining in DCT
Regulation by PTH in DCT

137
Q

Management of acid base balance in kidneys

A

Majority of HCO3 absorbed in PCT

HCO3 +H is formed in tubular epithelium by CA after absorption of H2O and CO2
HCO3 absorbed and H+ secreted into lumen

138
Q

Urea absorption in kidneys

A

Waste product not actively reabsorbed
But as water moves out- conc increases so small is passively reabsorbed

139
Q

Criteria for substance to measure GFR

A

*must be filtered by the glomerulus
*must not be reabsorbed
*must not be secreted
*must not be metabolized

140
Q

Nervous control of micturition

A

Para- sacral outflow S2-4- innervate bladder, internal sphincter. Also run in pudendal nerve and control external sphincter

Symp- L1-2 -hypogastric plexus - inhibit detrusor and increase contraction of internal

141
Q

Bladder abnormalities from spinal cord injury

A

Reflex/autonomous Bladder – Spinal Cord Transection Above T12

In this case, the afferent signals from the bladder wall are unable to reach the brain, and the patient will have no awareness of bladder filling. There is also no descending control over the external urethral sphincter, and it is constantly relaxed.

There is a functioning spinal reflex-the bladder automatically empties as it fills – known as the reflex bladder.

Flaccid/atonic Bladder – Spinal Cord Transection Below T12

A spinal cord transection at this level will have damaged the parasympathetic outflow to the bladder. The detrusor muscle will be paralysed, unable to contract. The spinal reflex does not function.

In this scenario, the bladder will fill uncontrollably, becoming abnormally distended until overflow incontinence occurs.

142
Q

Hypothalamus location

A

Forebrain
Floor of third ventricle

143
Q

Pituitary gland tissue origin

A

Anterior- ectoderm in oral cavity - linked to hypothalamus via hypophyseal portal system

Posterior- continuous with hypothalamus

143
Q

Causes of SIADH

A

*tumours, e.g. lung, pancreas, lymphomas
*TB
*lung abscess
*CNS lesions, e.g. meningitis, abscess, head injury
*metabolic, e.g. alcohol withdrawal
*drugs, e.g. carbamazepine.

144
Q

Synthesis of thyroid hormones

A

*active pumping of iodide ions in from the extracellular space to the follicular epithelium
*iodide ions enter the colloid and are converted to iodine by TPO
*iodine is combined with tyrosine.
*Two forms are produced: monoiodotyrosine (1 MT) and diiodotyrosine (2 DT); these then combine to form the two thyroid hormones:
*triiodothyronine (T3): MT + DT
*thyroxine (T4): × 2 DT.
*More T4 is produced but T3 is more biologically active.
*Thyroid hormones are stored in the colloid of the follicle and released into the circulation as needed (the thyroglobulin is detached).

145
Q

How thyroid hormones cause effect

A

T3 and T4 cross the cell membrane via diffusion; most of the T4 is converted to T3 in the cell.
*Thyroid hormone then bonds to nuclear receptors and initiates increased DNA transcription and protein production.

146
Q

MOA of thioamides

A

Competitively inhibit TPO
Block coupling of iodotyrosine
PTU_ inhibits deionisation fo T4

147
Q

Effects fo thyroid hormones

A

Metabolic- increased
Increased catabolism of FA and protein
Increased absorption of glucose

Increase HR, PVR, CO

Increased GI motility

148
Q

Cause of secondary hyperthyroidism

A

Very rare
Pituitary tumour
Metastatic thyroid- well differentiated
Choriocarcinoma- usually HCG but can produce susbstances similar to TSH
Ovarian teratoma

149
Q

Lab results of sick euthyroid

A

TSH and T3/4 can both be abnormally low

150
Q

Cause of hypoparathyroidism

A

*congenital, e.g. DiGeorge syndrome
*autoimmune
*iatrogenic: following total thyroidectomy or parathyroidectomy
*hypomagnesaemia: low magnesium levels prevent the release of PTH.

151
Q

Cause of vit D def

A

*dietary insufficiency: particularly common in vegans
*lack of sunlight: common in elderly patients and Asian women
*malabsorption: particularly after gastric surgery, coeliac disease and disorders of bile salt production
*renal disease: leads to inadequate conversion to the active form 1,25-dihydroxycholecalciferol
*hepatic failure
*Vitamin-D-resistant rickets: a familial condition with hypophosphataemia, phosphaturia and rickets.

152
Q

Hypophosphataemia symptoms

A

*confusion
*convulsions
*muscle weakness: acute hypophosphataemia can lead to significant diaphragmatic weakness and delay weaning from a ventilator in patients in the intensive treatment unit
*left shift of oxyhaemoglobin curve: this results in decreased oxygen delivery to tissues and is due to the reduction in 2,3-DPG.

153
Q

Release of hormones in adrenal medulla

A

Nerve fibres from the splanchnic nerves innervate the medulla; these release acetylcholine, which stimulates hormone release.
- pre ganglionic - Ach
*The chromaffin cells release a variety of hormones when stimulated to do so; they are stored in granules and exit the cells into the circulation via exocytosis.
*The adrenal medulla produces:
*epinephrine (adrenaline)- made from tyrosine
*norepinephrine (noradrenaline)
*dopamine
*β-hydroxylase (enzyme involved in catecholamine synthesis)
*ATP
*opioid peptides (metenkephalin and leuenkephalin).

154
Q

Synthesis of steroids in adrenals

A

Cholesterol is converted to pregnenolone in mitochondria

Can go to progesterone- corticosterone- aldosterone

Or to progesteroneto 17a progesterone- cortisol

Or 17progester to Testosterone via 20 then to- oestradiol

155
Q

What is cortisol bound to in the blood

A

Transcortin 75%
Albumin 15%
Rest active or free

156
Q

Cortisol secretions is stimulated by

A

ACTH
Circadian rhymth- highest in the morning

*stress
*trauma
*burns
*infection
*exercise
*hypoglycaemia.

157
Q

Effects of cortisol

A

Metabolic- opposite to insulin- breakdown of protein, converted to glucose- stored as glycogen
Lipolysis

Euphoria

Anti-inflammatory - synthesis of lipocortin- inhibits phospholipase A2

158
Q

Secondary hyperaldosteronism causes

A

*renal artery stenosis
*congestive cardiac failure
*cirrhosis.

159
Q

Effects of excess aldosterone secretion

A

*Na+ and water retention, leading to ↑ blood pressure
*renal K+ loss, leading to hypokalaemia
*renal H+ loss, leading to metabolic alkalosis.

160
Q

congenital adrenal hyperplasia (CAH) most common cause and symptoms

A

The commonest defect affects the enzyme 21-hydroxylase.

decrease in cortisol secretion and as a result increases in ACTH secretion; this has the effect of driving the unused cortisol precursors into the androgenic hormone synthetic pathways.

*The clinical effects depend on the sex of the affected individual:
*male: there is rapid growth in childhood and early sexual development (precocious puberty); due to early fusion of the epiphysis, these patients are often shorter than average
*female: there is masculinization of the external genitalia with hypertrophy of the clitoris, a male body shape and hair distribution.

161
Q

Gigantism vs acromegaly

A

Gigantism- childhood- before epiphyseal fusion

Acromegaly- after

162
Q

GH metabolic effects

A

*↑glycogenolysis
*↓glucose uptake by cells
*promotes amino acid uptake into cells
*promotes protein synthesis
*↑lipolysis and release of free fatty acids (FFAs)
*↓LDL cholesterol.

163
Q

Sx of acromegaly

A

Prominent supra orbital ridges
Visual defects
Broad nose
Heart failure
High BP
Galactohoea
Carpal tunnel

164
Q

Insulin metabolic effects

A

Anabolic hormones

Promotes glucose uptake - except brain
Glycogen storage

Amino acid uptake
Protein synthesis

Inhibits lipolysis
Stimulates lipogenesis

165
Q

Stimulants of somatostatin

A

*↑ plasma glucose
*↑ plasma amino acids
*↑ plasma glycerol.

166
Q

Glucagon metabolic effects

A

Catabolic hormones

Increase glycogenolysis
Gluconeogenesis

Lipase- to increase FFA and glycerol

167
Q

Effects of somatostatin

A

*inhibits the release of insulin and glucagons
*↓ gastrointestinal motility, secretion and absorption.

168
Q

Other hormones effects on glucose regulation

A

GC-hypo- anti insulin
Promote lipolysis, gluconeo, glycogen

GH- fasting
Anti inuslin
Promote lipolysis, glucogenolysis

TH- low conc- anabolic
High- catabolic- hyperglycaemia

Catecholamines- when hypo
Glycogenolysis
Lipolysis

168
Q

Secondary Diabetes mellitus causes

A

pancreatic disease:
*pancreatitis
*pancreatic cancer
*pancreatectomy
*cystic fibrosis

antagonists to insulin:
*acromegaly (GH)
*Cushing’s syndrome (glucocorticoids)
*hyperthyroidism (thyroid hormone)
*phaeochromocytoma (catecholamines)
*glucagonoma (glucagon)

*drugs, e.g. corticosteroids, thiazide diuretics
*liver disease
*genetic syndromes, e.g. Down’s syndrome, Friedreich’s ataxia
*insulin receptor abnormalities, e.g. congenital lipodystrophy

169
Q

Pancreatic endocrine tumours

A

Insulinoma- B cell- whiles triad - 10% malignant

Gastrinoma- G cells- Malignant >50%

VIPoma- watery diarrhoea, low K, achlorhydria

Glucagonoma- a cell- 75% malignant- secondary diabetes mellitus; other symptoms include anaemia, weight loss and a characteristic rash called necrolytic migratory erythema

Somatostatinoma- d cells- diabetes, cholethiasis, steatorrhoea

170
Q

Metabolic changes following surgery

A

divided into two phases: the ebb phase and the flow phase:
*the ebb phase is the initial response to injury and is a phase of reduced energy expenditure and metabolic rate that lasts for approximately 24h

*the flow phase follows: this is a catabolic phase with increased metabolic rate, hyperglycaemia, negative nitrogen balance and increased O2 consumption. The flow phase has significant effects on the metabolism of carbohydrates, lipids and proteins:

*carbohydrates: hyperglycaemia- this is stimulated by catecholamines and glucocorticoids (insulin resistance prevents cell uptake). After 24h the glycogen is exhausted and the hyperglycaemia is maintained by gluconeogenesis

*lipids: lipolysis is stimulated by catecholamines, the sympathetic nervous system, cortisol and growth hormone.

*proteins: the demand for amino acids is met by skeletal muscle breakdown; the greater the insult, the greater the breakdown and nitrogen loss. The amino acids are used in gluconeogenesis and synthesis of acute phase proteins.

171
Q

Clinical changes post surgery

A

-hypovolaemia: this type of fluid loss is referred to as ‘third space’ loss; the vasodilatation and increased vascular permeability lead to fluid being sequestered in the interstitial space

*renal changes: following injury there is reduced excretion of free water and sodium; this continues for about 24h and is due to the release of aldosterone and ADH

*fever: injury (even in the absence of infection) is associated with a rise in temperature; this is due to changes in the thermoregulatory set point in the hypothalamus by IL-1

*haematological changes: there is a leukocytosis; albumin levels fall due to decreased production and loss into injured tissue. The coagulation system is activated. This is primarily to reduce bleeding after the injury; however, it leads to a state of hypercoagulability and an increased risk of deep vein thrombosis (DVT)

*electrolyte and acid–base changes: the electrolyte changes include ↓Na+ (due to dilution from retained water), ↑K+ (as a result of cell death and tissue injury), metabolic alkalosis (the absorption of Na+ stimulated by aldosterone leads to K+ and H+ excretion) and metabolic acidosis (this occurs with more severe injuries with hypotension, poor perfusion and consequent anaerobic metabolism).

-hyperglycaemia, lipolysis, ketones - form sympathetic innervation

  • increased resp drive - resp alkalosis
  • CO increases
172
Q

Insulin post surgery

A

Low in ebb phase
Increase in flow phase- but hyperglycaemia due to resistance

173
Q

Types of neurglial cells and function

A

Astrocytes- form BBB
Microglia- phagocytose
Oligodendrolgia- myelin in CNS

174
Q

Autoregulation of cerebral blood flow

A

Occurs between 60-160mmHg

Myogenic - When the blood pressure rises, the vessels constrict, thus decreasing flow; when the blood pressure falls, the cerebral vessels dilate in order to increase flow.

Metabolic- increased activity results in a decrease in PaO2 and increase in PaCO2 and H+, the changes resulting in local vasodilatation of cerebral blood vessels and thus increased perfusion.

Neural- some sympathetic vasoconstrictor and parasympathetic vasodilator innervation, but their effect is very weak

Local- Increases in PaCO2 are associated with an increase in CBF due to marked cerebral vasodilatation; however, just as hypercapnia results in vasodilatation, then a fall in PaCO2 (hypocapnia) results in cerebral vasoconstriction.
The effect of changes in PaO2 is not as marked; hypoxia has a significant effect only when it falls below 8 kPa.
Increases in PaO2 can cause mild cerebral vasoconstriction; indeed hyperbaric oxygen therapy can reduce CBF by 20–30%.

175
Q

Calculating CPP

A

DBP+1/3(systolic-diastolic) -ICP

176
Q

CSF function

A

Hydraulic cushion
Stable ionic environment

177
Q

Where CSF is reabsorbed

A

Arachnoid villi- which drain into venous sinuses

178
Q

Features of BBB

A

Lipid soluble molecules can pass freely

Rather than the freely permeable fenestrated capillaries found in other tissues, the cerebral capillaries have very tight cell-to-cell junctions in the endothelium. In addition, the end-feet of astrocytes cover the basement membrane.

the endothelium contains transport proteins (carriers) for nutrients such as sugars and amino acids
*certain proteins, e.g. insulin and albumin, may be transported by endocytosis and transcytosis

179
Q

Areas of BBB with fenestrated capillaries

A

third and fourth ventricles: allow drugs and noxious chemicals to trigger the chemoreceptor area in the floor of the fourth ventricle; this in turn triggers the vomiting centre. In addition angiotensin II passes to the vasomotor centre in this region to increase sympathetic outflow and causes vasoconstriction of peripheral vessels

*posterior lobe of pituitary: allows the release of oxytocin and antidiuretic hormone (ADH) into the circulation

*hypothalamus: this allows the release of releasing or inhibitory hormones into the portal–hypophyseal tract.

180
Q

Brainstem death tests

A

7 areas- all must be absent

1.No pupillary response to light, direct or consensual: this reflex involves cranial nerves II and III.

2.Absent corneal reflex – normally would result in blinking; this reflex involves cranial nerves V and VII.

3.No motor response in the cranial nerve distribution to stimuli in any somatic area, e.g. supraorbital or nailbed pressure leading to a grimace.

4.No gag reflex: back of the throat is stimulated with a catheter; this reflex tests cranial nerves IX and X.

5.No cough reflex: no response to bronchial stimulation with a suction catheter; this reflex tests cranial nerves IX and X.

6.No vestibulo-ocular reflex: head is flexed to 30° and 50mL of ice-cold water is injected over 1min into each external auditory meatus; there should be no eye movements; this reflex tests cranial nerves III, VI and VIII.

7.Apnoea test: the patient is preoxygenated with 100% O2 for 10min; PaCO2 is allowed to rise to 5 kPa (before testing); the patient is disconnected from the ventilator and O2 is insufflated at 6L/min; PaCO2 is allowed to rise to 6.5 kPa; there should be NO respiratory effort.

181
Q

Consequences of SOL

A

Raised ICP
Incracranial shift and herniation
Hydrocephalus- as will interrupt CSF flow

182
Q

Site specific brain herniation

A

*transtentorial: the lesion lies within one hemisphere; leads to herniation of the medial part of the temporal lobe over the tentorium cerebelli (uncal)

*tonsillar: caused by a lesion in the posterior fossa; the lowest part of the cerebellum pushes down into the foramen magnum and compresses the medulla

*subfalcial: caused by a lesion in one hemisphere; leads to the herniation of the cingulate gyrus under the falx cerebri

*diencephalic: generalized brain swelling; leads to the midbrain herniating through the tentorium; this is termed coning

183
Q

Systemic and clinical effects of raised ICP

A

*Cushing’s response: ↓ respiratory rate, bradycardia and hypertension
*neurogenic pulmonary oedema
*Cushing’s ulcers
*preterminal events include bilateral pupil constriction followed by dilation, tachycardia, ↓ respiratory rate, and hypotension.

*headache
*nausea and vomiting
*papilloedema
*decreased conscious level.

184
Q

Clinical manifestation of transtentorial hernia

A

*oculomotor nerve compression: ipsilateral pupil dilation (transtentorial)
*cerebral peduncles: contralateral hemiparesis (transtentorial)
*posterior cerebral artery: cortical blindness (transtentorial)
*cerebral aqueduct: hydrocephalus (transtentorial)

185
Q

Which hernia can cause compression in medulla resulting in death

A

Tonsillar

All can cause compression of midbrain resulting in death

186
Q

Changes in Na and K as action potential starts

A

The Na+ channel activates much faster than the K+ channel. This explains the rapid influx of Na+; the channel also closes much faster; the K+ channel remains open over a longer period than the Na+ channel and is responsible for repolarization as K+ is released and the membrane potential falls back to its negative value.

187
Q

Membrane potential valve

A

Resting -70mv
Depolarised- +50

188
Q

Determinants of conductions velocity

A

Axon diameter
Myelination

189
Q

Where are action potentials generated between myelin

A

Nodes of Ranvier

Causes AP to jump- saltatory conduction

190
Q

Types of nerve fibre, function, speed and diameter

A

Aα Motor proprioception 100m/s 15–20um
Aβ Touch and pressure 50 5–10
Aγ Muscle spindles 30 3–6
Aδ Pain, temperature and touch 20 2–5
B Autonomic 10 3
C Pain 1 0.5–1

191
Q

Synaptic transmission

A

*the action potential depolarizes the presynaptic membrane by opening voltage-gated Ca2+ channels
*Ca2+ enters the axon down an electrochemical and concentration gradient
*the increase in Ca2+ results in the vesicles fusing with the presynaptic membrane and releasing neurotransmitters into the synaptic cleft
*the neurotransmitters then bind with receptors on the post-synaptic membrane
*binding of neurotransmitters initiates secondary signals within the cell and opens ion channels, thus generating a depolarizing current
*the transmitter is released from the receptor and is broken down by specific breakdown pathways.

192
Q

Types of neurotransmitters, function and what they are broken down by and into

A

Ach- excitatory - broken down to acetate and choline by acetylcholinesterase

*amines: this group includes catecholamines (adrenaline, noradrenaline, and dopamine), 5-hydroxytryptamine (serotonin) and histamine. The catecholamines are formed from the amino acid tyrosine. Two enzymes degrade catecholamines: monoamine oxidase breaks down transmitter taken up by the presynaptic neuron; and catechol-O-methyl transferase breaks down catecholamines taken up by the postsynaptic neuron

Amino acids: several amino acids act as neurotransmitters; these include:
*glycine: inhibitory
*glutamate: excitatory or inhibitory (can be converted to GABA)
*aspartate: excitatory

Peptides: examples of peptide transmitters include:
*substance P: involved in the transmission of pain sensation
*endorphins: inhibit pain pathways

193
Q

Types of pain nerve fibres and function

A

*Aδ fibres: these are myelinated nerves; as a result, they have a high conduction speed and diameter. They are responsible for the sharp initial pain
*C fibres: these are unmyelinated nerves and thus have a smaller diameter and lower conduction velocity. They are responsible for the longer-lasting dull pain.

here they synapse in lamina I and III in the dorsal horn.

194
Q

Pain transmission

A

Transduction- involves the production of electrical impulses; following tissue damage there is the release of inflammatory substances, i.e. prostaglandins, histamine, serotonin, bradykinin and substance P.

Transmission- pain sensation is along Aδ and C fibres to the spinal cord; here they synapse in lamina I and III in the dorsal horn.

Modulation of pain involves the ‘gate control theory’- These include inhibitory inputs from the periaqueductal grey matter and nucleus raphe magnus (both releasing serotonin) and the locus coeruleus (releases noradrenaline). In addition there is the release of the naturally occurring enkephalins and endorphins.

195
Q

Connections and location of sympathetic NS

A

Pre- found in- in the thoracic and upper 2–3 lumbar segments of the spinal cord
*preganglionic neurons lie in the lateral horn of the spinal grey matter
*preganglionic axons leave via the ventral root of the spine to join the spinal nerve
*post-ganglionic neurons have their cell bodies either in the sympathetic chain or in a named plexus along the aorta, i.e. coeliac, superior and inferior mesenteric.

*Spinal nerves are connected to the sympathetic chain by two small branches: the lateral white ramus communicantes (myelinated), and the medial grey ramus communicantes (unmyelinated).

*The sympathetic innervation of the head and neck is via preganglionic neurons synapsing with post-ganglionic bodies within the sympathetic chain; the post-ganglionic neurons then leave via the grey rami communicantes to join the spinal nerve.

196
Q

Difference in connections of head vs abdo SNS

A

*The sympathetic innervation of the abdominal and pelvic organs differs from that of the head and neck. Preganglionic neurons pass straight through the sympathetic chain to their individual plexuses and synapse with post-ganglionic cell bodies within the plexus.

197
Q

Neurotransmitters of SNS

A
  • Pre are Ach
    *The neurotransmitter of the sympathetic nervous system is noradrenaline (except sweat glands; these are innervated by cholinergic fibres).
198
Q

Pre ganglion of PNS vs SNS

A

PNS pre ganglion longer
Cell bodies of post ganglion- lie closer to organ

199
Q

Composition of sarcomere

A

*the dark bands or A bands are composed of the thicker myosin filaments
*the light bands or I bands are composed of the thinner actin filaments
*the I band is divided by the Z line; the space between Z lines is called a sarcomere
*at the Z lines the membrane of the muscle cell (sarcolemma) forms narrow tubes that traverse the sarcomere; these are called the T-tubules

200
Q

Actin filament proteins

A

*actin: a thin contractile protein, arranged in a double-stranded helix
*tropomyosin: lies in the groove between the actin filaments
*troponin: lies at regular intervals along the filament, attached to both actin and tropomyosin; it also has binding sites for Ca2+ and is involved in the regulation of contraction. Troponin and tropomyosin block the myosin-binding site on actin.

201
Q

Types of skeletal muscle and properties

A

*type I or slow twitch: act as postural muscles, e.g. in the back; they are designed to perform slow, sustained contractions and resist fatigue well. They rely on aerobic metabolism and contain myoglobin

*type II or fast twitch:
*type IIa or fast oxidative fibres, e.g. calf muscles: they rely on aerobic metabolism and contain myoglobin; they have moderate resistance to fatigue
*type IIb or fast glycolytic fibres, e.g. extraocular muscle: do not contain myoglobin and thus appear white; they contain a large amount of glycogen and rely on anaerobic metabolism.

202
Q

Sliding filament hypothesis

A

*When ATP binds to the head section of myosin it dissociates from its binding site on the actin filament.
*The ATP is hydrolysed (by ATPase on head) and changes the angle of the myosin head (relative to its tail); as the ATP has been hydrolysed, the myosin is again able to bind to the actin filament.
*The release of phosphate from the myosin head restores the angle and moves the actin filament along the myosin filament; this is called the power stroke.
*ATP will bind to myosin and start the process again.
*Creatine phosphate is present in very high concentrations within muscle and provides sufficient energy reserves for the above processes to take place. The enzyme creatine kinase catalyses the transfer of the phosphate group from creatine phosphate to ADP, thus replenishing ATP stores.

203
Q

How Ca causes muscle contraction

A

Depolarization of the cell leads to the release of Ca2+ from the sarcoplasmic reticulum within the cell. The rise in Ca2+ activates contraction by binding to troponin on the thin filaments; this leads to a conformational change and removes troponin and tropomyosin from the myosin binding site on actin.
*As the cell repolarizes, the Ca2+ is actively pumped back into the sarcoplasmic reticulum.
*The Ca2+ is removed from the troponin and thus the troponin and tropomyosin block the myosin binding site.

204
Q

Muscle reflex pathway

A

*muscle spindle is stretched: this causes the receptor region to depolarize; this generates an action potential in the afferent nerve (Ia afferent)
*the afferent impulse enters the spinal cord via the dorsal horn and synapses with an α motor neuron that supplies the stretched muscle
*the action potential in the α motor neuron signals the muscle to contract to oppose the stretch
*the afferent impulse also synapses with inhibitory neurons that synapse with α motor neurons that supply antagonist muscles (reciprocal inhibition). This reduces resistance to contraction of the stretched muscle.

205
Q

Gamma reflex

A

After stretch

Intrafusal muscle fibres stretched- 1a efferent then type 2 slower- to provide proprioception info - causing a motor to contract

Gamma neurons to cause contractions of these fibres - causing stretching of mid portion that doesn’t have contractility- opening stretch Na channels- increasing resting potential- increasing likelihood of AP

206
Q

Golgi Tendon Organ Reflex

A

The reflex they are involved in is an inhibitory response. It involves:
*afferent impulse 1b - acting on interneuron- via glutamine
Interneuron via glycine acts on α motor neurons that supply the contracting muscle
*reduction in the level of active contraction
*the reflex is protective and limits muscle/tendon tension

207
Q

Withdrawal reflex

A
  • withdrawal to painful stimulant- detected by cutaneous afferent neuron
    *α motor neurons: this results in stimulation of flexors in the limb in which the painful stimulus was experienced, thus withdrawing the affected limb
    *inhibitory signals are passed to α motor neurons in the opposing extensor muscles
    *this pattern is reversed in the opposing limb: flexor muscles are inhibited and extensor muscles are stimulated; this is called the crossed extensor reflex
208
Q

Descending motor pathways

A

*corticobulbar tracts: supply the motor portions of the cranial nerves
*corticospinal tracts: supply the spinal motor neurons; they are concerned with voluntary movements.

209
Q

4 descending inputs from brainstem

A

Extrapyrimidal- involuntary control

1.The rubrospinal tract: originates in the red nucleus- cross over and primarily innervates distal limb muscles.- fine control in hands

2.The tectospinal tract: fibres arise in the superior colliculus of the midbrain; it receives inputs from the visual cortex and is believed to control reflex activity in response to visual stimuli.

3.The vestibulospinal tract: originates in the vestibular nuclei; it supplies muscles of the ipsilateral side of the body. It innervates muscles concerned with balance and posture in response to inputs from the vestibular apparatus.

4.The reticulospinal tract: fibres -The medial reticulospinal tract arises from the pons. It facilitates voluntary movements, and increases muscle tone.
The lateral reticulospinal tract arises from the medulla. It inhibits voluntary movements, and reduces muscle tone.

210
Q

Metaraminol MOA

A

a1 agonsit
Used for acute hypotension

211
Q

Which cells contribute the most to complement

A

Hepatocytes

212
Q

Where are paneth cells found

A

Crypt of Lieberkuhn

213
Q

Factors to increase flow rate

A

Short length, large diameter, low viscosity and high pressure

214
Q

Renal blood flow following obstruction in first few hours

A

Initial increase due to prostaglandin and vasodilators
Then decrease due to vasoconstriction

215
Q

Clearance calculation

A

U x V/P

urine conc x urine production /plasma conc

216
Q

JVP waves and relations

A

a- atrial contraction just before carotid pulse

x- rapid atrial filling

c- ventricles begin to contract- bulge tricuspid back

v- atrial filling

y- opening of tricuspid

eMRCS questions (45 decks)

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