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Y2 - BRS 2 > Listy Things For SAQs > Flashcards

Listy Things For SAQs Flashcards

1
Q

How do we classify the types of motor units? (3)

A

Speed of contraction
Fatiguability
Amount of tension generated

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2
Q

What 4 factors influence tissue distribution of a drug?

A

Regional blood flow
Plasma protein binding
Capillary permeability
Tissue localisation

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3
Q

What 3 protective mechanisms are there to protect following reflux?

A 
Volume clearance (oesophageal peristalsis reflex)
pH clearance (saliva buffers lowered pH)
Epithelium (barrier properties)
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4
Q

What are the 4 anatomical contributions to the LOS?

A

3-4cm distal oesophagus within abdomen
Diaphragm surrounds LOS (Lt and Rt crux)
Intacct phrenoesophageal ligament
Angle of His

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5
Q

What 4 things contribute to mucosal protection?

A

Mucus film
HCO-3 secretion
Epithelial barrier
Mucosal blood protection

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6
Q

What 3 mechanisms repair epithelial defects

A

Migration
Gap closed by cell growth
Acute wound healing

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7
Q

Give 3 indication of a thyroid storm

A 
Hyperthyroidism (blood tests)
\+ any 2 of:
- Hyperpyrexia (>41 degrees C)
- Accelerated tachycardia/arrythmia
- Cardiac failure
- Delirium/frank psychosis
- Hepatocellular dysfunction (jaundice)
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8
Q

Give 3 properties of a disease for a screening programme to be successful

A

Should be able to identified early/before critical point (detectable)
Treatable
Prevent/reduce morbidity/mortality

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9
Q

Give 3 properties of a good screening test

A

Acceptable/easy to administer
Cost effective
Reproductible and accurate results

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10
Q

What are 3 components of the healthy child programme

A

Screening
General examination and immunisation
Health education/programme

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11
Q

What 3 things contribute to the massive antigen load in the GI tract

A

Resident microbiota 1014 bacteria
Dietary antigens
Exposure to pathogens

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12
Q

How can the epithelial barrier provide mucosal defense

A 
Mucus layer - Goblet cells
Epithelial monolayer - Tight junctions
Paneth Cells (small intestine):
->Bases of crypts of Lieberkühn.
->Secrete antimicrobial peptides (defensins) & lysozyme.
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13
Q

What are the 4 domains of a developmental assessment?

A

Speech and language skills
Social skills
Gross motor skills
Fine motor skills

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14
Q

What 3 factors affect the amount of drug bound by a plasma protein?

A

Free drug concentration
Affinity for the protein binding sites
Plasma protein concentration

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15
Q

How do prostaglandins in gastric mucosal cells protect from acid?

A
  • Increased bicarbonate production (buffer)
  • Increased mucous production (buffer)
  • Increased blood flow (repair)
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16
Q

Give 4 functions of the tear film

A
  • Maintains smooth cornea-air surface
  • Oxygen supply to cornea (no blood vessels)
  • Remove debris (tear film and blinking)
  • Bactericide
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17
Q

How is the airway remodelling in allergic asthma

A
  • Recruitment of eosinophils (and other immune cells)
  • Increased goblet cells (mucus secreting)
  • Thicker airway (more matrix, increased size and no. of smooth muscle cells)
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18
Q

What are 5 characteristics of vulnerable plaques?

A
  • Large soft eccentric lipid-rich necrotic core
  • Increased VSMC apoptosis
  • Reduced VSMC and collagen content
  • Thin fibrous cap
  • Infiltrate of activated macrophages expressing MMPs
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19
Q

What are 3 roles of PDGF (platelet derived growth factor)

A

Vascular smooth muscle cell chemotaxis
Vascular smooth muscle cell survival
Vascular smooth muscle cell division (mitosis)

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20
Q

What are 2 roles of TGF-B (transforming growth factor beta)

A

Increased collagen synthesis

Matrix deposition

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21
Q

What 5 key functions are controlled by the endothelium

A 
Inflammation
Permeability
Vascular Tone
Thrombosis (coagulation)
Angiogenesis
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22
Q

What are the 4 mechanisms that contribute to the formation of atherosclerotic plaques?

A

Leukocyte recruitment
Permeability
Shear stress
Angiogenesis

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23
Q

5 stages of gastrulation

A 
Formation of the primitive streak
Formation of the primitive groove
Formation of the definitive endoderm
Formation of the ectoderm
Formation of the mesoderm
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24
Q

What organs are formed by the ectoderm

A

CNS and neural tract
Skin epithelia
Tooth enamel

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25
Q

What organs are formed by the endoderm

A

GI tract
Liver, pancreas
Lung
Thyroid

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26
Q

What organs are formed by the mesoderm

A

Blood (endothelial cells, red and white blood cells)
Muscle (smooth, skeletal and cardiac)
Gonads, kidney and adrenal cortex
Bone, cartilage

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27
Q

Functions of oxytocin

A

Increases connectivity of myocytes in myometrium (syncytium)
Destabilise membrane potentials to lower threshold for contraction
Enhances liberation of intracellular Ca2+ ion stores

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28
Q

Which 2 factors affect extend of passive drug reabsorption

A

Drug metabolism

Urine pH

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29
Q

What are the 2 principles of motor control (brain)

A

Hierarchical Organisation Principle

Functional Segregation Principle

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30
Q

OCP Function

A
  1. Anovulation
  2. Thickening of Cervical Mucus
  3. Thinning of Endometrial Lining
    to reduce implantation
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31
Q

Why is there increased risk of foot ulceration in T2DM

A

Reduced sensation to feet (peripheral neuropathy)

Poor vascular supply to feet (peripheral vascular disease)

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32
Q

How does rising estrogen levels drive prostaglandin action in the uterus (2)

A
  1. Rising estrogen activates phospholipase A2 enzyme, generating more arachidonic acid for PG synthesis
  2. Estrogen stimulation of oxytocin receptor expression promotes PG release.
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33
Q

What causes severe disease in pneumonia (3)

A
  1. Highly pathogenic strains (zoonotic)
  2. Absence of prior immunity
  3. Predisposing illness/conditions
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34
Q

Respiratory epithelium defence mechanism (5)

A
  • Tight junctions –prevents systemic infection
  • Mucous lining and cilial clearance –prevents attachment, clears particulates
  • Antimicrobials –recognise, neutralize and/or degrade microbes and their products
  • Pathogen recognition receptors–recognise pathogens either outside or inside a cell.
  • Interferon pathways –activated by viral infection. Promotes upregulation of anti-viral proteins and apoptosis.
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35
Q

What is the effect of disturbed blood flow on the endothelial (4)

A
  • Thrombosis, inflammation (WBC adhesion)
  • Endothelial apoptosis
  • SMC proliferation
  • Loss of NO production
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36
Q

What is the effect of laminar blood flow on the endothelial (4)

A
  • Promotes anti-thrombotic, anti-inflammatory factors
  • Endothelial survival
  • Inhibition of SMC proliferation
  • NO production
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37
Q

What are the effects on NO on the endothelium (6)

A

(Multiple protective effects)

  • Dilates blood vessels
  • Reduces platelet activation
  • Inhibits monocyte adhesion
  • Reduces SMC proliferation
  • Reduced released of superoxide radicals
  • Reduces oxidation of LOL cholesterol (major component of plaques)
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38
Q

What processes are angiogenesis essential for (3)

A

Embryonic development
Menstrual cycle
Wound healing

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39
Q

How do endothelial cells contribute to the initiation and propagation of covid19 (3)

A

SARS-CoV2 Infection

  • > Cytokine storm
  • > Endothelial activation
  • > Procoagulant switch
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40
Q

What are some examples of a good screening test (newborn) (3)

A
  • Newborn check (developmental checks)
  • Newborn heading screen (deafness)
  • Blood spot check (heel prick test, some biochemical disorders)
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41
Q

What is one test undertaken pre-conception, first trimester, 2/3rd trimerster, newborn period (4)

A
  • Diabetic eye screening (for existing T1+T2DM)
  • Sickle cell and thalassaemia (blood test)
  • Down syndrome and fetal abnormality US
  • Newborn blood spot
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42
Q

Methods of antigen sampling in the gut (2)

A 
Microfold cells (FAE, Peyer's patches)
Trans-epithelial dendritic cells
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43
Q

Things that cause dysbiosis (5)

A 
Infection/inflammation
Diet
Xenobiotics
Hygiene
Genetics
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44
Q

Things that dysbiosis causes (6)

A 
Brain -> MS
Lung -> asthma
Liver -> NAFLD/NASH
Adipose tissue -> obesity
Intestine -> IBD
Systemic diseases -> T1DM
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45
Q

What is assessed in the MSE (Mental State Examination) (7)

A 
Appearance and behaviour
Speech
Mood
Thoughts
Perceptions
Cognition
Insight
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46
Q

What are some examples of EPSE (extra-pyramidal side effects) (4)

A

Parkinsonism
Acute dystonia
Tardive dyskinesia
Akathisia

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47
Q

ADHD (attention deficit hyperactivity disorder) (3)

A

Inattention
Hyperactivity
impulsivity

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48
Q

How is the cytoarchitecture of the brain organised classified (3)

A

Cell size
Spacing/packing density
Layers

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49
Q

How are primary cortices’ localisation of function

A

Function predictable
Organised topographically
Symmetry between left and right

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50
Q

How are secondary cortices’ localisation of function

A

Function less predictable
Not organised topographically
Left-right symmetry weak or absent

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51
Q

How can the brain function be assessed (3)

A

Imaging
Encephalography
Brain stimulation

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52
Q

What features can be seen on MRI for a patient with Alzheimer’s disease (4)

A

Medial temporal loss bilaterally
Hippocampal volume loss replaced with CSF
Dilated and enlarged ventricles
Narrowed gyri and widened sulci

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53
Q

What are the neuroadaptations ass. with chronic alcohol consumption (3)

A

Reduced function in the inhibitory system
GABA-A receptors become less sensitive
An upregulation of the excitatory system.

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54
Q

What is measured in a water deprivation test (3)

A 
Urine volumes
Urine concentration (osmolality)
Plasma concentration (osmolality)
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55
Q

What are the depression triads (3)

A

Core symptoms: low mood, anergia (low energy), anhedonia
Biological symptoms: sleep, libido, appetite
Psychological symptoms: the world, the future, oneself

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56
Q

What factors affect exercise capacity (4)

A
  • Neurological (e.g. motor control, coordination)
  • Respiratory (e.g. ability for lungs to ventilate, pulmonary perfusion, gas exchange)
  • Cardiovascular (e.g. ability for heart to receive blood from lungs and pump to working muscles)
  • Muscular (e.g. local perfusion, muscle cell enzymes)
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57
Q

Name 3 tests used to evaluate exercise capacity (3)

A

Cardiopulmonary exercise testing
The six minute walk test
Incremental shuttle walk test

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58
Q

What are the 4 stages of secondary (indirect) healing (4)

A

Endochondral healing

  • Haematoma formation
  • Soft callus formation
  • Hard callus formation
  • Remodelling
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59
Q

When does hypoglycaemia become a problem (4)

A
  1. Excessive frequency
  2. Impaired awareness (unable to detect low blood glucose)
  3. Nocturnal hypoglycaemia
  4. Recurrent severe hypoglycaemia
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60
Q

Risks of hypoglycaemia (6)

A 
Risks of hypoglycaemia
Seizure / coma/ death (dead in bed)
Impacts on emotional well-being
Impacts on driving
Impacts on day to day function
Impacts on cognition
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61
Q

What is done in DM annual foot check (3)

A
  • Look for foot deformity, ulceration
  • Assess sensation(monofilament, ankle jerks)
  • Assess foot pulses (dorsalis pedis and posterior tibial)
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62
Q

Management of diabetic foot disease - peripheral neuropathy (3)

A
  1. Regular inspection of feet by affected individual
  2. Good footwear
  3. Avoid barefoot walking
    Podiatry and chiropody if needed
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63
Q

Management of diabetic foot disease - peripheral neuropathy with ulceration (6)

A
  1. Multidisciplinary diabetes foot clinic
  2. Offloading
  3. Revascularisation if concomitant PVD
  4. Antibiotics if infected
  5. Orthotic footwear
  6. Amputation if all else fails
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64
Q

What are the 4 drug-receptor interactions (4)

A

Electrostatic interactions
Hydrophobic interactions
Covalent bonds
Stereospecific interactions

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65
Q

What are the 3 major routes for excretion in the kidney (3)

A

Glomerular filtration
Active tubular secretion (main)
Passive reabsorption from tubule

66
Q

Function of the lens (5)

A 
Transparency
Regular structure
Refractive Power 1/3 of the eye focusing power -higher refractive index than aqueous fluid and vitreous
Accommodation
Elasticity
67
Q

What is the near response triad (3)

A

Pupillary constriction
Convergence
Accommodation

68
Q

What is the indirect evidence of 5-HT hypofunction in depression (5)

A
  • Anti-hypertensive drug (reserpine) causes 5HT depletion → could cause depression
  • Antidepressant action
  • Post mortem after suicide shows reduced 5HT in brainstem
  • MAO A higher in MDD
  • Tryptophan depletion triggers MDD relapse
69
Q

What are the 3 models of addiction (3)

A
  • Reward deficiency (positive reinforcement)
  • Overcoming adverse state e.g withdrawal (negative reinforcement)
  • Impulsivity, compulsivity
70
Q

What can cause haemolytic anaemia (4)

A

Spherocytes + Elliptocytes
Sickle cell
G6PD deficiency
Hypersplenism

71
Q

Laboratory evidence of haemolysis (3)

A
  • LDH raised
  • Unconjugated hyperbilirubinaemia
  • Reduced haptoglobins
72
Q

What are causes of microcytic anaemia (4)

A

Defect in haem synthesis
•Iron deficiency anaemia (Case 4)
•Anaemia of chronic disease (Case 5)-Defect in globin synthesis (thalassaemia
•Defect in α chain synthesis (α thalassaemia
•Defect in β chain synthesis (β thalassaemia)

73
Q

What are causes of normocytic anaemia (7)

A

Recent blood loss:
-Gastrointestinal haemorrhagee
-Trauma
Failure of production of red cells
-Early stages of iron deficiency
-Bone marrow failure or suppression (e.g. chemotherapy)
-Bone marrow infiltration (e.g. leukaemia)
Pooling of red cells in the spleen
-Hypersplenism, e.g. liver cirrhosis
-Splenic sequestration in sickle cell anaemia`

74
Q

What are the causes of macrocytic anaemia (4)

A
  • Lack of vitamin B12or folic acid (megaloblastic anaemia, Case 6)
  • Use of drugs interfering with DNA synthesis
  • Liver disease and ethanol toxicity
  • Haemolytic anaemia (reticulocytes increased)
75
Q

What are the causes of haemolytic anaemia (4)

A

–Integrity of the membrane: Hereditary spherocytosis (Case 1), Autoimmune haemolytic anaemia (Case 2)
–Haemoglobin structure and function: Sickle cell anaemia
–Cellular metabolism: G6PD deficiency (Case 3)

76
Q

What are the 4 functions of the kidney (4)

A

Homeostatic function
Endocrine function
Excretory function
Glucose metabolism

77
Q

What are 3 ways to classify a pituitary tumour (3)

A 
Radiological (MRI):
•Size
•Sellar or suprasellar
•Compressing optic chiasm or not
•Invading cavernous sinus or not

Function
Benign or malignant

78
Q

What else can cause a raised prolactin (3)

A

Physiological
•Pregnancy/breastfeeding
•Stress: exercise, seizure, venepuncture
•Nipple/chest wall stimulation

Pathological
•Primary hypothyroidism
•Polycystic ovarian syndrome
•Chronic renal failure

Iatrogenic
•Antipsychotics
•Selective serotonin re-uptake inhibitors
•Anti-emetics
•High dose oestrogen
•Opiates
79
Q

What can untreated hyperparathyroidism cause (3)

A 
Osteoporosis
Renal calculi (kidney stones)
Impaired mood and mental function
80
Q

What causes increase APPT, normal PT (4)

A

Haemophilia A
Haemophilia B
Factor XI def
Factor XII def

81
Q

What causes increased PT, normal APPT (1)

A

Factor VII def

82
Q

What causes increased PT and APPT (4)

A

Liver disease
Anticoagulant drugs eg. warfarin
DIC
Dilution following red cell transfer

83
Q

What can use cerebral venous thrombosis (4)

A

Thrombophilia
Pregnancy
Dehydration
Behcets

84
Q

Features of Blood Brain Barrier disruption (5)

A 
Endothelial layer dysfunction
Collagen dysfunction
Fibrinogen leakage
Astrogliosis
Astrocytic end-feet change (damage)
85
Q

Types of saccade (4)

A

Reflective saccade to external stimuli
Scanning saccade
Predictive saccade to track objects
Memory-guided saccade

86
Q

What can be used to classify ARDS (4)

A 
Berlin Definition
Timing (within 1 week)
Chest imaging (bilateral opacities)
Origin of oedema
Oxygenation (Pa02/Fi02 ratio)
87
Q

What can be used to classify the severity of ARDS (4)

A 
Murray Score
Pa02/Fi02 (on 100% air)
CXR
PEEP
Compliance (ml/cmH20)
88
Q

List 3 common causes of acute respiratory failure

A 
LRT infection
Aspiration
Trauma
Pancreatitis
Pulmonary vascular disease
TRALI
PE
89
Q

List the 3 mechanisms of acute lung injury (3)

A
  1. inflammation
  2. infection
  3. immune response
90
Q

Name 2 imaging modalities that can be used to guide diagnosis and treatment in the management of ARDS

A

X-ray
CT
USS

91
Q

List the advantages of using extra corporeal membrane oxygenation (6)

A

Advantage:
Improve O2 delivery
Improve C02 removal
Rest lung and prevent ventilator associated lung injury
Resolve respiratory acidosis
Reduce multiple organ dysfunction arising from hypoxaemia and hypercapnia

92
Q

List the disadvantages of using extra corporeal membrane oxygenation (6)

A

Case selection
Not universally available/inequality of provision of care
Bleeding: intra-cerebral, venepuncture sites, epistaxis, haemoptysis
Haemolysis
Infection from central dwelling cannulae
Cost

93
Q

What is the inclusion criteria for ECMO (2)

A

Severe respiratory failure (non-cardiac cause, ie Murray lung injury score 3.0 or above)
Positive pressure ventilation is not appropriate (eg. significant tracheal injury)

94
Q

What is the exclusion criteria for ECMO (3)

A

Contraindication to continuation of active treatment
Significant co-morbidity -> dependency to ECMO support
Significant life limiting co-morbidity

95
Q

What are the types of ventilation for ARDS (4)

A

Volume controlled
Pressure controlled
Assisted breathing modes
Advanced ventilatory support

96
Q

What 3 risk factors are involved in the risk factor multiplication in atherosclerosis (3)

A

Hypertension
High cholesterol
Smoking

97
Q

What are the two classes of monocyte-macrophages (2)

A

Inflammatory macrophages

Resident macrophages

98
Q

What do inflammatory macrophages do (1)

A

Adapted to kill microorganisms

99
Q

What do resident macrophages do (4)

A

Normally homeostatic - supress inflammatory activity
Alveolar resident macrophages - surfactant lipid homeostasis
Osteoclasts - calcium and phosphate homeostasis
Spleen - iron homeostasis

100
Q

What roles do macrophages in plaques have (5)

A

I. Generate free radicals that further oxidise lipoproteins
II. Phagocytose modified lipoproteins, & become foam cells
IIIa. Express cytokine mediators that recruit monocytes
IIIb. Express chemo-attractants & growth factors for VSMC
IIIc. Express Proteinases that degrade tissue

101
Q

What free radicals are generated by macrophages in plaques (2)

A

NAPDH oxidase

Myeloperoxidase

102
Q

What are the ketone bodies (3)

A

Synthesized FROM Acetyl CoA:

Acetoacetate
Acetone
3-OH-hydroxybutyrate

103
Q

4 important things to consider when treating NoF fractures

A

Intra/extracapsular
Displaced or undisplaced
Age of patient
Mobility of patient

104
Q

Factors affecting tissue healing (6)

A

Mechanical environment:
Movement
Forces

Biological environment
Blood supply
Immune function
Infection
Nutrition
105
Q

What are the general complications of a fracture (4)

A

Fat embolus
DVT
Infection
Prolonger immobility (UTI, chest infections, sores)

106
Q

What are the specific complications of a fracture (6)

A 
Neurovascular injury
Muscle/tendon injury
Non union/mal union/ Delayed union
Local infection
Degenerative change (intraarticular)
Reflex sympathetic dystrophy
107
Q

What nuclei are involved in the corticobulbar tract (6)

A 
Oculomotor nucleus
Trochlear nucleus
Trigeminal motor nucleus
Abducens nucleus
Facial nucleus
Hypoglossal nucleus
108
Q

Name the 4 extrapyramidal tracts

A

Vestibulospinal
Reticulospinal
Tectospinal
Rubrospinal

109
Q

What are the 2 phases of micturition?

A

Filling phase

Voiding phase

110
Q

3 places where the urethra is slightly constricted

A

Pelvic ureteric junction
Pelvic brim
As passes through bladder wall

111
Q

3 things to look for the in synovial fluid analysis for crystal arthritis

A

Crystal (type)
Shape
Bifringence

112
Q

What 4 biologicals can be used to treat RA

A

Inhibition of tumour necrosis factor-alpha (TNF-a)
Modulation of T cell co-stimulation
Inhibition of interleukin-6 signalling
B cell depletion

113
Q

When does developmental assessment occur (2)

A
  • Opportunistically

* Planned as part of programme of reviews

114
Q

With whom does developmental assessment occur (4)

A
  • Parents
  • All doctors
  • Nursery nurses
  • Teachers
115
Q

Patterns or abnormal development (3)

A

Slow but steady
Plateau
Regression

116
Q

Types of delay (5)

A

Global delay

Specific delay - language, motor, sensory, cognitive

117
Q

4 areas of child development

A

Gross motor
Vision and fine motor
Hearing, speech and language
Social, emotional and behavioural

118
Q

4 primitive reflexes

A

Morrow reflex
Standing reflex
Grasp reflex
Parachute reflex

119
Q

What things could caused delayed development (4)

A

Ill-health
Decreased inherent potential (genetics)
Sensory/motor impairment
Lack of physical and/or pyscholoigcal stimuli

120
Q

Causes of motor delay (7)

A
  • Cerebral palsy
  • Global delay eg Down’s syndrome
  • Congenital dislocation hip
  • Social deprivation
  • Muscular dystrophy-Duchenne’s
  • Neural tube defects: spina bifida
  • Hydrocephalus
121
Q

Causes of language delay (6)

A 
•Hearing loss
•Learning disability
•Autistic spectrum disorder
•Lack of stimulation
•Impaired comprehension of language
  -Developmental dysphasia
•Impaired speech production
  -stammer, dysarthria
122
Q

Causes of global delay (5)

A

•Chromosomal abnormalities
e.g. Down’s syndrome, Fragile X

•Metabolic
e.g. hypothyroidism, inborn errors of metabolism

•Antenatal and perinatal factors
Infections, drugs, toxins, anoxia, trauma, folate def

  • Environmental-social issues
  • Chronic illness
123
Q

Factors which affect the developing human at any time in the lifecycle (3)

A

Prenatal- iron, folatye, vit b12
Perinatal- check for o2 depeation, drugs uses like glcuoce can egect hear
Postnatal - traiuma, mengitis

124
Q

What are the two ways to prevent DOHaD mechanism leading to disease?

A

NHS Healthy Child Programme

Sure start

125
Q

Associations between early environmental exposures and which diseases?

A
  • Cardio-vascular disease
  • Type 2 diabetes
  • Lung disease
  • Cancer risk
  • Neurological, special sense and intellectual development
  • Allergic and auto-immune diseases
126
Q

Aims of the the NHS Healthy Child Programme?

A

Aims to prevent disease and promote good health
•universal
•reduce health inequalities

127
Q

Things to measure for Murrary Score (4)

A

02 saturation
Positive end point pressure
Chest radiology
Compliance

128
Q

What does TNM8 lung cancer staging use to score lung cancer progression (4)

A

Primary tumour site
Tumour size
Regional lymph node metastases
Extrathoracic metastasis

129
Q

What else imp. to know before carrying on with treatment (lung cancer) (3)

A

Comorbidities
Medication history
Lung function

130
Q

How could inhibiting prostaglandin action prevent pre-term birth (5)

A 
Inhibit leukocyte recruitment
Inhibit interleukin release
Inhibit membrane destabilization
Inhibit monocyte connectivity
Inhibit lower uterus relaxation
131
Q

What prostaglandins are involved in labour (3)

A

PGE2
PGF2 alpha
PGI2

132
Q

What is the action of PGE2 (3)

A

Cervix re-modelling:
Promotes leukocyte infiltration into the cervix
IL-8 release
Collagen bundle re-modelling

133
Q

What is the action of PGF2 alpha (2)

A

Myometrial contractions:
Destabilises membrane potentials
Promotes connectivity of myocytes (with Oxytocin)

134
Q

What is the action of PGI2 (2)

A

Myometrium:
Promotes myometrial smooth muscle relaxation
Relaxation of lower uterine segment

135
Q

What is implicated in cervical remodelling (3)

A

PGE2
Peptide hormone - relaxin
Nitric oxide (NO)

136
Q

What promotes connectivity of myocytes (2)

A

PGF2 alpha

Oxcytoxin

137
Q

Consequences of persistent gastro-oesophageal reflux disease (4)

A

Oseophagitis
Peptic stricture
Barett’s oseophagus
Oseophageal cancer

138
Q

What is the role of labour (3)

A

Safe expulsion of the fetus at the correct time
Expulsion of the placenta and fetal membranes
Resolution/healing to permit future reproductive events

139
Q

How does rising estrogen levels drive prostaglandin action in the uterus (2)

A
  1. Rising estrogen activates phospholipase A2 enzyme, generating more arachidonic acid for PG synthesis
  2. Estrogen stimulation of oxytocin receptor expression promotes PG release.
140
Q

Maternal oxygen and perfusion changes (4)

A

-Maternal cardiac output increases
30% during first trimester (stroke vol & rate)
-Maternal peripheral resistance decreases
up to 30%
-Maternal blood volume increases to
40% (near term (20-30% erythrocytes, 30-60% plasma)
-Pulmonary ventilation increases
40%

141
Q

What factors may affect timely diagnosis of physical disorders in people with mental illness (4)

A
  • Illness behaviour
  • Diagnostic overshadowing
  • Stigma
  • Lack of resources
142
Q

Three ways to classify psychiatric drugs (3)

A

Based on chemical structure- just have the name e.eg: Clomipramine - WHO Classification System
Based on what illnesses they treat- e.g: antidepressants
Based on their pharmacology - NbN ; Neuroscience based Nomenclature

143
Q

Types of treatment in psychiatry (4)

A

Chemical –drugs/medicines
e.g. drugs for psychosis e.g. drugs for depression
Electrical stimulation
e.g. ECT for depression e.g. neurostimulation for pain syndromes
Structural rearrangement - surgery & orthopaedics
e.g. psychosurgery/deep brain stimulation for severe depression
Talking (pycho) therapies
e.g Cognitive Behaviour Therapy (CBT) e.g. exposure for phobias

144
Q

What are the 4 components of clubfoot (4)

A

Cavus
Adductous of foot
Varus
Equinous

145
Q

How can we describe child fractures (5)

A 
Pattern
Anatomy
Intra/Extra-articular
Displacement
Salter-Harris Criteria
146
Q

2 ways in which gradient is created for water reabsorption

A

Countercurrent multiplication

Urea recycling``

147
Q

How do you classify mechanical intestinal obstruction?

A

Speed of onset
Site
Nature
Aetiology

148
Q

What are 3 important things regarding pharmacodynamics (3)

A

Where is the effect produced
What is the target of the drug
What is the response of after drug interaction with a target

149
Q

What are 4 important things regarding pharmacokinetics

A

Absorption
Distribution
Metabolism
Excretion

150
Q

Surgical Tx for stress UI (3)

A

Mid-urethral sling
Colposuspension
Periurethral bulking agents

151
Q

What systems deficits can limit exercise (4)

A

Neurological
Respiratory
Cardiovascular
Muscular

152
Q

Why do enterocytes and goblet cells have such a rapid turnover (36h lifespan)? (3)

A
  • Enterocytes are the first line of defence and may be directly affected by toxic substances (in the diet or from bacteria)
  • Effects of agents which interfere with cell function will therefore be diminished.
  • Any lesions will be short lived.
153
Q

Bebenefits of gut microbiota (4)

A
  • provide essential nutrients that we can’t manufacture
  • metabolise indigestible compounds
  • defence against colonisation opportunistic pathogens
  • contribute to intestinal architecture
154
Q

What are the risks with thyroid surgery? (4)

A

Risk of voice change
Risk of also losing parathyroid glands
Scar
Anaesthetic

155
Q

What is key in growth arrest? (2)

A

Location

Timing

156
Q

What are red flags of lower back pain (4)

A

Weight loss
Fever
Night pain
Less than 19yrs

157
Q

What are the red flags of leg pain (3)

A

Bowel/bladder dysfunction
Saddle anaesthesia
Profound neurological deficit

158
Q

What are the goals of surgery for acute mesenteric ischaemia (2)

A

Restoration of SMA blood flow

Resection of nonviable bowel

159
Q

CRH functions in labour (3)?

A
  • promotes fetal ACTH and cortisol release
  • Increasing cortisol drives placental production of CRH -> Positive feedback!
  • stimulates DHEAS production by the fetal adrenal cortex -> substrate for estrogen production
160
Q

What do neurotrophic factors do (2)?

A

Prevent neuronal death

Promote growth of neurons after injury

161
Q

What 3 things does montelukast do?

A

Decreased:
Eosinophil migration
Bronchoconstriction
Inflammation-induced oedema

162
Q

What are the 4 types of nerual crest cells?

A

Cranial NC
Cardiac NC
Trunk NC
Vagral & Sacral NC

Y2 - BRS 2 (5 decks)

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