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MRCOG Part 1 > Physiology > Flashcards

Physiology Flashcards

1
Q

Fluid balance

A

Total body volume = 42L (60% total body weight)
Blood volume = 5.6L (plasma + RBC)

Losses via lungs (400ml/day), skin (1L/day), faeces (100ml/day), urine (1.5L/day)

So maintenance fluid requirement 30ml/kg/day

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2
Q

Hormones regulating extracellular fluid volume

A

ADH directly

ANP (atrial natriuretic peptide) indirectly

Renin-angiotensin system - plasma osmolarity and indirectly blood volume via aldosterone

Minor regulators - glucocorticoids and catecholamines

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3
Q

Osmolarity vs osmolality

A

Osmolarity = number of osmoles of solution per litre of solution (Osm/L), measure of solute concentration

Osmolality = osmoles of solute per kg of solvent (Osm/kg)

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4
Q

Osmosis

A

= movement of water from low solute concentration to higher concentration via semi-permeable membrane

Opposed by hydrostatic power
1osmol/L depresses freezing point by 1.86degrees

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5
Q

Plasma osmolarity

A

= 300mOsm/L

Na+ = 140 (main contributor)
Cl- = 140
K+ = 4
Anion = 4
Glucose = 5
Urea = 5

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6
Q

Starling’s law of capillaries

A

Relating to fluid movement across the capillary membrane as a result of filtration

Starling’s forces show relationship between hydrostatic and oncotic pressures:
Oncotic - 26mmHg blood, 1mmHg interstitial
Hydrostatic - 35mmHg arterial, 16mmHg venous, 0 interstitial

Net filtration pressure NFP = pressure promoting filtration - pressure promoting reabsorption

so NFP arterial= (35+1) - (26+0) = 10mmHg
NFP venous = (16+1) - (16+0) = -9mmHg

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7
Q

Oedema

A

Increased fluid in interstitial space
Anasarca is generalised oedema with SC tissue swelling

Due to - increased hydrostatic pressure, reduced plasma oncotic pressure, lymphatic obstruction, sodium retention, inflammation

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8
Q

Acid-base balance and anion gap

A

Regulated by respiratory, kidneys, blood, bones, liver

Anion gap normally 8-16mEq/L.
= Na - (HCO3 + Cl)

Raised anion gap (more +ve)
- lactic acidosis (methanol, salicylate, paraldehyde)
- ketoacidosis
- hypoalbuminaemia

Reduced anion gap (less +ve)
- bromide
- myeloma

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9
Q

Henderson-Hasselbach equation

A

HA + H2O <-> A- + H3O+
H2O + CO2 <-> H+ + HCO3-

If H+ generated, reaction shifts to left. So generates CO2, consumes HCO3-.

If HCO3- lost, reaction shifts to right. So generates H+, consumes CO2.

Net gain in H+ is the same as a net loss in HCO3-

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10
Q

pH and compensation

A

Logarithmic relationship

pH = pK + log10[HCO3-]/[CO2]

Respiratory compensation
- only in metabolic disorders, instantaneous

Metabolic compensation
- via kidneys, slower
- for respiratory disorders or metabolic disorders not originating in kidneys

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11
Q

Normal arterial maternal/fetal blood values

A

Maternal arterial:
O2 sats >97%
pO2 100mmHg
pCO2 40mmHg/4kPa
Base excess -2 to 2
HCO3- 24mEq/L
pH 7.34-44
Hb 12gm/dL

Fetal
O2 sats venous 75%, arterial 25%
pO2 venous 35mmHg, artery 25mmHg
pCO2 8-10kPa
Base excess venous -1 to 9, artery -2.5 to 10
pH venous 7.17-7.48, arterial 7.05-7.38
Hb 18gm/dL

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12
Q

HCO3-

A

Alkaline
Manufactured in DCT and collecting duct (PCT is not involved in acid-base balance)

DCT cells produce CO2, which reacts with water to form carbonic acid (H2CO3) with carbonic anhydrase as catalyst
H2CO3 is unstable organic acid, so rapidly dissociates into H+ and HCO3-
CO2 + H2o -> H2CO3 -> H+ + HCO3-

HCO3- enters circulation, in urine is buffered by NH4+ (ammonium - increases during acidosis) and HPO4^2- (hydrogen phosphate)

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13
Q

Long-term acidosis effect on K+

A

H+ enters cell (as high extracellular concentration)
K+ driven out of cell to maintain electrical neutrality

-> hyperkalaemia

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14
Q

Base excess/deficit

A

= the amount of acid or alkali required to restore 1L of blood to a normal pH (7.4), at a pCO2 of 5.3kPa, and temp 37
Need serum bicarb concentration and pH values to calculate
Normal range -2 to 2 mEq/L

Negative BE = metabolic acidosis
Positive BE = metabolic alkalosis (excess, excess bicarb)

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15
Q

Acid-base changes in fetus

A

Cord compression -> respiratory acidosis

Placental insufficiency -> metabolic acidosis

Anaerobic metabolism (when O2 sats <25%) -> increased lactate -> acidosis

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16
Q

Electrolyte changes in pregnancy

A

Osmolarity decreases by 10mOsm/L (in response to progesterone)

HCO3- decreases in response to decreased CO2

Na+ decreases in response to fall in HCO3- and reset of plasma osmolarity

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17
Q

Calcium functions and distribution

A

Functions - bone formation, muscle contraction, enzyme co-factor, blood clotting (coag cascade), secondary messenger, stabilisation of membrane potentials

Required intake 1g/day, or 1.5g/day when pregnant

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18
Q

Calcium distribution in body

A

1kg total body calcium, 99% in skeleton
Extracellular (plasma) calcium is 45% ionised, 55% bound to plasma proteins, phosphate, bicarbonate
- in acidosis, increased ionised calcium

Plasma (extracellular) ionised Ca2+ 12,000x more concentrated than intracellular
Intracellular it is sequestrated out of cytosol and within endoplasmic reticulum and mitochondria, only released in certain circumstances or cell damage

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19
Q

Calcium modulation

A

Via PTH and PTHrP (parathyroid hormone related peptide), and calcitonin

Absorption from GI tract via
- active uptake - Na+/Ca2+ ATPase
- transcellular transport - calbindin
- endocytosis - Ca2+-calbindin complex via TRPV6 membrane Ca channel

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20
Q

Phosphate functions

A

Intracellular metabolism (ATP synthesis)
Phosphorylation of enzymes
Forms phospholipids in membranes

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21
Q

Parathyroid hormone

A

Peptide hormone - 84 amino acids, many isoforms
Acts on G-protein receptors
Half life in minutes, store supplies last 90 mins
Does not cross the placenta

INCREASES Ca
DECREASES phosphate
ANTAGONISES calcitonin

Acts on:
- Bone to increase resorption
- Kidney to increase absorption from DCT, decrease re-absorption from PCT, increase vitD production by increasing 1α-hydroxylase, and promoting calcitriol formation
- Gut to increase calcium and phosphate absorption

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22
Q

Calcitonin

A

Polypeptide, 32 amino acids
Produced by C cells (parafollicular) in thyroid
Secreted in response to high phosphate and calcium

Decreases circulating calcium by:
- preventing osteoclast action
- decreasing reabsorption of phosphate and calcium in PCT
- decreasing calcium absorption in GI tract

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23
Q

Phosphaturic hormone

A

Decreases phosphate in blood, increases phosphate in urine

Counteracts the actions of vitD
Predominantly made by osteoblasts

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24
Q

Vitamin D

A

Pro-hormone
In two forms - ergocalciferol (D2) and cholecalciferol (D3)

Made in skin, placenta, decidua

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25
Q

Calcitriol

A

= 1,25(OH)2D3
Active form of vitD
Short half life of 0.25days, its intermediate 25(OH)D3 is stored with half life 1.5months

Function
- controls osteoblast and osteoclast differentiation
- increases calcium uptake from GI tract
- increases calcium and phosphate reabsorption from kidneys
(- inhibits calcitonin, opposite effects)
- anti-tumour activity

Deficiencies cause secondary hyperparathyroidism (renal osteodystrophy), rickets, osteomalacia

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26
Q

Synthesis of calcitriol

A

7-dehydro-cholesterol (from skin) converted with UV light to vit D3 (cholecalciferol)

VitD3 in the liver is converted with 25-hydroxylase to 25(OH)D3

25(OH)D3 in the kidney is converted with 1α-hydroxylase to 1,25(OH2)D3 (calcitriol)

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27
Q

Primary hyperparathyroidism

A

Causes hypercalcaemia

Cause:
80% benign parathyroid adenoma
15% primary parathyroid hyperplasia
2% parathyroid carcinoma - can be part of autosomal dominant familial endocrinopathies eg MEN1, MEN2A, isolates familial hyperparathyroidism

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28
Q

Secondary hyperparathyroidism

A

In response to lower calcium

Causes:
- kidney disease
- decreased vitD
- decreased serum Ca

Results in renal osteodystrophy by increased Ca absorption from bones, reduced glomerular filtration rate by 50%

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29
Q

Pathological calcification

A

Abnormal deposition of Ca salts with smaller amounts of other mineral salts, common process

2 forms:
Dystrophic calcification - local deposition in dying tissues or areas of necrosis, despite normal serum levels and normal calcium metabolism
Metastatic calcification - deposition in normal tissues due to hypercalcaemia

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30
Q

Causes of hypercalcaemia

A
  1. Hyperparathyroidism
  2. Renal failure - accumulation of phosphate and reduced absorption of Ca, leading to secondary hyperPTH
  3. VitD disorders - eg sarcoidosis, VitD excess, Williams’ syndrome
  4. Destruction of bone - bone tumours, immobilisation, Paget’s disease (accelerated turnover)
  5. Drug induced - vitA intoxication, thiazide diuretics, lithium, oestrogens
  6. Endocrinopathies - thyrotoxicosis, phaeochromocytoma
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31
Q

Features of hypercalcaemia

A

STONES - renal
BONES - osteoporosis, osteomalacia, rickets, osteitis fibrosa
ABDOMINAL GROANS - constipation, vomiting, peptic ulcer, pancreatitis
PSYCHIC MOANS - depression, memory loss, psychoses, coma

Other - proximal muscle weakness, keratitis, conjunctivitis

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32
Q

Treatment of hypercalcaemia

A

Rehydration
Pamidronate disodium (bisphosphonate drug to inhibit osteoclastic bone resorption)
Calcitonin
Plicamycin

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33
Q

Hypocalcaemia causes

A

Vit D deficiency
Hypoparathyroidism (surgical/radiation, idiopathic, neonatal, familial, autoimmune (DiGeorge), deposition of metals)
Hypomagnesaemia
Acute pancreatitis
Citrated blood transfusion

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34
Q

Hypocalcaemia features

A

Perioral tingling
Paraesthesia
Tetany - Trousseau’s, Chvostek’s, carpopdeal spasm
Cardiac arrhythmias
ECG changes - prolonged QT, prolonged ST
Subcapsular cataract

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35
Q

Bone remodelling

A

Cycle takes 90-200 days
Turnover at bone surfaces - periosteal and endosteal
Peak bone density around age 25

OsteoBlasts BUILD - modulated by PTH, oestrogen, glucocorticoids, thyroid hormone

OsteoClasts CRUNCH - modulated by TNF, IL-1/IL-6, GM-CSF (not PTH receptors)

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36
Q

Biochemical markers of bone turnover

A

Aluminium phosphate
Type 1 collagen (urine)
Hydroxyproline (urine)
Pyridinolines (urine)
TRAP - tartrate-resistant acid phosphatase

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37
Q

Osteoporosis

A

Reduced bone mineral density and disruption of bone microarchitecture
More in women (50% in >50)

Causes:
- environmental - smoking, alcohol, malnutrition, immobilisation
- autoimmune - diabetes, coeliac
- drugs - immunosuppressive, steroids, PPIs
- endocrine - hyperthyroid, hyperPTH, hypogonadal, cushing’s, pregnancy, lactation, hyperprolactinaemia
- haematological - lymphoma, myeloma, sickle cells
- metabolic - haemochromotosis

So RFs are BMI <19, family history fractures, untreated premature menopause, chronic medical disorders, immobility

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38
Q

T score interpretation

A

BMD <1SD = normal
BMD 1-2.5SD = osteopenia
BMD >2.5SD = osteoporosis

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39
Q

Treatment of osteoporosis

A

1g Calcium
800IU VitD
Bisphosphonate - if >75 no need for DEXA, if 65-75 give if OP confirmed on DEXA, if <65 give if low BMD or high risk factors
HRT or raloxifene
Teriparatide (form of PTH for <65yo)
Strontium
Calcitonin
Calcitriol
Testosterone

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40
Q

Calcium in pregnancy

A

Hypocalcaemic state (though free ionised levels stable) caused by
- active transplacental transport of Ca to fetus
- increased renal loss of Ca (increased GFR)
- decreased serum albumin

Associated increased calcitriol, increased PTH, increased calcitonin

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41
Q

Fetal calcium

A

Hypercalcaemic compared to mother (1.4:1)
Ca and phosphate actively transported across placenta
Ossification occurs in 3rd trimester
PTH produced from 12 weeks

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42
Q

Cardiac anatomy

A

Approx fist sized
3 layers - epicardium (part of pericardium), myocardium and inner endocardium

Tricuspid - between RA and RV
Pulmonary - between RV and pulmonary trunk, semilunar
Mitral valve - between LA and LV, bicuspid
Aortic - between LV and aorta, semilunar

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43
Q

Cardiac cycle

A

Electrical impulses SAN -> AVN -> Bundle of His -> Purkinje fibres

Phases 0.8s total:
0.4s relaxation
0.1s ventricular filling
0.3s ventricular contraction

P wave - atrial depolarisation
PR - time between atrial depolarisation and ventricular depolarisation, 0.1-0.2s
QRS - ventricular depolarisation, 0.12s
ST - time between ventricular depolarisation and repolarisation
T wave - ventricular repolarisation

1st heart sound - AV valve closure (tricuspid and mitral)
2nd - semilunar valve closure (pulmonary and aortic)
3rd heart sound common in pregnancy and young adults due to rapid ventricular filling

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44
Q

Causes of change to QT interval

A

Normally 0.3-0.4s

Increased QT - hypokalaemia, hypocalcaemia, quinidine

Decreased QT - hyperkalaemia, hypercalcaemia, digoxin

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45
Q

Pressures in cardiac chambers

A

RA - 1-7mmHg
LA - 10-15mmHg

RV - 35mmHg systolic, 4mmHg diastolic
LV - 140mmHg systolic, 10mmHg diastolic

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46
Q

Stroke volume

A

Volume ejected by ventricles during systole

SV (80ml) = end systolic volume (120ml) - end diastolic volume (40ml)

Ejection fraction 0.67, EF = SV/ESV

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47
Q

Cardiac output

A

CO = SV x HR

Resting 5.5L/min male, 4.5L/min female

Cardiac index = CO/body surface area = 3.2L/min/m^2

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48
Q

Starling’s law

A

Force of contraction is proportional to fibre length
Fibre length is proportional to stretch of ventricular muscle (dilatation)
Ventricular dilatation is proportional to venous return

Venous return (pre-load) depends on - intrathoracic pressure, total blood volume, gravity, calf muscle action, venous tone

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49
Q

Baroreceptors

A

For cardiac autonomic control
INHIBITORY

Carotid sinus - at bifurcation of common carotids, innervated by glossopharyngeal
Aortic body - at aortic arch, sensitive to partial pressure of O2/CO2 and pH
Floor of 4th ventricle - sensitive to CSF pressure, Cushing’s reflex means raised CSF pressure leads to raised BP

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50
Q

Chemoreceptors

A

For cardiac autonomic control

Carotid body - at bifurcation of carotid artery, sensitive to pO2, pCO2 and pH
Central chemoreceptor - sensitive to CO2

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51
Q

Blood vessel walls

A

Tunica interna
Tunica media - thickest layer in artery, smooth muscle
Tunica externa - thickest layer in vein

Capillaries just single layer of tunica interna

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52
Q

Blood pressure

A

BP = systemic vascular resistance x CO

Depends on blood volume, viscosity, elasticity of vessel walls, length and diameter of blood vessels, hormones (ADH, ACE, Adrenaline)

SVR depends on neurogenic, metabolic, endocrine

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53
Q

Mean arterial pressure

A

MAP = diastolic pressure + 1/3x(systolic - diastolic)

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54
Q

Blood flow

A

Poiseuille’s law - resistance is proportional to length of tube, inversely proportional to radius of tube
Proportional to pressure, radius, 1/viscosity, 1/length

Viscosity increases when haematocrit >45%

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55
Q

Blood components

A

55% plasma

45% blood cells (from stem cells by haemopoiesis)
- erythrocytes - biconcave discs, 8mm diameter, no nucleus, containing Hb with lifespan 120 days
- leukocytes - 1%, contain nuclei
- thrombocytes - release serotonin causing vasoconstriction, forms platelet plug

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56
Q

Blood groups

A

Based on presence/absence of inherited antigens on surface of RBCs

ABO
- O - no antigens, a/b antibodies in plasma, only O can donate to
- A - a antigens, b antibodies in plasma, A or O can donate
- B - b antigens, a antibodies in plasma, B or O can donate
- AB - a/b antigens, no antibodies, any can donate

Rhesus
- 80% of caucasians Rh+

Also Kell and Lewis systems

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56
Q

Cardiac output changes in pregnancy

A

CO rises by 40% from 4.5 to 6L/min. Plateaus at 24-30weeks, then further rise by 2L/min in labour.

HR rises by 20%
SV rises by 30%
Peripheral vascular resistance decreases by 5%
BP decreases by 10%
Vasodilation due to progesterone

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57
Q

ECG changes in pregnancy

A

LV hypertrophy and dilatation
Apex shifted anteriorly and to left
LAD 15 degrees
Inverted T waves lead 3
Q wave in lead 3 and aVF
Non-specific ST changes

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58
Q

Haematological changes in pregnancy

A

Plasma volume rises by 50%, from 2600 to 3800ml, plateaus at 32weeks
Total volume of RBCs rises by 18% - so haemodilution, physiological anaemia with HCT decrease
Leukocytes increase, clotting factors increase

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59
Q

Endothelial changes in pregnancy

A

Vasodilatation due to increased nitric oxide, decreased asymmetrical dimethylarginine, increased PGI2 (prostacyclin)
Pro-coagulant state

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60
Q

Pharynx

A

130mm length total

Nasopharynx - contains eustachian tube opening and pharyngeal tonsils (adenoids)

Oropharynx - separated from oral cavity by uvula and pillars of fauces (anterior fold palatoglossal arch, posterior fold palatopharyngeal arch), contains palatine tonsils

Laryngopharynx

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61
Q

Larynx

A

aka voice box

4 cartilages:
- epiglottis
- thyroid cartilage
- cricoid cartilage
- arytenoid cartilage

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62
Q

Trachea and bronchi

A

Trachea
120mm length
16-20 incomplete cartilage rings

Bronchi
Bifurcation at carina - right bronchus more acute for 3 lobes
Incomplete cartilage rings

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63
Q

Muscles of ventilation

A

Diaphragm
Intercostals (11 pairs)
Accessory muscles (sternocleidomastoid, platysma, scalene)

Supplied by phrenic nerve from C3-5

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63
Q

Pulmonary vascular resistance

A

PVR depends on:
- lung volume - when small, PVR high. Initial increase then PVR falls, but further increase then PVR rises exponentially.
- pulmonary vascular tone via NO action
- hypoxia, leads to pulmonary vasoconstriction
- pulmonary artery and venous pressure

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64
Q

Respiration

A

Physiological respiration
- ventilation - movement of air in and out of lungs as a result of pressure difference
- pulmonary gas exchange
- gas transport
- peripheral gas exchange

Cellular respiration (to obtain energy)
- metabolic process, O2 + glucose -> CO2 + H2o + ATP

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65
Q

Ventilation

A

Inspiration - active (based on Boyle’s law)
Expiration - passive

Affected by airway compliance and resistance

Minute ventilation = tidal volume x RR, = the total volume of gas entering lung per minute

Alveolar ventilation = (TV - dead space volume) x RR, = 4.2L/min, the volume of gas that reaches the alveoli

Dead space ventilation = the volume of gas per min that remains in airways, not involved in gas exchange

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66
Q

Control of ventilation

A

Nervous control - resp centre in brainstem
Chemical control - medulla oblongata centrally, aortic and carotid bodies peripherally
Bezold-Jarisch reflex - causes hypopnoea and bradycardia, due to increase in parasympathetic activity, caused by veratrum alkaloids, nicotine and antihistamines
J-receptors (proprioceptors) - in lung innervated by vagus nerve, stimulation causes increase in breathing

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66
Q

Intrapleural pressure

A

Prevents tendency of lung to collapse due to elastic recoil

Resting IP = -5cmH2O

Falls during inspiration, becomes positive during forced expiration (can get up to +30)

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66
Q

Gaseous exchange

A

Fick’s law describes diffusion - resp surfaces must have large surface area, thin permeable surface, moist exchange surface

Affected by:
- temperature (high temp - increased velocity - increased pressure)
- composition
- diffusion gradient

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67
Q

Lung compliance changes

A

= 200mL/cmH2O, = change in lung volume per unit change in pressure
Laplace’s law - transpulmonary pressure is proportional to wall tension, and inversely proportional to radius.

Surfactant secreted by type 2 pneumocytes, composed of dipalmitylphosphatidylcholine and cholesterol, to reduce wall tension and thus compliance

Elastance = 1/compliance (elastic recoil of lung)

Increased in
- obstructive lung disease (asthma, COPD, CF)
- expiration
- old age
Decreased in
- restrictive lung disease (interstitial lung disease, scoliosis, neuromuscular disorders)

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68
Q

Airway resistance

A

Poiseuille’s law
- resistance proportional to length of tube
- inversely proportional to radius of tube

Diameter of airways influenced by respiratory secretions, lung volumes, smooth muscles of respiratory tree

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69
Q

Lung volumes

A

Vital capacity - inspiratory reserve + tidal volume + expiratory reserve
Residual volume - volume that remains in lungs following maximal expiration
Inspiratory reserve volume - volume that can be inspired above the tidal volume
Total lung volume = VC +RV
Inspiratory capacity = TV + IRV

Functional residual capacity = volume left in the lung at the end of quiet respiration (RV +ERV)
- increased in obstructive lung disease, CPAP
- decreased in restrictive lung disease, pregnancy, anaesthesia

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70
Q

Spirometry

A

FVC = total amount of air that can be forcibly exhaled after inspiration
FEV1 = forced expiratory volume in 1s
FEV1/FVC = 75-80%

Peak expiratory flow rate around 600ml/breath

OBSTRUCTIVE PATTERN
- total lung volume increase
- FRC increase
- RV increase
- PEFR decrease
- reduced FEV1/FVC

RESTRICTIVE PATTERN
- all lung volumes reduced
- FEV1/FVC increased or normal

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71
Q

Dead space in respiration

A

Volume of inspired air that is not involved in gas exchange

3 types:
- anatomical - approx = body weight in lbs
- alveolar - ventilated but not perfused
- physiological (= anatomical + alveolar, 2-3mL/kg)

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72
Q

Respiratory changes in pregnancy

A

Due to progesterone:
Tidal volume increase by 30-40%, so resp minute volume increases, so oxygen consumption rises, pO2 up to 14kPa, pCO2 down to 30mmHg
Exp reserve decreases
Total lung volume decreases but vital capacity unchanged

Anatomically - bronchiole relaxation, decreased airway resistance
Mechanically - increased O2 demand, more diaphragmatic than thoracic breathing

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73
Q

Maternal and fetal oxygen transport

A

Cyanosis when deoxyhaemoglobin >5g/dL
Decrease in O2 sats by 1% causes increase in ventilation by 600ml/min
Haematocrit of venous blood is 3% higher than that of arterial blood

Carbon monoxide 240 times more affinity for haemoglobin than oxygen

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74
Q

Oxygen dissociation curve

A

Sigmoid shape, with plateau at pO2>60mmHg

P50 = the pO2 in blood where Hb is 50% saturated, 26.6mmHg

LEFT SHIFT - higher affinity for O2, decreased unloading, decrease in P50
- carbon monoxide
- fetal Hb
- decreased 2,3-DPG

RIGHT SHIFT - decreased affinity for O2, increased unloading, increase in P50, so higher pressures are required to maintain sats
- hyperthermia
- acidosis
- hypercapnia

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75
Q

Bohr effect

A

In the presence of CO2, the O2 affinity for dissociation of respiratory pigment decreases
So oxyhaemoglobin dissociation curve to the right when the pH is low, even with a relatively high PO2

+ Haldane effect - deoxygenation of blood increases its ability to carry CO2

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76
Q

CO2 transport

A

3 forms:
Solution - 10% - CO2 is 24x more water soluble than O2
Carbamino compounds - 30%
Hydration - 60% - CO2 + H2O -> H2CO3 -> H+ + HCO3- in RBCs
(RBCs have carbonic anhydrase, plasma does not)

In Cl- shift, HCO3- leaves RBCs and moves into plasma, Cl- moves into RBCs to maintain electrical neutrality

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77
Q

2,3-DPG changes

A

Product of glycolysis

Increases in
- exercise
- high altitude
- elevated androgens
- elevated thyroxine
- elevated growth hormone
SO CAUSES RIGHT SHIFT

Decreases in
- acidosis
SO LEANS TO LEFT SHIFT

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78
Q

Teeth and salivary glands

A

Deciduous milk teeth - 20, from 6 months
Permanent teeth - 32, from 6 years

Salivary glands
- parotid - duct opens at 2nd upper molar
- submandibular - ducts open on either side of tongue frenulum
- sublingual - ducts on floor of mouth
1.5L saliva produced per day
Contains amylase

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79
Q

Layers of digestive tract and gastric secretions

A

Mucosa
Submucosa - has blood vessels, nerves, lymph, and submucosal plexus. Responsible for secretions.
Muscular layer - has mesenteric plexus
Serosa - continuation of peritoneum

Gastric secretions - 3L produced per day
- HCl (pH 1.5-3.5)
- pepsinogen
- intrinsic factor (for B12 absorption)

80
Q

3 phases of digestion

A

Cephalic - saliva containing amylase, 1.5L/day

Gastric - gastrin secreted, continues until stomach emptied and pH 1.5
- takes 2-6 hours, protein stays the longest

Intestinal
- gastric inhibitory peptide (GIP) inhibits gastric motility and secretion
- secretin inhibits gastric secretion
- cholecystokinin (CCK) inhibits gastric emptying
- emptying takes 3-5 hours, making chyme (digested food)

81
Q

Small intestine

A

pH 7.5
Microvilli brush border
3L intestinal secretions per day
Peristalsis and segmentation to move food

Ileum is only site of absorption of B12 and bile salts, critical in fluid and Na conservation. Motility 3x slower than jejunum. So in resection, loss of bile salts, reduced water and salt absorption, diarrhoea, increased transit time, short gut syndrome, renal calculi.

Jejunum contents are isotonic

82
Q

Large intestine

A

Mucus secreting, no enzymes
Commensal bacteria produce some vitBs, vitK
90% efficiency of salt and water absorption
Transit time 24-150hours

Flatus = hydrogen, methane, CO2

83
Q

Bile

A

1L produced per day
Alkaline
Contains bile salts, bile pigments, cholesterol

Bile salts = bile acids (cholic acid and chenodeoxycholic acid) conjugated to glycine or taurine for absorption of fat and fat-soluble vitamins

84
Q

Bilirubin

A

Is a bile salt!
Product of Hb breakdown
Lipophilic
Converted to stercobilin (excreted in faeces) and urobilinogen (excreted in urine)

Physiological jaundice common at day 3-7 of life, due to immature liver enzymes and haemolysis of fetal RBCs
- can cause kernicterus (deposition of bilirubin in basal ganglia)

85
Q

Pancreatic juices

A

1.5L produced per day
Alkaline

Contains:
- water
- sodium chloride
- sodium bicarbonate
- enzymes (trypsinogen, chymotrypsinogen, proelastase, amylase, lipase)

86
Q

Recommended nutrition intake

A

2200kcal/day non-pregnant
2400kcal/day pregnant
2800kcal/day lactating

400g carb
100g fat
Protein - 1.5g/kg body weight/day non-pregnant, 2g when pregnant
6g salt
400microgram folic acid
2.8mg/day iron non-pregnant, or 6mg/day pregnant

87
Q

Iron deficiency anaemia

A

When iron <12micromol/L
TIBC saturation <15%
Microcytic
Microchromic

Total body iron = 40mg/kg body weight

88
Q

Recommended vitamin intake (in microgram/day)

A

ADEK are fat soluble

A - retinol - 800
B1 - thiamine - 1000
B2 - riboflavin - 1500
B3 - niacin - 15000
B6 - pyridoxine - 2000
B12 - cobalamin - 2
C - ascorbic acid - 30000
D - calciferol - 10
E - tocopherol - 10000

89
Q

Recommended mineral intake (in micrograms/day)

A

Ca - 800
Iron - 12
Na - 3000
Cl - 3500
K - 1000
Iodide - 0.1
Zinc - 150
Mg - 300

90
Q

Vitamin A

A

Retinol, active form is retinoic acid

Deficiency - keratomalacia, night blindness
Toxicity - hypervitaminosis A

91
Q

Vitamin B1

A

Thiamine

Deficiency - beribero, Wernicke-Korsakoff syndrome
No known toxicity

92
Q

Vitamin B2

A

Riboflavin

Deficiency - Ariboflavinosis
No known toxicity

93
Q

Vitamin B3

A

Niacin

Deficiency - pellagra
Toxicity - liver damage

94
Q

Vitamin B5

A

Pantothenic acid

Deficiency - paraesthesia
No known toxicity

95
Q

Vitamin B6

A

Pyridoxine

Deficiency - microcytic anaemia, peripheral neuropathy
Toxicity - impaired proprioception

96
Q

Vitamin B7

A

Biotin

Deficiency - dermatitis, enteritis
No known toxicity

97
Q

Vitamin B9

A

Folic acid

Deficiency - macrocytic anaemia
No known toxicity

98
Q

Vitamin B12

A

Cobalamin

Deficiency - megaloblastic anaemia
No known toxicity

99
Q

Vitamin C

A

Ascorbic acid

Deficiency - scurvy
Toxicity - vitC megadosage

100
Q

Vitamin D

A

Calciferol

Deficiency - rickets, osteomalacia
Toxicity - hypervitaminosis vit D

101
Q

Vitamin E

A

Tocopherol

Deficiency - haemolytic anaemia in newborns
Toxicity - haemorrhage/anti-coagulant

102
Q

Vitamin K

A

Phylloquinone

Deficiency - bleeding diathesis (hypocoag)
No known toxicity

103
Q

Formation of urine

A
  • Glomerular filtration
  • Selective tubular reabsorption
  • Tubular secretion (H+ and K+)

GLOMERULUS - mass of capillaries in Bowman’s capsule, containing afferent and smaller efferent arterioles
PCT - reabsorbs water passively and solutes actively, 80% filtrate reabsorbed here, inc glucose when in physiological range. Renal threshold reduced in pregnancy
LOOP OF HENLE - to concentrate urine, solute reabsorption at ascending loop (impermeable to water), water reabsorption at descending loop
DCT - influenced by ADH and aldosterone, only 5% filtrates reach here, mostly for water absorption

104
Q

Juxtaglomerular apparatus

A

Ascending loop of Henle - macula densa - measures Na concentration
Afferent arteriole - juxtaglomerular cells - modified endothelial cells are pressure sensitive

105
Q

Synthetic functions of kidney

A

Glucose
EPO
Vitamin D: 25(OH)D3 is converted with 1α-hydroxylase to 1,25(OH2)D3 (calcitriol)

106
Q

Structure of ureters and bladder

A

3 layers of ureter: outer fibrous, middle muscular, inner transitional epithelium

Bladder is 4 layers (mucosa, inner longitudinal, circular, outer longitudinal muscles) is stimulated at 300ml volume, capacity 500ml
Nerve supply via Lee-Frankenhauser plexus

107
Q

Micturition

A

Under voluntary control - mediated by pontine reticular formation in cerebellum
Bladder contractility from sacral spinal reflex
Urethral function by pudendal nerve

STORAGE - as bladder fills, bladder wall receptor -> pelvic splanchnic nerve -> sacral root S2-4 -> lateral spinothalamic tract -> higher centres
INITIATION - relaxation of pelvic floor and suppression of descending inhibitory impulses via parasympathetic system (M2 and M3 muscarinic receptors in bladder)
VOIDING - when the rising intravesical and falling urethral pressures equalise

(descending inhibitory reflexes via sympathetic NS - alpha receptors in bladder neck and urethra to increase outlet resistance, beta receptors on detrusor muscle to cause relaxation)

108
Q

Normal urodynamic values

A

Residual <50ml
1st sensation 200ml
Voiding volume 400ml
Capacity 600ml

Flow rate >15ml/s

Pressures:
- negligible rise in detrusor pressure on filling (<15cmH2O)
- maximum voiding detrusor pressure <50cmH2O
- intraurethral at rest (contracted sphincter) 50-100
- no systolic detrusor pressure during filling

109
Q

Urinary system changes during pregnancy

A

Increased uterus size -> nocturia, frequency
Lower renal threshold -> glycosuria
Renal hypertrophy -> increased renal size (no hyperplasia)

Mild renal pelvis and ureteric dilatation due to progesterone and obstruction from uterus
Increased renal blood flow
Increased GFR
Decreased filtration fraction

Urine output increases for 7 days post partum

110
Q
A
110
Q

Renal metabolic changes in pregnancy

A

Decreased HCO3- (decreased CO2)
Decreased Na
Decreased osmolarity (progesterone)
Decreased urea
Decreased creatinine (frmo 73 to 47)

111
Q

Folliculogenesis

A

Growth and development of follicle, in two main phases:
Pre-antral - independent of FSH
Antral (Graafian) - dependent on FSH
Lasts 375 days - 13 menstrual cycles

Based on 2-cell 2-gonadotrophin hypothesis for oestrogen production
- in response to LH, thecal tissues produce androgens, which are then converted to oestrogen in granulosa cells via FSH-induced aromatisation
- FSH for early folliculogenesis
- LH for final stages of follicle maturation and growth of dominant follicles

Primordial -> primary -> secondary -> graafian -> dominant

112
Q

Theca cells

A

Secrete androgens and progesterone
Do NOT secrete testosterone as lack 17beta-HSD
Only have LH receptors

113
Q

Granulosa cells

A

Secrete oestrogen and progesterone
(androgens converted to oestrogen via FSH)
P450 aromatase
Have LH and FSH receptors

114
Q

Primordial follicles

A

Primary oocyte surrounded by a single layer of granulosa cells and basal lamina
Formed at 6 months gestation (5-7million), down to 2million by birth, 300-500,000 by puberty

114
Q

Primary follicle

A

When granulosa cells in the primordial follicle change from flat to cuboidal -> zona pellucida forms around the ovum
FSH receptors develop
Independent of gonadotrophin stimulation

115
Q

Secondary follicle

A

When primary follicle attains second layer of granulosa cells, by recruited theca cells (theca interna and externa)
With capillary network between theca layers
At day 5 of cycle
Follicle mitotic activity high

115
Q

Graafian follicle

A

aka tertiary/antral follicle
Marked by formation of fluid-filled cavity between granulosa cells
Corona radiata = granulosa cells immediately surrounding the ovum
Dependent on FSH
Grows to >1cm
Secretes oestrogen

115
Q

Pre-antral follicle

A

Secondary follicle in late stage of development

Contains:
Oocyte
Zona pellucida
9 layers of granulosa cells
Basal lamina
Theca interna
Capillary network
Theca externa

116
Q

Preovulatory follicle

A

Graafian follicle in late stages of development
5-7 preovulatory follicles enter menstrual cycle and compete to become the dominant follicle
Follicles with low FSH receptors will stop developing and undergo atresia, leaving one dominant follicle to undergo ovulation

117
Q

Oogenesis

A

Process to form mature ova, from primordial germ cell -> oogonium -> primary oocyte -> secondary oocyte -> ovum:
Oocytogenesis
Ootidogenesis
Maturation

118
Q

Primordial germ cells -> oocyte

A

Primordial germ cells migrate from yolk sac to ovaries, mature to oogonia

Oogonia are diploid (46 chromosomes) then divide by mitosis to form primary oocyte at 3rd month gestation

119
Q

Primary -> secondary oocyte

A

Primary oocyte is diploid 46 chromosomes, then undergoes meiosis 1 at 5th month gestation, arrests at prophase 1 and is not completed until ovulation (dictyate = resting phase)

At ovulation, completes meiosis 1 -> secondary oocyte and 1st polar body

Secondary oocyte is haploid 23 chromosomes
- primitive ovum, surrounded by secondary follicle
- enters meiosis 2, arrests at metaphase 2 and then is not completed until fertilisation occurs

At fertilisation, completes meiosis 2 -> ovum and 2nd polar body

120
Q

Menstrual cycle

A

= proliferation and shedding of functional layer of endometrium

Menstruation day 1-5 - due to withdrawal of progesterone, usual loss 50-150ml
- oestrogen + progesterone low, so GnRH increase -> FSH increase -> stimulates secondary follicle to secrete oestrogen

Proliferation day 6-15 = follicular phase, influenced by oestrogen from Graafian follicle (oestrogen inhibits release of FSH and stimulates LH, so ovulation)

Secretion day 16-28 = luteal phase, influenced by corpus luteum secreting progesterone, which decreases LH levels

121
Q

Hormone levels in menstrual cycle

A

FSH - low at beginning, rises in response to GnRH, then inhibited by oestrogen for ovulation, low by the end

LH - rises through follicular phase (GnRH), mid-cycle surge (oestrogen) then rapid decline (progesterone)

Oestradiol rises up to mid-cycle, falls, then peaks in luteal phase

Progesterone starts low then has one peak in luteal phase

122
Q

Ovulation

A

When ovarian follicle ruptures and releases ovum
Defines transition from follicular to luteal phase
18 hours after peak LH
Ruptured follicle becomes corpus luteum - produces oestrogen and progesterone, has LH receptors

  • Mittelschmerz (mid-cycle pain)
  • fluid in POD
123
Q

Corpus luteum in fertilisation / not

A

FERTILISATION
corpus luteum degenerates only when placenta takes over function (between 3-6 months)

NO FERTILISATION
corpus luteum decays after 14 days to become corpus albicans (mass of fibrous scar tissue) and start menstruation

124
Q

Menarche

A

Age 10-16, average 12.8 Western 12.3 African
Does NOT signal that ovulation has occurred - usually around 3 years post menarche

In response to
- sufficient body mass (48kg with 17% fat)
- activation of GnRH pulse generator
- ovarian oestrogen-induced growth of uterus
- fluctuating oestrogen levels

125
Q

Primary amenorrhoea

A

Failure of menarche to occur
- 3 years after thelarche (breast development)
- by age 16 in presence of normal secondary sexual characteristis
- by age 14 in absence of other secondary sexual characteristics

126
Q

Menopause

A

45-55years, average in UK 51
- age reduced by smoking, hysterectomy (even with ovarian conservation, by around 4 years), uterine artery embolisation
- process takes 6months - 3years

Biochemically
- fall in oestradiol (predominant oestrogen will be oestrone)
- decreased levels inhibin
- rise in LH and FSH

127
Q

Premature menopause

A

If before age 40
1% of women, higher incidence in identical twins (5%)

128
Q

Symptoms of menopause

A

Vasomotor - hot flushes, migraine
Urogenital - vaginal atrophy, urinary urgency/frequency
Skeletal - osteopenia, osteoporosis
Psychological - mood disturbance, memory loss, insomnia
Sexual - decreased libido, dyspareunia

129
Q

Spermatogenesis

A

= spermatogonium -> primary spermatocyte -> secondary spermatocyte -> spermatid -> spermatozoa

Produced in seminiferous tubule, when mature move into lumen
70-80 days to produce, new cycle every 16 days
Under influence of FSH

130
Q

Spermatocytogenesis, and spermatidogenesis

A

Spermatogonium undergoes mitosis to produce primary spermatocyte (diploid 46 chromosomes)

Then undergoes meiosis 1 to produce seoncdary spermatocyte (haploid 23)

Then undergoes meiosis 2 to produce 4 spermatids

131
Q

Spermiogenesis

A

Maturation of spermatids under the influence of testosterone

Structural changes:
- axoneme forms
- golgi apparatus becomes acrosome (head)
- body contains mitochondria
- centriole of cell becomes tail of sperm
- DNA becomes highly condensed
- excessive cytoplasm removed

Spermiation = release of mature spermatozoa from sertoli cells into lumen of seminiferous tubule

132
Q

Hormonal control in spermatogenesis

A

GnRH - released at age 10, to produce FSH and LH

FSH - acts on seminiferous tubules (sertoli cells) to stimulate spermatogenesis

LH - acts on leydig cells to stimulate testosterone production

Testosterone - inhibits GnRH and LH

Inhibin - produced by sertoli cells in response to increased sperm, to inhibit FSH

133
Q

Semen

A

Secretions from - seminal vesicles, prostate, bulbourethral (Cowper’s) glands, hyaluronidase (to aid passage through cervical mucus)

Seminal fluid composed of carnithine, inositol, glycerophosphocholine, phosphatase, fructose, citric acid

134
Q

Semen analysis

A

> 15million spermatozoa per ml
39million sperm per ejaculate
Vitality >55%
Leukocyte <1million/ml
300million sperm produced per day
pH 7.2-7.6
Survive for 3-4 days
Total motility >38%
Normal morphology >3%

135
Q

Spermatozoa journey

A

Semen coagulates in vagina
Cervical passage - glycoprotein molecules arrange in parallel lines, sperm form reservoir in cervical crypt
Capacitation - sperm surface glycoprotein removed in uterus via uterine fluid, initiates whiplash movement of sperm tail
Acrosome reaction - allows sperm to penetrate the zona pellucida

136
Q

Bone formation

A

Made of collagen, phosphate and water

Influenced by growth hormone, thyroid, PTH, oestrogen, testosterone

Ossification is membranous, eg top of skull/clavicle, or direct (endochondral), eg long bones, vertebrae, pelvis

Primary centre in diaphysis, secondary centre in epiphysis

137
Q

Types of bone tissue

A

Compact/cortical
- hard and dense
- composed of sheets (lamellae)
- arranged in concentric cylinders (Haversian systems), at the centre is Haversian canal
- osteocytes lie in lacunae within lamellae and canaliculi radiate from here

Cancellous
- interior of bones
- irregular honeycomb of thin plates (trabeculae)
- contains red bone marrow

138
Q

Types of bone

A

Long - shaft is compact, epiphysis is cancellous

Short - mainly cancellous, cortex is compact

Flat - two parallel plates of compact bone surrounding a layer of cancellous bone

Irregular

Sesamoid - forms in areas of pressure, in tendons

139
Q

Bone healing

A

Haematoma forms
Macrophages phagocytose the haematoma
Osteoblast lay down callus (new bone)
Osteoclast reshape bone and form central medullary canal

140
Q

Types of muscle

A

Skeletal (voluntary/striated)
- type 1 - slow twitch fibre, red, high levels myoglobin, aerobic
- type 2 - fast twitch fibre, white, large reserve of glycogen, anaerobic

Smooth (involuntary/visceral) - spindle shaped cells connected by gap junctions

Cardiac - branched fibres connected via intercalated disc

Organisation: actin + myosin, in sarcomeres, in myofibrils, in fascicles, in muscle

141
Q

Myofibrils

A

Contain actin (thin filament) and myosin (thick filament)

Enclosed in endomysium (single muscle cell), then perimysium (covers bundle), then epimysium (whole muscle)

142
Q

Muscle contraction

A

Skeletal:
Action potential -> Ca release from sarcoplasmic reticulum into cytosol -> Ca bind to troponin on actin -> displacement of tropomyosin and exposure of myosin-binding site on actin -> actin and myosin cross link -> myosin slides on actin

Smooth muscle:
Associated with calmodulin
Contraction following phosphorylation of myosin

143
Q

Muscle fuels

A

Phosphocreatine
Glycogen
Blood glucose
Fatty acids

144
Q

MSK changes in pregnancy

A

Muscle relaxation - via progesterone, suppression of mRNA production for oxytocin, oxytocin receptor and prostaglandin F receptor, increase in cAMP, decreased number of gap junctions
- takes up to 3mo postpartum for muscle tone to normalise

Relaxation of sacroiliac joints

Separation of pubic symphysis - normal joint space up to 9mm, if >10mm then significant separation

145
Q

Cells of the nervous system

A

Neurones - cell body, dendrites, axon, presynaptic terminal

Glial cells - non-neuronal, non-excitable
- to provide support and nutrients to neurones, and form myelin
- 4 types of glial cell in CNS - astrocytes, oligodendrocytes (make myelin in CNS), microglia, ependyma (membrane lining cavities)
- 3 types of glial cell in the PNS - schwann (make myelin in PNS), satellite, enteric glial

146
Q

Nerve fibres

A

= axon of nerve cell, organised into fascicle bundles, nerves are grouped fascicles

A fibres
- largest diameter, shortest refractory period, myelinated, 12-130m/s, for touch/pressure/joint position/temperature, motor innervation to skeletal muscles

B fibres
- myelinated, 15m/s, found in autonomic NS

C fibres
- unmyelinated, smallest diameter, longest refractory period, 2m/s, for pain, and viscreal motor fibres to heart and smooth muscle

147
Q

Coverings of nerve fibres

A

Endoneurium covers individual groups of axons

Perineurium covers groups of fascicles

Epineurium covers the nerve

148
Q

Axonal degradation pathway

A

Degeneration of synaptic terminal distal to lesion (Wallerian degeneration) -> myelin degeneration -> debris clean-up by microglia, macrophages and schwann cells -> chromatolysis (neuronal cell body change) -> transneuronal degeneration

149
Q

Action potentials

A

Plasma membranes
- have membrane potential (electrical voltage difference across membrane), resting MP -70mV (inside of cell negative)
- due to unequal distribution of ions
- calculated by Goldman equation
- impermeable to ions, good insulator, but has ion pumps and ion channels (leak or gated, which can depend on voltage, chemicals, pressure, light)

150
Q

Potential

A

Graded - due to chemical/mechanical/light-gated ion channels
OR
Action - all-or-none
- lasts 1ms
- continuous in non-myelinated, but saltatory in myelinated jumping between nodes of Ranvier
- depolarisation (Na inflow, less negative), rapid opening of voltage-gated Na channels
- repolarisation (K outflow, more negative), slow opening of voltage-gated K channels and closure of Na channels
- then hyperpolarisation after repolarisation phase, due to open voltage-gated K channels

151
Q

Refractory period

A

Time when an excitable cell cannot generate another action potential

Absolute (irrespective of stimulus) or relative (only with large stimulus)

152
Q

Neurotransmitters

A

Acetylcholine
Amino acids - excitatory (glutamate and aspartate), or inhibitory (GABA and glycine)
Catecholamines - noradrenaline, adrenaline, dopamine, serotonin
Neuropeptides - endorphins, enkephalins, substance P, CCK, gastrin
Gases - nitric oxide, carbon monoxide

153
Q

Transmission at synapses

A

RELEASE
Nerve impulse -> depolarisation of synaptic membrane -> voltage-dependent Ca channels open -> higher intracellular Ca triggers exocytosis of synaptic vesicles into synaptic cleft -> transmitter binds to neurotransmitter receptor on postsynaptic membrane

REMOVAL
via diffusion, enzymatic degradation, reuptake into cells

154
Q

Impulse conduction and synaptic transmission is influenced by

A

pH
- alkalosis increases excitability of neurones, acidosis depresses
Neurotransmitter agonists/antagonists
Receptor site antagonists
Anticholinesterase agents eg neurostigmine, physostigmine

155
Q

Fuel for brain

A

Cerebral blood flow is 15% of CO, 750ml/min
MAP must be >70mmHg for adequate cerebral perfusion
Brain is 2% body weight and consumes 20% oxygen at rest
Fuelled by - glucose, liver glycogen (after glycogenolysis), muscle protein (after gluconeogenesis), and ketone bodies
CANNOT use fatty acids

155
Q

Reflexes

A

Involuntary response to stimuli - somatic or autonomic

Reflex arc: receptor -> sensory neurone -> control centre (brain/spinal cord) -> motor neurone -> effector
- can be MONOSYNAPTIC (always ipsilateral eg stretch/tendon reflexes) or POLYSYNAPTIC (eg flexor or crossed extensor reflex)

Reflex receptors
- for stretch, =muscle spindles, causes contraction so change muscle length
- for tendon, = Golgi tendon organ, causes relaxation so monitors change in muscle tension to prevent overload

156
Q

Autonomic nervous system fibres

A

All preganglionic fibres are cholinergic

Postganglionic
- parasympathetic are cholinergic
- sympathetic are adrenergic (except sweat glands which are cholinergic)
- absent in adrenal gland as chromaffin cells of medulla are essentially postganglionic cells

157
Q

Sympathetic NS

A

FIGHT OR FLIGHT
- preganglionic nerve fibres from T1 to L2
- sympathetic ganglia - paravertebral (sympathetic trunk, paired either side of spinal cord with 22 ganglia each) and prevertebral (coeliac, SupMes and IM ganglions)
- postganglionic nerve fibres

158
Q

Parasympathetic NS

A

REST AND DIGEST
- preganglionic nerve fibres from cranial nerves (oculomotor, facial, glossopharyngeal, vagus) and vertebral levels S2-S4
- parasympathetic ganglia in wall of visceral organs
- postganglionic nerve fibres

159
Q

Lymphatic system

A

Flow always towards heart, via at least one lymph node before a duct
Maintained by valves, pressure from muscular contraction/pulsating arteries, suction (negative pressure from heart contraction)
Composition similar to plasma
Tissue in lymph nodes (several afferent but only one efferent vessel, contains lymphocytes and macrophages), spleen, thymus
Functions - immune, collect excess fluid, transport fatty acids

160
Q

Epidermis

A
  • stratified squamous epithelium
  • 4 cell types - keratinocytes, melanocytes, langerhans cells (type of immune cell produced by bone marrow), merkel cells (involved in touch)
  • 4 layers - stratum corneum (superficial), stratum lucidum, stratum granulosum, stratum spinosum
161
Q

Dermis

A
  • contains hair follicles, blood vessels, glands (SEBACEOUS in hair follicles and ECCRINE/merocrine sweat glands produce watery secretions all over body, APOCRINE sweat glands produce viscous secretions associated with sexual excitement in axilla, pubic area, areola), nerves
  • papillae in dermis give rise to ridges eg fingerprints
162
Q

Skin changes in pregnancy

A

Striae gravidarum - due to increased cortisol
Chloasma - due to increased melanocyte-stimulating hormone production
Increased skin pigmentation
Linea nigra (darkened linea alba)
Increased activity of sebaceous and sweat glands - due to increased thyroid hormone

163
Q

Sight

A

Three layers to eye - sclera, choroids, retina
Retina has rods (mainly at peripheries) and cones (sensitive to bright light and colour, make up the macula densa)

164
Q

Hearing

A

Ear in temporal bone
Three parts:
- outer ear
- middle ear - eustachian tube and tympanic cavity (malleus, incus, stapes)
- inner ear - has oval window and round window openings to middle ear, stapes attaches to oval. Consists of labyrinth (bony and membranous, filled with perilymph between layers and endolymph within membranous labyrinth) and semicircular canals)

165
Q

Taste

A

3 zones on tongue:
Front - sweet and salt
Lateral - sour
Rear - bitter

Innervation by facial, vagus, and glossopharyngeal nerves

166
Q

Olfaction

A

Smell detected by olfactory sensory neurones in roof of nasal cavity, olfactory epithelium
Sensitivity depends on proportion of olf to resp epithelium in nasal cavity

Odor molecules travel:
superior nasal concha -> olfactory receptor cells -> cribriform plate -> mitral cells in olfactory bulb -> olfactory nerve -> brain

167
Q

Touch

A

Consists of touch and pressure

Mechanoreceptors in humans
- Meissner’s corpuscles - encapsulated unmyelinated nerve endings, sensitive to light touch (NOT pain), in papillae of skin and genital region
- Pacinian corpuscles - sensitive to pressure and vibrations, deep in skin
- Merkel’s disc - pressure and sustained touch
- Ruffini corpuscles - skin stretch

168
Q

Pain

A

= unpleasant sensory or emotional experience associated with actual or potential tissue damage

SOMATOGENIC
Nociceptive
- superficial - localised pain from skin/superficial tissues
- deep - somatic (poorly localised, dull/aching, initiated by nociceptors in ligaments, tendons, muscles, bones, fascia, blood vessels) and visceral
Neuropathic
PSYCHOGENIC

169
Q

Amniotic fluid volumes by gestation

A

10 weeks - 30ml
12 weeks - 50ml
16 weeks - 190ml
35 weeks - 900ml
>35 weeks volume decreases

170
Q

Formation and clearance of amniotic fluid

A

In 1st trimester - made and cleared by placenta, can transport across fetal skin (until it keratinises around 22-25weeks)

In 2nd trimester
- urine - first at 8-11 weeks, increased function/volume through pregnancy (700-900ml/day at term) but full development of renal system not until several months post delivery
- swallowing - first at 12 weeks, 250ml/day
- lung secretions - 200-400ml/day
- placenta

171
Q

Amniotic fluid composition

A

Osmolality = 275mOsm/L
Fluid exchange 500ml/day

Composition
- urine
- cells - epithelial, glial, non-embryonic stem cells
- hormones - progesterone, cortisol, oestrogen, prolactin, rennin
- antibacterial - zinc, lysozyme, peroxidase, interferon-α
- albumin, lecithin, sphingomyelin, bilirubin (decreases in 3rdT)
- α-fetoprotein - less than in fetal blood, peaks at 10-12 weeks
- NO fibrinogen

172
Q

Fetal membranes

A

AMNION
- amniotic cavity formed by day 7
- 5 layers - cuboidal epithelium, basement membrane, compact layer, fibroblast layer, spongy layer
- no blood vessels, lymphatics or nerves

CHORION
- 4 layers - cellular, basement membrane, reticular layer, trophoblast

173
Q

Fetal lung development

A

Pseudoglandular period - 5-17 weeks

Canalicular period - 16-25 weeks
- primitive alveoli
- low diffusing capacity (huge separation from resp tissue and capillaries)

Terminal sac period - 24w-term
- potential for gas exchange improves
- surfactant synthesis by type2 pneumocytes

Alveolar period - late fetal life - age 8
- alveolar-like structures present at 32w, then final growth

174
Q

Surfactant

A

To increase lung compliance
From 24 weeks, by type 2 pneumocytes
Triggered by increase in cortisol (at 32weeks), thyroid hormone, thyrotrophin-releasing hormone, prolactin
Predominant phospholipid is dipalmitoyl phosphatidylcholine DPPC

Lung maturity confirmed by amniotic fluid levels of lecithin:sphingomyelin ratio 2:1

175
Q

First breath following delivery

A

10-60ml
For lung inflation to occur - first inspiratory effort needs transpulmonary pressure 60cmH2O, second inspiratory effort needs 40cmH2O
Triggered by hypercapnia and hypoxia in partial occlusion of umbilical cord
Promoted by tactile stimulation and reduced skin temp

176
Q

Respiratory distress syndrome

A

10-15% prem babies
Due to surfactant deficiency
More in males, caesareans, perinatal asphyxia, maternal diabetes, 2nd twin

177
Q

Fetal circulation

A

Only 10% CO enters lungs

  • umbical vein - ductus venosus - IVC -> right atrium
  • RA to foramen ovale - left atrium - left ventricle -> ascending aorta
    OR - RA to RV - pulmonary artery - ductus arteriosus -> descending aorta
  • aorta -> umbilical artery
178
Q

4 shunts in fetal maternal circulation

A
  1. Placenta
  2. Ductus venosus (bypass liver)
  3. Foramen ovale (between RA and LA)
  4. Ductus arteriosus (aorta to pulmonary artery, patency mediated by prostaglandins)
179
Q

Cardiopulmonary adjustments at birth

A
  • Vasoconstriction of umbilical arteries
  • Autotransfusion - blood from fetal side of placenta enters baby as umbilical veins (placenta-baby) do not constrict
  • Opening of pulmonary circulation due to decreased pulmonary vascular resistance (expansion of lungs and pulmonary vasodilation)
  • Closure of foramen ovale due to increased LA pressure, decreased RA pressure
  • Closure of ductus venosus within 3hrs
  • Closure of ductus arteriosus within few hours - rapid rise in pO2 causes smooth muscle contraction and fall in prostaglandin levels, then permanent closure at 1week old
180
Q

Hypoxia effects on newborn

A

Pulmonary vascular resistance remains high
- so ductus arteriosus remains patent
- so right-to-left shunt persists

181
Q

Fetal erythropoiesis location

A

Begins at 3weeks - in placenta and yolk sac

By 4 weeks - endothelium of blood vessels and liver

By end of 1stT - bone marrow and spleen

Early fetal erythrocytes are nucleated. 5% reticulocyte count at term (1% in adults). Life span depends on gestation, but 80 days at term.

182
Q

Placenta structure

A

Weight 600g at term, 25cm diameter, 3cm thick
Surface area 14m^2 at term
Blood flow 1.5L/min
Consumes 1/3rd of oxygen supplied

Villi (syncitiotrophoblast (multinucleated, no mitotic activity, hormone synthesis), cytotrophoblast (uninucleated), mesenchyme) arranged as lobules, each receiving spiral artery
40-60 lobules

183
Q

Development of placenta

A

Trophoblasts differentiate from day12

Extravillous trophoblast invasion and conversion of spiral arterioles:
Wave 1 - 8-10 weeks
- intestitial cells migrate to inner 1/3rd of myometrium and form giant cells
- endovascular migration down spiral arteries
Wave 2 - 16-18weeks

Leads to loss of smooth muscle of spiral arterioles, dilatation, and loss of vasoreactivity, low-pressure and high capacity vessels

184
Q

Placental blood circulation

A

Umbilical artery - 50mmHg (deoxygenated blood from fetus to placenta)
Umbilical vein - 20mmHg (oxygenated blood to fetus)
Maternal spiral artery - 70mmHg
Intervillous space - 10mmHg

Placental barrier:
Syncitiotrophoblasts outer - contacts maternal blood
Cytotrophoblasts
Extra-embryonic mesoblast - contains Hofbauer cells (macrophages involved in restructuring stroma to ensure plasticity during villi development)
Fetal capillaries

185
Q

Functions of placenta

A

Maternal-fetal transport
- passive diffusion of urea, free fatty acids, respiratory gases
- facilitated transport of glucose
- active transport of amino acids
- receptor-mediated endocytosis of IgG (from 35 weeks)

Hormone synthesis - hCG(chorionic gonadotrophin), hPL (placental lactogen), placental growth hormone between 10-20 weeks, progesterone

Barrier to pathogens

Immunological interface

186
Q

How does the placenta make oestrogen?

A

It does NOT synethesize de novo

  • placenta works with fetal adrenals to synthesize DHEA (dihydroepiandosterone)
  • fetal liver converts DHEA -> oestriol (can measure this for fetal wellbeing)
  • placenta then converts DHEA to oestradiol and oestrone
187
Q

Length of twin pregnancy?

A

3 weeks shorter than singleton

188
Q

Fetal adrenal glands

A

Fetal zone (80-90% of cortex volume) disappears soon after birth
Role in maturation via cortisol production - of lungs, liver, thyroid, GI tract
Role in development - hypothalamic function, pituitary-thyroid axis, hepatic enzymes
Role in sequential change of placental structure
Promote thymic involution

189
Q

Meconium

A

Consists of amniotic fluid, mucus, desquamated GI mucosa cells, fatty acids, bile salts
Usually passed within 48hrs of delivery
1/10 present intrapartum - due to post-dates or fetal distress
1/1000 aspirate -> mechanical lung obstruction, displacement of surfactant, pneumonitis, decreased efficiency of gas exchange. Can lead to pneumothorax or persistent pulmonary hypertension of the newborn

190
Q

Neonatal skin

A

Sterile in utero
Milia - enlarged sebaceous glands on nose and cheek

Protected by
- vernix caseosa - fatty film that develops over the skin from 20weeks
- lanugo - fine covering of hair from 20weeks until 36weeks (usually shed)

191
Q

Fetal weight at 16, 20, 24, 36, 40 weeks

A

16w - 150g
20w - 330g
24w - 670g
28w - 1200g
32w - 1950g
36w - 2810g
40w - 3620g

(so doubles roughly every 4w 16-28w. Then gains slow to 6-700g per 4w)

192
Q

Cardiovascular changes in pregnancy

A

Increased plasma volume by 40-50% (2600-3800ml) up until 32w
Increased red cell mass by 18% (1400ml-1650ml)
Increased CO by 40%
HR rise by 20%
BP decrease by 10%

193
Q

Pulmonary changes in pregnancy

A

RR unchanged
Tidal volume rises by 30-40%
Exp reserve decreases
Total lung volume decreases
Vital capacity unchanged
O2 consumption rises by 20%
- 20ml/min to fetus, 6ml/min for raised CO, 6ml/min for increased renal work, 18ml/min to increased maternal metabolic rate

194
Q

GI changes in pregnancy

A

Sphincter tone decreases
GI emptying time increases
(GI reflux, constipation)

195
Q

Liver changes in pregnancy

A

ALP increases by 3x (placental production)
CCK release decreases
Gallbladder contractility decreases (more cholestasis, gallstones)

196
Q

Renal changes in pregnancy

A

Increased renal flow 25-50%
GFR increases
Serum urea and creatinine falls
Glycosuria
Urinary acid excretion rate rises

197
Q

Metabolic changes in pregnancy

A

Lower bicarb
Lower Na
Lower osmolarity
Increased iron demand and absorption
Increased volume of distribution
Increased drug excretion

198
Q

Haematological changes in pregnancy

A

Increased EPO and hPL
Physiological anaemia and thrombocytopenia
Increased WBC
Hypercoaguable - increase in all coagulant factors, increased fibrinogen

MRCOG Part 1 (14 decks)

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