PPCS2

Question 1

Misoprostal

Answer 1

200mcg tablet
Dose- 800mcg - 4x200mcg
Sublingual or rectal
Indications- primary or secondary PPH where there is excessive bleeding from the birth canal which is uncontrolled by syntometrine or is contraindicated or unavailable.
Confirmed miscarriage or termination with excessive bleeding from birth canal uncontrolled by syntometrine.
Contra-indications- any suspicion of another fetus in the uterus, don’t administer any uterotonics
Known anaphylaxis to misoprostol or any other component of the product, or to other prostaglandins
Onset is 7-10 mins.

Question 2

TXA in PPH

Answer 2

500mg/5ml - 2 vials for dosage 1g/10ml over 10 minutes
Criteria-
Bleeding from genital tract over 500ml - usually within 4 hrs but can be 24hrs
TXA should be given after misoprostal
Suspected uterine trauma - bleeding could be intra-abdominal
Uterotonic drugs are contraindicated
If breastfeeding, TXA should be administered in life-threatening circumstances
Obstetric-
Life-threatening bleeding due to disorders of obstetric origin

Question 3

Oxytocin

Answer 3

Estradiol from ovaries induces oxytocin receptors on uterus.
Oxytocin from fetus & mother’s posterior pituitary - stimulates uterus to contract - stimulates placenta to make prostaglandins - stimulated more contractions of uterus.
Melatonin strengthens effects of oxytocin.
Adrenaline- counterbalances oxytocin - remain calm and try to keep the environment stress free

Question 4

PPH

Answer 4

Primary PPH- 500mls or more/clinical signs of hypovolaemic shock within 24 hours of birth
Secondary PPH- excessive bleeding from birth canal between 24 hours & 6 weeks of birth.
Lie mother down- high flow O2- stop bleeding
Placenta delivered or not administer syntometrine 1ml IM if not hypertensive or misoprostal 800mcg
If placenta delivered- massage uterus to encourage contraction- atonic uterus feels high & soft- cupped hand circular motion when contracted it will feel lower & firmer
If placenta not delivered - do not massage unless life threatening haemorrhage
Administer IV TXA 1g over 10 minutes & call maternity unit
Check for external perineal tears
Apply direct pressure using gauze or maternity pad
Fluid resuscitation- IV access - if bleeding 500ml fluid replacement
Tissue- retained placenta or membranes need to be treated in hospital
All passed products to come to hospital
Transfer to nearest consultant led obstetric unit with pre alert obs & monitoring
Continue uterine massage

Question 5

Cord prolapse

Answer 5

When the umbilical cord enter the birth canal in front of the baby- can block or completely cut off the baby’s maternal oxygen & blood supply as it is compressed in the birth canal by the baby’s head.
Can result in brain injury.
Usually results in immediate c-section

Question 6

Obstetric cardiac arrest

Answer 6

Confirm arrest & call for help
Lie flat & manually displace uterus to the left
Commence CPR
Identify team leader
Defib pads & check rhythm
Maintain airway & ventilation
Circulation - IV/IO access
Emergency hysterotomy - doctor
Post resus from haemorrhage - haemorrhage protocol

Question 7

Stages of labour

Answer 7

Normally within a week of due date
Progesterone levels drop around week 37
Estrogen stays high- causes uterine muscle to be more sensitive to other hormones.
Stage 1- fetus drops in uterus- contraction of uterus (oxytocin & prostaglandins) & dilation of the cervix- placenta secretes relaxin & opens pelvic outlet & helps to dilate cervix. Mucus plug evacuates, amniotic sac ruptures. True labour->active labour
Stage 2- expulsion - foetal head enters birth canal, uterus continues to contract. When head crowns- baby rotates (with assistance) baby is delivered, baby dried & placed on mom, cord gets cut.
Stage 3- afterbirth- birth of the placenta- uterus continues to contract. After placenta uterus still contracts for involution of uterus for pregestation size. Also other abdominal organs return to normal locations.

Question 8

Pre-eclampsia

Answer 8

Mild/moderate- BP of >140/90 proteinuria & sometimes oedema
If BP elevated on two occasions in labour/immediately after birth pt needs to be seen by consultant at obstetric unit.
BP of 150/100 or more in pregnancy, labour, or after birth requires urgent treatment & rapid transfer to consultant led obstetric unit - if time critical, correct any ABC abnormalities & transfer to nearest suitable receiving hospital with a pre-alert.
If not time critical perform more thorough assessment & fetal assessment, measure BP & transfer to unit.
Severe- BP 160/110 or more with one or more of the following- headache (severe & frontal), visual disturbances, proteinuria, epigastric/RUQ pain, twitching, tremor, nausea, vomiting, confusion, rapidly progressive oedema —>
Correct time critical factors ABC
Pre-alert- be mindful of light & sirens as strobe & noise can precipitate convulsions
Transfer to nearest obstetric unit
Administer 4g magnesium sulfate IV over 5-15 mins if available

Question 9

Eclampsia

Answer 9

Tonic/clonic convulsion. Pre diagnosis of pre-eclampsia but eclampsia can be acute with no prior warning 1/3 present post delivery
Assess for time critical features eg recurrent?
Correct ABC & transport to consultant led obstetric unit
Gain IV access with large bore cannula/IO access
Do not administer fluid bolus due to oedema
Non time-critical- more thorough assessment
If hx of htn or pre eclampsia treat as eclampsia if not treat as for epilepsy
Place in full lateral position & protect airway
Monitor spo2
If recurrent or continuous (2-3mins or further seizure) administer 10mg/2ml diazepam IV/IO over 2 mins max dose 20mg
Pre-alert

Question 10

Shoulder dystocia

Answer 10

Prepare for newborn life support and position mother in McRobert’s position—> if shoulders do not release, attempt to deliver baby with hands on the baby’s head and apply gently axial traction with baby’s head in line with it’s spine for 30 seconds—> apply suprapubic pressure with mother in McRobert’s position, using CPR grip apply continuous pressure downwards for 30 seconds & encourage mother to push or perform gentle axial traction—> attempt intermittent rocking suprapubic pressure for 30 seconds/gentle axial traction—> change woman’s position to all fours & encourage to push —> transfer women in lateral position with legs separated to protect baby’s head

Question 11

Nuchal cord

Answer 11

Cord wrapped around baby’s neck-
If loose gently pull over baby’s head
If it’s tight keep baby’s head close to moms thigh on whatever way they’re coming out then somersault baby to release cord

Question 12

Shock

Answer 12

Occurs when the circulatory system is unable to keep up with the metabolic demands of the body- circulatory failure leads to reduced tissue perfusion causing cellular & tissue hypoxia
Perfusion triangle- heart, blood, blood vessels

Question 13

TXA

Answer 13

Anti-fibrinolytic, clots the blood to stop bleeding.
Trauma treatment- known or suspected severe external/internal haemorrhage (other than gastric)
2 vials 1g over 10 mins within 3 hours of bleeding.

Question 14

Hypovolaemic shock

Answer 14

Fluid loss- bleeding, burns, vomiting/diarrhoea, excess sweating, dehydration

Increased HR & RR, low BP, reduced GCS, delayed CBR, pallor, cool/cold to touch

Fluid therapy up until point of strong radial, tourniquets, pressure bandages, chito gauze, elevation, splint, TXA if within 3 hours, direct/indirect pressure

Question 15

Carcinogenic shock

Answer 15

Pump problem- the heart is unable to pump blood efficiently around the body
MI, extreme bradycardia/tachycardia, left heart failure, trauma
Also known as obstructive- PE, tension pneumothorax, cardiac tamponade

Question 16

Distributive shock

Answer 16

Fluid to wrong place- anaphylaxis, sepsis, toxins, neurogenic shock

Question 17

Adrenaline in anaphylaxis

Answer 17

Multiple adrenergic receptors.
Alpha-receptor agonist - reverses peripheral vasodilation & reduces tissue oedema.
Beta-receptor activity- dilates bronchial airway & increases myocardial force of contraction. Suppresses histimine & leukotrine release.
Acts directly on beta 2 adrenergic receptors on mast cells to inhibit activation- lesser the degree of IgE-mediated allergic reactions.

Question 18

Sepsis

Answer 18

A life-threatening organ dysfunction caused by a dis-regulated response to infection.
Normally when an infection infiltrates the body, it is engulfed by macrophages- part of the invader is expressed on the outside & picked up by a T-cell. The T-cell triggers a small number of cytokines to be released into the circulation= recruitment of inflammatory cells.
In sepsis- failure to control inflammatory cascade leading to a loss of capillary integrity, mastication of macro-vascular blood flow leading to organ injury & dysfunction.

Question 19

Anaphylaxis

Answer 19

Severe, life-threatening, generalised or systemic hypersensitivity reaction characterised by rapidly developing life-threatening airway and/or breathing and/or circulation problems usually associated with skin & mucosal changes
1. Antigen IgE interaction
2.The body releases chemical mediators into the bloodstream e.g histamine, leukotrines.
3. Smooth muscle contraction- bronchoconstriction
4. Vasodilation & plasma leakage
5. Vascular system changes e.g hypotension, vasoconstriction, decreased cardiac output

Question 20

Inflammatory process

Answer 20

Injury to cells= cell membrane floating round (phospholipid bilayer) —> phospholipase A2 breaks down phospholipid by hydrolysis—> aracadonic acid is produced (an inflammatory precursor)—> metabolised by lipoxygenase into leukotrines which cause bronchoconstriction and by cyclooxygenase (cox1&cox2) into prostaglandins (pain, vasodilation, swelling) and thromboxains (cause platelets to stick together)
Response- localised non specific immune reaction.
-any damaging stimulus triggers the response
-damaged tissue&immune cells secrete inflammatory chemicals.
-tissue mast cells release histamine & prostaglandins into extracellular fluid
-increase dilation & permeability of vessels (redness & heat)
-changes accelerate enzyme activity, boost phagocytosis & damage foreign proteins
-increased pressure & prostaglandins induce pain
-phagocytes (neutrophils & macrophages) squeeze through blood vessel & clear debris & dead cells from the site & stimulate cytokines to initiate tissue repair

Question 21

Organophosphate poisoning

Answer 21

On synapse acetylcholine binds to receptor sites & causes sodium channel to open. If they’re not broken down by acetylcholine esterase you get a constant contraction of the muscles.
Nerve gases bind to the esterase & stops it from working resulting in a constant contraction. Sarin nerve agent causes very tight contractions leading to death.
Atropine (anti nerve agent) binds to receptor sites & blocks acetylcholine binding, resulting in relaxation of the muscles.

Question 22

Heart sounds

Answer 22

Heard with stethoscope.
From valve closures.
4 sounds but only 2 are audible.
S1-Lubb- closure of AV valves when ventricular systolie starts- louder & longer than other heart sounds.
S2-Dubb- closure of semilunar valves at the start of ventricular diastolie.
S3&S4- from blood turbulence from ventricular filling and atrial systolie.
Murmurs- abnormal heart sounds- usually in children & older adults, but can be pathological.
Incompetent valve that fails to close completely-swishing sound.
A stenotic valve does not open completely- rumbling sound.

Question 23

Pharmacodynamics

Answer 23

The study of the impact of drugs on the body- focusing on molecular mechanisms by which drugs exert their therapeutic and adverse effects.
Receptors, agonists & antagonists.
Meds can act in 4 different ways:
-Bind to a receptor site
-Change physical properties of a cell
-Chemically bind with other chemicals
-Alter a normal metabolic pathway
Affinity- force of attraction between receptor& medication.
Efficacy- medications ability to cause desired response.
Avidity- the strength of the binding.

Question 24

Pharmacokinetics

Answer 24

What the body does to the drug.
ADME
Absorption- active or passive.
Distribution- transport of medication from site to the site of action
Metabolism- anabolism (building up) & catabolism (breaking down) includes first pass effect from liver.
Excretion- medication/metabolites moves from the tissues back into circulation to organs of excretion eg kidneys, liver, intestines, lungs, sweat.
Allows for safe & effective use of drugs in patients.

Question 25

Homeostasis

Answer 25

The regulatory process that organisms employ to maintain internal stability and metabolic efficiency despite external changes. Complex interactions between the nervous and endocrine systems to maintain balance. The ability of organisms to keep their internal chemical composition constant.

Question 26

Fibrinolysis

Answer 26

The biological process responsible for the dissolution or breakdown of fibrin clots. Fibrin clots are formed during haemostasis to prevent blood loss following a vascular injury.
tPA mainly activates plasminogen which generates enzyme plasmin causing proteolytic reactions. PAI-1 inhibits the activity of tPA and controls the rate of fibrinolysis.

Question 27

Coagulation

Answer 27

The physiological process that prevents excessive bleeding following vascular injury. Mechanisms that work together to seal off damaged blood vessels and restore normal blood flow.
Damaged blood vessel or tissue—> platelets & clotting factors are activated —> platelets stick together to form a haemostatic plug over the wound —> platelets release chemicals that form fibrin that act as a mesh to stop bleeding —> a clot forms over the damaged area which the body will dissolve when the injury heals.
Endothelial cells also play a crucial role in normal circumstances & when injury arises.

Question 28

Allergic reaction

Answer 28

A hypertensive immune response to a normally harmless substance

APC takes allergen & divides it up into fragments & displays them on surface —> APC activates Th2–> Th2 releases chemical signals that cause B cells to develop into antibody producing plasma cells which make IgE (allergen specific) —> distinct reaction & IgE binds to mast cells—> re-exposure —> allergen binds to specific IgE on mast cells—> release of histamines & leukotrines —> Th2 & mast cells induce further immune cells such as eosinophils & basophils—> further amplify symptoms

Question 29

Hemostasis

Answer 29

Series of rapid defensive reactions to stop excessive bleeding & promote healing after a vascular injury

Governed by clotting factors and platelets only at the injury site

Vascular phase- blood vessels constrict to reduce blood flow

Platelet phase- collagen from damaged endothelial cell lining initiates platelet adhesion - form loose platelet plug (platelet aggregation) & then releases clotting factors

Coagulation phase- clotting factors converts fibrinogen into insoluble fibrin strands = mesh work to solidify platelet plug into a stable clot

Question 30

Blood pressure imbalances & circulatory shock

Answer 30

Homeostatic imbalances can abruptly change blood pressure.
HTN = sustained bp of 130/80 or more (obesity, alcohol, stress, genetic predisposition)
Hypotension= 90/60 or less (dehydration, blood loss, or sepsis)

Circulatory shock- inadequate blood flow & reduced ability to supply nutrient & oxygen to tissues.