Concise Flashcards Sem 1

Question 1

List some major vital signs and indicate a normal range for each.

Answer 1

Vital Signs

• Heart rate – 60-100 bpm
• Respiratory rate – 12-20 breaths/minute
• Blood pressure – 90/60-140/90 mmHg
• Body temperature – 36.0-37.5°C
• Oxygen saturation – 95-100%

Question 2

List four standard precautions.

Answer 2

Standard Precautions

1. Handwashing – using correct technique
2. Barriers to Infection – Gloves, gowns, masks, goggles etc.
3. Appropriate Disposal of Sharps & Waste
4. Aseptic Technique – to avoid wound contamination

Question 3

Name the borders and contents of the femoral triangle.

Answer 3

Femoral Triangle.

• Floor: Psoas Major Muscle
• Lateral border: Sartorius Muscle
• Medial border: Adductor Longus Muscle
• Superior border (Base): Inguinal Ligament
• Contents (medial→lateral): Vein, Artery, Nerve (VAN out)

Question 4

Name the two major forces governing movement of fluid in and out of capillaries.

Answer 4

1. Hydrostatic Pressure – (Pc and Pif) – the force of water between the capillary and the interstitium (influenced by blood pressure)
2. Oncotic Pressure (πp and πIF) – the concentration gradient between the capillary and the interstitium, exerted by proteins (influenced by plasma protein concentration)

Question 5

List the rapid, intermediate and late responses to change in blood pressure.

Answer 5

Rapid/Immediate Response (seconds → minutes)

1. Baroreceptors
2. Chemoreceptors
3. Central Ischaemic Response
4. Intermediate Response (minutes → hours)

Volume Reflex (ANP)

1. Stress Relexation
2. Renin-Angiotensin System
3. Capillary Fluid Shift

Long-Term Response (days → weeks)

1. Renal Pressure Diuresis
2. Erythropoesis

Question 6

List the types of shock and summarise their pathogenesis.

Answer 6

Question 7

List some physiological effects of alcohol.

(10)

Answer 7

1. Slurred speech
2. Motor incoordination
3. Loss of balance
4. Impaired judgement
5. Memory loss
6. Diuresis (inhibition of ADH)
7. Cutaneous vasodilation
8. Inhibition of platelet aggregation
9. ↑ salivary and gastric secretions
10. Tolerance & dependence

Question 8

Outline a screening procedure for alcoholism.

Answer 8

CAGE during history taking to screen for alcoholism

• Cut Down - Have you ever felt you ought to cut down on your drinking?
• Annoyed - Have people annoyed you by criticising your drinking?
• Guilty - Have you ever felt bad or guilty about your drinking?
• Eye Opener - Have you ever had a drink first thing in the morning to steady your nerves?

Question 9

List 6 ethical duties required of doctors.

Answer 9

Ethical duties required of doctors.

1. Duty to diagnose and treat
2. Duty to attend (e.g. make house calls)
3. Duty to disclose – provide enough information for decision making
4. Duty to follow-up
5. Duty of confidentiality
6. Duty to disclose errors

Question 10

Is a doctor required to stop and help at a motor vehicle crash?

Answer 10

• No legal requirement to rescue in Australia (except NT) – exceptions e.g. doctor-patient relationship
• But doctors have a professional and ethical duty to provide aid in an emergency - failure to provide care may be regarded as unprofessional conduct
• Good Samaritan Legislation – no liability to a health practitioner who provides aid in an emergency if:
  
  • The negative action is done or omitted in good faith
  • The act is done without gross negligence (doctors have higher standard of care than students/public)
  • The act is performed without fee or expectation of fee

Question 11

Differentiate between civil and criminal law.

Answer 11

Question 12

Describe the general Evidence Based Medicine (EBM) process.

Answer 12

1. A specific question is asked regarding a patient’s problem
   
   • P = Patient/Population/Proble
   • I = Intervention/Indicator
   • C = Comparison/Control
   • O = Outcome
2. Literature is searched for articles related and relevant to the case
   
   • Cochrane library - collection of evidence-based databases containing information related to specific interventions (systematic reviews and RCTs)
   • Pubmed can be used to answer all types of clinical questions (clinical studies & systematic reviews)
3. The evidence gathered from research is evaluated on an individual basis for its validity and usefulness for application to the case in question
4. The findings, if useful, are applied to the case in question

Question 13

Name four processes involved in Medical medical self-regulation.

Answer 13

1. Education – MBBS → specialist training → CME
2. AMC accreditation of medical schools
3. Accreditation of general practice
4. Professional Services Review Scheme
5. Quality Assurance Committees
6. Adverse Events research/ safety & quality systems
7. Evidence-based medicine
8. Legal standards of care
9. Medical Boards

Question 14

Name four functions of the Medical Board of Australia.

Answer 14

1. To keep a register of medical practitioners
2. To receive complaints re: practitioners and initiate proceedings
3. To discipline practitioners, by imposing conditions on registration or bringing serious matters to the Health Practitioners tribunal
4. To receive reports of impaired practitioners, provide monitoring and rehabilitation, and impose conditions on impaired practitioners

Question 15

Name the layers of skin (in detail).

Answer 15

Layers of the Skin

• Epidermis
  
  • Stratum corneum
  • Stratum lucidum (only thick skin)
  • Stratum granulosum
  • Stratum spinosum
  • Stratum basale
• Dermis
  
  • Papillary dermis
  • Reticular dermis
• Hypodermis

Question 16

Summarise the nerve endings existing in the skin.

Answer 16

• Merkel Cells - Stratum Basale = sensory receptors for fine touch
• Free Nerve Endings – end in Stratum Granulosum
• Meissner’s Corpuscles – papillary dermis = fine touch/pressure, low-freq vibration
• Pacinian Corpuscles – reticular dermis/hypodermis = deep touch/pressure, vibration
• Krause’s End Bulbs – papillary dermis = like pacinian corpuscles
• Ruffini Endings – reticular dermis = mechanoreceptors

Question 17

Name the functions of skin (7).

Answer 17

Functions of skin.

1. Protection – mechanical, chemical, barrier
2. Waterproofing – lipids
3. Thermoregulation – vasodilation/constriction, sweating
4. Metabolism – fat storage, Vitamin D activation
5. Excretion – sebum, sweat, cerumin, milk
6. Sensation – hairs, nerve endings
7. Communication – colour, muscles, odour

Question 18

Describe the four processes involved in the pathogenesis of acne.

Answer 18

Pathogenesis of Acne

1. Poral Occlusion – from hyperkeratinisation, cosmetics, oils, tar, genetic factors
2. Sebum Production – androgen-dependant (especially high in puberty)
3. Bacterial Colonisation of Duct – by Propionibacterium acnes, feeding on sebum
4. Dermal Inflammation – chemical mediators

Question 19

Outline treatment options for acne.

Answer 19

Question 20

Outline the mechanism of abcess formation.

Answer 20

Mechanism of abcess formation

1. Presence of S. aureus
2. Inflammation – necrosis, neutrophil immigration
3. Pus –dead neutrophils, softened necrotic tissue
4. Abcess Formation – membrane - fibrinous exudates
5. Formation of Granulation Tissue (dense, fibrous)

Question 21

Name 7 virulence factors of Staphylococcus Aureus.

Answer 21

Virulence Factors of Staphylococcus Aureus

1. Lipase – degrades skin surface lipids
2. Catalase – resists oxidative destruction
3. Coagulase – catalyses fibrinogen → fibrin, forms layer of fibrin around abscess
4. Endotoxins
   
   • Leukocidin (kills WBC)
   • Haemolysin (kills RBC)
   • Enterotoxins
5. Capsule – resists opsinisation/phagocytosis
6. Protein A – binds Fc region of antibodies→ prevents clearance
7. Adhesins – Elastin, Collagen-binding proteins

Question 22

Outline the mechanisms of some major antibiotics.

Answer 22

Question 23

Outline the three complement pathways.

Answer 23

Question 24

Name the five signs of acute inflammation and outline their mechanisms.

Answer 24

Question 25

Outline the process of lymphocyte production and maturation.

Answer 25

Question 26

Outline the process of T lymphocyte-mediated killing.

Answer 26

Question 27

Outline the process of B cell activation (6 steps).

Answer 27

**B cell activation.** 1. Sensitised B cells migrate to lymphoid tissue through high endothelial venules 2. Antigen-presenting B cells (MHCII) are captured in the T cell zones (paracortex) of lymph nodes 3. Activated TH2 cells bind to the antigen presented by the naive B cells 4. IL-4 released by the T cell and CD40L on the T cell surface stimulate clonal expansion of B cells * Some B cells differentiate to plasma cells - IgM-secreting, immediate * Most B cells (and their corresponding T cells) migrate to the primary lymphoid follicles 5. In the primary follicles, B cells (now known as centroblasts) form a germinal centre where they undergo affinity maturation – involves: 6. Mature B cells differentiate into plasma cells and memory B cells * Plasma cells secrete antibodies (IgM, primary response * Memory B cells remain in circulation ready for a secondary response

Question 28

Name 6 functions of antibodies

Answer 28

**Functions of Antibodies** 1. **Neutralisation** – prevent activity of toxins, entry of microbes into cells 2. **Opsonisation** - phagocytosis (phagocytes express Fc receptors) 3. **Antibody-dependant cell-mediated cytotoxicity** (activate NK cells to undergo cytotoxic killing) 4. Complement Activation – classical complement pathway = opsonisation, recruitment, direct killing 5. **Triggering** of mast cells, basophils, activated eosinophils 6. **Recognition** of antigens by B cells (BCR)

Question 29

Identify specific characteristics of the different classes of antibody (GAMED)

Answer 29

**IgG** - Most common antibody * Involved in secondary immune response - complement activation * Crosses placental barrier – passive immunity from mother to child **IgA** - Neutralisation * Can form a dimer (with J chain) * Found in secretions – saliva, sweat, tears, breast milk (passive immunity from mother to child) **IgM** - Mostly in primary immune response – complement activation * Monomeric form on B cells, but pentameric form in circulation (+ J chain) **IgE** - Involved in allergic response- stimulates histamine release by mast cells and basophils **IgD** - B cell receptor (BCR)

Question 30

Describe four ways that antibodies develop diversity.

Answer 30

1. **Chain** **Diversity** – Different combinations of heavy and light chains 2. **Somatic** **Recombination** – Genetic switching of variability, domain and junction regions 3. **Junctional** **Diversity** – Alteration at the site of cleavage in the joining region 4. **Somatic** **Hypermutation** – Mutations in antibody genes which alter antibody structure

Question 31

Outline the pathogenesis of fever.

Answer 31

Question 32

Outline the process of determining an APGAR score.

Answer 32

Question 33

Name the ligaments that attach to the liver and where they connect to (6).

Answer 33

1. **Coronary** **ligament** - connects the liver to the diaphragm above 2. **Triangular** **ligaments** (left & right) – where the anterior and posterior coronary ligaments come together 3. **Falciform** **ligament** - connects liver to anterior body wall 4. **Round** **ligament** (ligamentum teres) - remnant of fetal umbilical vein 5. **Lesser** **ommentum** - connects the liver to the stomach, and contains the ligamentum venosum, a remnant of the fetal ductus venosus 6. **Porta** **hepatis** (transverse fissure) - transmits the portal vein, the hepatic artery proper, the common hepatic duct, nerves and lymphatics

Question 34

What valve controls the cystic duct?

Answer 34

Spiral valve/ valve of Hesler

Question 35

Explain the concept of zones within a liver acinus.

Answer 35

* **Zone I:** closest to periportal axis; well perfused with O2, nutrients & toxins – resists hypoxic damage but susceptible to drugs/toxins * **Zone II** – transitional zone; between I and III * **Zone III** – near central vein; blood is deoxygenated, low in nutrients and high in drug metabolising enzymes – susceptible to hypoxic damage and drugs (paracetamol)

Question 36

Name the seven Baltimore groups of viruses and give an example of each.

Answer 36

Question 37

Outline the stages of viral infection (7).

Answer 37

_Stages of Viral Infection_ 1. **Attachment** – viral protein contacts cell receptor 2. **Penetration** – fusion of viral coat with cell membrane 3. **Uncoating** - release of viral genome 4. **Transcription and/or Translation** * DNA viruses – transcription/replication occurs in the nucleus & proteins translated in the cytoplasm * RNA viruses – transcription/translation/ replication all occur in the cytoplasm 5. **Genome Replication** 6. **Assembly** – formation of viral particles from proteins 7. **Release** - lysis of cell or budding

Question 38

Outline the mechanisms of action of acyclovir, interferon-α and AZT.

Answer 38

* **Acyclovir** – inhibits DNA polymerase * **AZT** – inhibits reverse transcriptase * **Interferon**-**α** – stimulates cells to inhibit viral translation

Question 39

Describe some defining features of Hepatitis A, B, C and D.

Answer 39

Question 40

Describe some liver function tests and what abnormal levels indicate.

Answer 40

Question 41

Outline the process of heme catabolism.

Answer 41

Question 42

Outline the causes of jaundice.

Answer 42

**Causes of Jaundice** 1. **Pre**-**Hepatic** **Jaundice**: excessive bilirubin production from Haemolysis, glomerular nephritis * ↑ unconjugated bilirubin in blood, ↑ urobilinogen in urine & stools, normal urine and stool colour 2. **Hepatic** **Jaundice**: impaired liver function or hepatocellular damage from hepatitis, toxins, cirrhosis * ↓Uptake → ↑unconjugated plasma bilirubin, normal urine, pale stools * ↓Conjugation → ↑unconjugated plasma bilirubin, normal urine, pale stools * ↓Excretion (hepatic cholestasis) → ↑conjugated plasma bilirubin, dark urine & pale stools 3. **Post**-**Hepatic** **Jaundice**: blockage of outflow from liver from gallstones, head of pancreas cancer * ↑ unconjugated bilirubin in blood, dark urine & pale stools

Question 43

Outline some of the clinical features of Down Syndrome.

Answer 43

Question 44

Name some categories of notifiable diseases (8).

Answer 44

1. **Gastroenteric pathogens** (some transmitted by food or water) - e.g. salmonella • Sexually transmissible infections - e.g. HIV, gonorrhoea 2. **Vaccine preventable diseases** - e.g. Measles, pertussis, rubella 3. **Blood-borne viruses** - e.g. Hepatitis c 4. **Vector-borne infections** - e.g. Dengue fever 5. **Zoonotic infections** - e.g. Brucellosis, q-fever 6. **Invasive bacterial diseases** - e.g. Invasive meningococcal disease, invasive pneumococcal disease 7. **Potential bioterrorism agents** - e.g. Smallpox 8. **New and emerging infections** - e.g. Severe Acute Respiratory Syndrome (SARS)

Question 45

Name some retroperitoneal organs.

Answer 45

SAD PUCKER (retroperitoneal organs) * **S**uprarenals * **A**orta & inferior vena cava * **D**uodenum (descending & horisontal) * **P**ancreas (except tail) * **U**reters * **C**olon (ascending & descending) * **Ki**dneys * **(O)**Esophagus * **R**ectum (middle 1/3)

Question 46

dentify structures, blood supply and innervation of the foregut, midgut and hindgut.

Answer 46

Question 47

Identify anterior and posterior relations of the stomach.

Answer 47

**Posterior Relations** * Omental bursa * Left kidney * Diaphragm, spleen, * left adrenal * Pancreas * Transverse mesocolon **Anterior Relations** * Diaphragm (fundus) * Left lobe of liver * Anterior abdominal wall

Question 48

Identify distinguishing features of the ileum and jejunum.

Answer 48

Question 49

What parts of the colon are mobile and what parts are fixed?

Answer 49

1. Ascending colon - fixed 2. Transverse colon - mobile 3. Descending colon – fixed 4. Sigmoid colon - mobile

Question 50

Identify the two plexuses of the enteric nervous system.

Answer 50

1. **Myenteric (Auerbach’s) Plexus** * Outer plexus between the longitudinal and circular muscle layers * Controls movements throughout the length of the GIT 2. **Submucosal (Meissner’s) Plexus** * Inner plexus within the submucosa * Controls GIT secretion and blood flow – more localised

Question 51

List types of diarrhoea and give a mechanism and example for each.

Answer 51

DOMES * Deranged Motility * Osmotic * Malabsorptive * Exudative * Secretory

Question 52

Name some common gastrointestinal pathogens, their incubation period and duration of illness.

Answer 52

Question 53

Outline the pathogenesis of infection with Entero- haemorrhagic E. Coli.

Answer 53

_Pathogenesis of E. Coli_ 1. EHEC ingested * Eating undercooked, contaminated ground beef * Drinking raw milk or contaminated water 2. 2-4 day latency period 3. Abdominal cramps, non-bloody diarrhoea (1-2 days) 4. Bloody diarrhoea (5-7 days) 5. Resolution or → haemolytic uraemic syndrome * 5% chronic renal failure * 30% proteinuria * 3-5% death * 6% resolution

Question 54

dentify four types of protozoa, describe them and give an example.

Answer 54

1. **Flagellates** –with whip-like flagella (e.g. Giardia lamblia) 2. **Amoebae** – temporary pseudopodia (e.g. Entamoeba histolytica) 3. **Sporozoa** – non-motile ‘spores’ (e.g. Cryptosporidium parvum) 4. **Ciliates** – hair-like cilia (e.g. Balantidium coli)

Question 55

Name the major causes of anaemia (9).

Answer 55

1. **Acute** blood loss (haemorrhage) 2. **Chronic** blood loss (e.g. lesion in GIT) 3. **Extravascular** **haemolysis** – reduced RBC deformability means they can’t fit through sinusoids and are sequestered in the spleen --\> phagocytosis (sickle cell, hypersplenism) 4. **Intravascular** **haemolysis** * Mechanical Trauma, RBC infections (malaria), autoimmune/drug-induced haemolysis, toxins (lead poisoning, snake venom), membrane lipid abnormalities 5. Genetic disorders - fanconi anaemia 6. **Malnutrition** * B12 (pernicious anaemia), folate, iron deficiency anaemia 7. Aplastic anaemia - hematopoietic failure 8. Pure red cell aplasia - suppression of erythrocyte progenitors 9. Iron sequestration (inflammation)

Question 56

Explain some of the parameters used to assess anaemia.

Answer 56

Question 57

Name some principles of a balanced diet.

Answer 57

* **Variety &** **Moderation** – No single food included/excluded * **Energy** **Intake** - Slightly less than needed to maintain current body weight * **Nutritional adequacy** * **Small Portions** – Be satisfied, not stuffed * **Low Energy Density** – More satiety for fewer calories – water, fibre, low fat * **Lots of Water** – Increases fullness, reduces hunger and helps the GI tract adapt to a high fibre diet * **High Fibre** – High fibre foods tend to be nutrient dense and lower in energy, promoting satiety * **Minimal Empty Calories** – Especially sugar and alcohol

Question 58

Outline some causes of the mortality discrepancy between indigenous and non-indigenous Australians.

Answer 58

**Socioeconomic Causes** 1. Less education, employment and income 2. Poor nutrition 3. Poor housing and sanitation 4. Increased exposure to violence 5. Increased incidence of substance abuse 6. Reduced quality of healthcare 7. Distance to health services - isolation **Cultural Causes** 1. Family Structure 2. Community view of disease 3. Hesitation about western medicine

Question 59

Define the terms prevalence, indicence, epidemic and endemic.

Answer 59

* **Prevalence**: the number of existing cases of a disease that are present in a population at a specified time * **Incidence**: the number of new cases of a disease per unit of population over time * **Endemic**: disease present/prevalent at a steady state in a population at all times * **Epidemic**: a sudden and significant increase in prevalence clearly in excess of normal

Question 60

Outline the blood supply, lymphatic drainage of the stomach.

Answer 60

* **Arterial** **supply**: branches of the coeliac trunk * Coeliac trunk = left gastric artery * Common hepatic artery = right gastric artery * Gastroduodenal artery = right gastro-omental artery * Splenic artery = left gastro-omental artery * **Venous** **drainage**: feeds into the portal vein and splenic vein * **Lymphatic** **drainage**: coeliac lymph nodes

Question 61

List 4 features of granulomatous inflammation.

Answer 61

_Features of granulomatous inflammation_ 1. **Fibrosis** – collagen deposition and ECM protein synthesis (repair, not regeneration) 2. **Angiogenesis** – proliferation of small blood vessels 3. **Granuloma** = aggregate of epitheloid macrophages, surrounded by lymphocytes & plasma cells 4. **± necrosis & giant cells**

Question 62

Name 6 hormones that inhibit gastric secretion/motility.

Answer 62

1. Somatostatin 2. Prostaglandin E2 3. Secretin 4. Cholecystokinin (CCK) 5. Gastric Inhibitory Peptide (GIP) 6. Vasoactive Intestinal Peptide (VIP)

Question 63

Explain the stages of gastric secretion.

Answer 63

Question 64

Name 8 virulence factors of Helicobacter pylori.

Answer 64

1. **Flagella** – motility; allows bacteria to propel itself through viscous mucus layer 2. **Adhesins** – facilitate binding to host cells – includes haemoglutinin, sialic acid binding protein A (SabA) 3. **Acid** **Inhibitory** **Protein** – blocks secretion of acid by parietal cells 4. **Mucinase** – breaks down gastric mucus, making the mucosa sensitive to acid 5. **Urease** – converts urea → ammonia, neutralising gastric acid in the bacteria’s immediate vicinity 6. **Superoxide** **Dismutase (SOD) & Catalase** – neutralise oxygen radicals from phagocytes 7. **CagA (some strains)** – stimulates gastric cells to release pro-inflammatory cytokines 8. **Vacuolating Cytotoxin (VacA)** – induces vacuolation in epithelial cells, stimulates neutrophil migration

Question 65

Outline the treatment approach for peptic ulcers (4).

Answer 65

1. **Neutralise** **secreted** **acid** * antacids ( aluminium hydroxide, calcium carbonate) 2. **Inhibit acid secretion** * **H2 antagonists** (ranitidine) – block histamine receptors →↓acid secretion * **Arachidonic acid agonists** (misoprostol) – ↑prostaglandins → ↓acid secretion * **PPIs** (pantoprazole) – inhibit proton pump that secretes H+ 3. **Protect the mucosa from damage** * Bismuth subcitrate (pepto-bismol) – coats the mucosa and protects it from acid irritation 4. **Eradicate the causative agent (H. pylori)** * **Antibiotics** (clarithromycin, amoxicillin, metronidazole) – kill H. pylori

Question 66

Explain the anabolic and catabolic pathways of appetite regulation.

Answer 66

**Catabolic pathway** 1. Stimulated by insulin, leptin and cholecystokinin 2. POMC/CART neurons secrete melanocortins (eg α-MSH) 3. Second order neuron stimulates TRH/CRH release 4. Stimulation of the nucleus tractus solitaris (NTS) → sympathetic activation, energy expenditure **Anabolic Pathway** 1. Stimulated by ghrelin, inhibited insulin and leptin 2. NPY/AgRP neurons secrete neuropeptide Y and agout-related peptide (AgRP) * AgRP acts as an antagonist of melanocortin receptors 3. Second order neuron stimulates release of melanin-concentrating hormone (MCH), other orexins 4. Stimulation of feeding centre, inhibition of NTS (↓SNS and energy expenditure)

Question 67

Identify the BMIs for classification of normal, overweight and obese patients.

Answer 67

Question 68

Explain 7 different methods for measuring body composition and body fat.

Answer 68

1. **BMI** -body mass index (weight/height2) - the current standard for assessing body fat 2. **Underwater** **Weighing** - measures the body’s density – adipose tissue is less dense than lean tissue 3. **Skin** **Fold** **Calipers** – measures the thickness of skin folds at specific areas – thicker skinfolds → more fat 4. **Waist-to-Hip Ratio (WHR)** - differentiates body types – apples (centralised obesity) vs. pears (generalised) 5. **BIA** (bioelectrical impedance analysis) - electrical impulses are used to measure the impedance of the body, indicative of body water – used to estimate fat-free body mass - determine total body fat 6. **DEXA scans** - High & low energy X-ray beams differentiate fat mass, fat- free mass and bone mass 7. **Growth Charts** – for children

Question 69

List the diagnostic criteria for anorexia nervosa and bulemia nervosa.

Answer 69

**Anorexia** * Refusal to maintain body weight * \<85% of expected weight or BMI \<17.5 * Fear of gaining weight * Denial of illness * Amenorrhoea – absence of 3 consecutive menstrual cycles **Bulemia** * 2 binge eating episodes and inappropriate compensatory behaviour for \> 3 months

Question 70

List the four elements required for informed consent.

Answer 70

1. **Information Disclosure** - A practitioner must take reasonable care in providing enough information for the patient to make a decision * **Proactive disclosure** – what a reasonable person in the patient’s case would want to know * **Reactive disclosure** – what the doctor should know the particular patient would want to know 2. **Comprehension** – The patient must understand and accept the information given to them 3. **Voluntariness** – the decision must be made voluntarily and without coercion from the physician, family members or authority figures (e.g. police, lawyers) 4. **Competence** – the patient must be competent – must understand their condition and how it affects them

Question 71

Explain what is required as grounds for involuntary admission (6).

Answer 71

_Involuntary Admission Requirements_ 1. Patient must be suffering from a recognised mental illness 2. The illness must require immediate treatment 3. The treatment must be available at an authorised mental health service 4. The illness must have the capability to cause immanent harm to the patient or others 5. There must be no less restrictive way to treat the illness 6. The person must lack the capacity to consent – or has unreasonably refused treatment

Question 72

Explain the different types of enzyme inhibition, as well as how they affect Km and Vmax.

Answer 72

**Competitive Inhibition** – the inhibitor binds to the enzyme’s active site, preventing binding of the substrate * ↑Km but Vmax is unchanged because competition can be overcome by ↑ substrate concentration **Non-competitive Inhibition** – the inhibitor binds to the enzyme somewhere other than the active site, causing a change in the conformation of the enzyme and preventing the substrate from binding * ↓Vmax but Km is unchanged **Uncompetitive Inhibition** – the inhibitor binds to the enzyme only when it is bound to substrate (enzyme:substrate complex), preventing the reaction from occurring. * Both ↓ Vmax and ↓Km

Question 73

List the products of each acetyl CoA invested in the citric acid cycle.

Answer 73

* 2 CO2 * 3 NADH molecules * 1 FADH2 molecule * 1 GTP molecule

Question 74

Identify some causes of hypoglycaemia.

Answer 74

**1. Fasting - EXPLAIN** * **EX**ogenous drugs * Insulin, sulfonylureas * Alcohol * **P**ituitary insufficiency * **L**iver failure/inherited enzyme defect * **A**ddison’s disease - ↓cortison * **I**slet cell tumours * **N**on-pancreatic neoplasms **2. Reactive** * Drug-induced * Metabolic disease * Gastric surgery

Question 75

Name some relations of the pancreas.

Answer 75

* **Anterior** – stomach * **Posterior** – inferior vena cava, aorta, superior mesenteric artery, left kidney, left adrenal, common bile duct, right dome of diaphragm, portal vein * **Right** – head lies in the C-shape of the duodenum * **Left** – tail associates with hilum of spleen * **Inferior** – transverse mesocolon

Question 76

Distinguish major features of Diabetes type I and II.

Answer 76

Question 77

Outline the pathogenesis of symptoms related to diabetes type I and II.

Answer 77

Question 78

What is the clinical definition of DKA?

Answer 78

Blood glucose \> 11 mmol/L Venous pH \< 7.3 Ketonaemia and ketonuria

Question 79

Explain the mechanisms behind some major oral hypoglycaemics.

Answer 79

1. **Sulfonylureas** * Stimulate insulin release, and decrease glucose production (in the liver) 2. **Biguanides** – e.g. Metformin * Decrease glucose release by inhibition of gluconeogenesis in liver and muscle 3. **Thiazolidinediones** – e.g. pioglitazone * Increase tissue sensitivity to insulin by activating transcription factors – PPARs (Peroxisome proliferator activated receptors) α, γ, δ (especially γ) which stimulate: 4. **α-Glucosidase inhibitors** – e.g. Miglitol * Delay intestinal absorption of glucose by inhibiting intestinal glucoside hydrolase enzymes and delaying breakdown of complex carbohydrates

Question 80

List some causes of unconsciousness.

Answer 80

**AEIOUTIPS** * **A**lcohol/drugs * **E**ndocrine/electrolytes * Insulin * **O**xygen * **U**raemia * **T**rauma * **I**nfection/intercranial pressure * **P**oison/porphyrins * **S**eizure/stroke/space-occupying lesion/ sub-arachnoid haemorrhage

Question 81

Outline assessment of consciousness using the Glasgow coma scale.

Answer 81

Question 82

Explain the physiology of sound conduction (6 steps).

Answer 82

1. Sound travels through EAC and causes vibration of tympanic membrane 2. Movement of the tympanic membrane causes displacement of the ossicles - sound is amplified as it travels through the ossicles due to reduction of surface area from the tympanic membrane to the oval window 3. Movement of the stapes at the oval window causes pressure waves in the vestibular duct, which cause vibration in the cochlear duct – the waves then travel through the tympanic duct out the round window 4. Pressure waves transmitted to the cochlear duct cause distortion of the basilar membrane under hair cells * Pitch - different pulsation frequencies – high frequency near the oval window * Intensity is measured by the amount of energy in the waves 5. Vibration of the basilar membrane causes movement of hair cells against the tectorial membrane – movement of stereocilia and kinocilium leads to opening of ion channels and depolarisation – triggers neurotransmitter release and stimulation of sensory neurones – more sterocilia affected → greater intensity 6. The spiral ganglion receives sensory input regarding the region and intensity of the stimulation and relays it to the medulla via the cochlear branch of cranial nerve VIII

Question 83

Distinguish between conductive and sensorineural hearing loss.

Answer 83

Question 84

Outline the branching of the airways.

Answer 84

**Conducting Airways** 1. Trachea 2. Primary bronchi 3. Lobar bronchi 4. Segmental bronchi 5. Intrasegmental bronchi 6. Bronchioles 7. Terminal bronchioles **Respiratory Airways** 1. Respiratory bronchioles 2. Alveolar ducts 3. Alveolar sacs 4. Alveoli

Question 85

List some causes of tubal obstruction in the body.

Answer 85

Question 86

List 8 consequences of tubal obstruction.

Answer 86

_Consequences of tubal obstruction_ 1. Upstream dilatation -build-up of luminal contents 2. Upstream muscular Hypertrophy 3. Downstream atrophy of tissues - as an adaptive response to the obstruction 4. Infection – from lack of flushing 5. Retention of Secretions in lumen 6. Stone Formation – e.g. renal calculi 7. Necrosis of Mucosa 8. Loss of Function

Question 87

Describe the 6 classes of mutation leading to cystic fibrosis.

Answer 87

1. **Defective protein synthesis** - complete lack of CFTR at the apical epithelial surface 2. **Abnormal protein folding/processing/trafficking** * Defective processing from the endoplasmic reticulum to golgi body * Complete lack of CFTR at apical surface * ∆F508 – the most common (70%) CFTR mutation – is in class 2 3. **Defective** **regulation** - activation of CFTR prevented by blocking ATP binding or hydrolysis * Presence of CFTR at apical surface, but non-functional 4. **Decreased conductance** - less movement of Cl- ions * Presence of CFTR at apical surface, but decreased function – milder phenotype 5. **Reduced abundance** - defect in intron splicing or promoter * Protein is normal but less is expressed – milder phenotype 6. **Altered regulation of other ion channels** * CFTR also regulates other ion channels e.g. ENaC and ORCC * Altered regulation can lead to changes in other ions e.g. Na+ * Some mutations affect conduction and regulation (e.g. ∆F508)

Question 88

Describe how a CFTR mutation affects cell transporters in the cells of the lung.

Answer 88

Question 89

Define some major terms involved in the global burden of disease, specifically life expectancy, HALE, YLL, YLD and DALY.

Answer 89

* **Life Expectancy (LE):** The number of years an individual can expect to live * **Healthy Life Expectancy (HALE):** the number of years an individual can expect to live without a disability * **Years of Life Lost (YLL):** the number of years an individual would have lived if they had not died prematurely * **Years of Life Lived with a Disability (YLD)** – incorporates incidence, duration and severity * **Disability Adjusted Life Years (DALY):** total ‘lost health’

Question 90

Name some of the muscles involved in inspiration.

Answer 90

**Principal** 1. External intercostals 2. Interchondral part of internal intercostals 3. Diaphragm **Accessory** 1. Sternocleidomastoid 2. Scalenes

Question 91

List the normal PO2 and PCO2 in the atmosphere, alveoli, systemic arteries and veins.

Answer 91

* **Atmosphere**: 160, 0.3 * **Alveoli**: 100, 40 * **Arteries**: 100, 40 * **Veins**: 40, 45

Question 92

Name four things that shift the oxygen saturation curve to the right.

Answer 92

1. reduced pH 2. increased CO2 3. increased temperature 4. increased bisphosphoglycerate

Question 93

List some respiratory and non- respiratory causes of hypoxaemia.

Answer 93

_Respiratory Causes_ 1. **Hypoventilation** - upper airway obstruction, trauma to chest, muscular/neural dysfunction, respiratory centre depression (drugs), severe presentations of asthma, COPD etc. 2. **Impaired** **Diffusion** - oedema, emphysema 3. **Shunt** - blood arrives in arteries without being oxygenated * Can be due to V/Q mismatch (physiologic shunt) * Intrapulmonary aterio venous malformations 4. **V/Q mismatch** - asthma, COPD, pulmonary embolism _Non-Respiratory Causes_ 1. **Intra-cardiac R--\>L shunt** - congenital defects 2. **Reduced inspired O2** - increased altitude = less oxygen 3. **Reduced O2 content** - anaemia

Question 94

Identify some causes of asthma.

Answer 94

_Causes of Asthma_ 1. **Atopic** **Asthma** – triggered by environmental antigens (allergens – dust, pollens, food) = increased IgE 2. **Non-atopic Asthma** – triggered by respiratory viruses = no IgE 3. **Drug-induced Asthma** – e.g. NSAIDs 4. **Occupational Asthma** – from fumes, organic/chemical dusts, gases, smoking

Question 95

Describe 6 airway changes involved in asthma.

Answer 95

1. **Inflammation** * Mediated by activated T2H lymphocytes – secrete cytokines o IL-5 – activation of eosinophils * IL-4/IL-13 – expression of IgE on mast cells & eosinophils * IL-4 - expression of eosinophil-chemotactic factors on endothelium 2. **Bronchoconstriction** * Proteases from mast cell degranulation 3. **Oedema** * From inflammation 4. **Increased mucus secretion** 5. **Smooth muscle hypertrophy** * GFs from inflammatory cells 6. **Damage to epithelium & shedding** * From inflammation

Question 96

List the treatments used for asthma and outline their mechanism of action.

Answer 96

Question 97

List the five clinical steps involved in smoking cessation.

Answer 97

1. Ask 2. Assess 3. Advise 4. Assist 5. Arrange/follow up

Question 98

Outline the four septation steps involved in the embryology of the heart.

Answer 98

1. **Atrioventricular**: Endothelial cushions invade heart, leaving AV canals 2. **Atrial**: Septum primum (ostium primum/secondum) → septum secondum (foramen ovale) 3. **Aorticopulmonary**: Truncoconal swellings form the spiral-shaped aorticopulmonary septum 4. **Interventricular**: Muscular septum grows up, membranous septum grows down

Question 99

Outline the three shunts involved in foetal circulation.

Answer 99

1. **Ductus** **Venosus** – O2 blood from the umbilical vein bypasses the liver and enters the IVC 2. **Foramen** **Ovale** – O2 blood flows from LR atrium, bypassing the lungs 3. **Ductus** **Arteriosus** – Mixed blood flows from the pulmonary trunk to the aorta, bypassing the lungs

Question 100

List some social determinants of health.

Answer 100

* Low socioeconomic status * High levels of stress * Poor conditions during childhood * Unemployment * Work that is high demand, repetitive and offers poor reward and low levels of control * Drug and alcohol use * Poor nutrition * Transport and its effects on health * Social exclusion and isolation * Social support

Question 101

List the layers of the heart.

Answer 101

1. **The Pericardium** 1. **Fibrous pericardium** – anchors heart to surrounding tissue 2. **Serous** **pericardium** – prevents friction during activity of the heart * **Parietal** **pericardium** – attached to fibrous pericardium * **Pericardial** **cavity** – contains serous fluid that prevents friction * **Visceral** **pericardium** – also known as epicardium 2. **The Heart Wall** 1. **Epicardium** – visceral pericardium 2. **Myocardium** – muscular layer; thicker in the ventricles (especially left ventricle) than the atria 3. **Endocardium** – inner endothelial layer

Question 102

Outline the transport of lipids.

Answer 102

Question 103

Outline the clotting cascade.

Answer 103

Question 104

Name the four steps in haemostasis.

Answer 104

1. Vasoconstriction/Spasm 2. Platelet Plug Formation 3. Blood Coagulation – The Clotting Cascade 4. Restoration of Normal Bloodflow

Question 105

Outline the fibrinolytic cascade.

Answer 105

Question 106

Outline three risk factors for thrombosis.

Answer 106

1. **Endothelial** **injury** – atherosclerosis, hypertensive damage, MI 2. **Abnormal** **Bloodflow** – stasis, turbulence, hyperviscosity 3. **Blood** **Hypercoagulability** – primary (genetic), secondary (acquired changes in clotting factors)

Question 107

Outline the pathogenesis of atherosclerosis.

Answer 107

1. Endothelial damage 2. Accumulation of Low Density Lipoproteins (LDL) in vessel wall 3. Monocyte entry into intima & differentiation to macrophages 4. Oxidation of LDL by free radicals from macrophages 5. Uptake of oxidised LDL by macrophages  foam cells (fatty streak) 6. Death of foam cells (necrotic core) 7. Release of chemoattractant factors stimulating migration of smooth muscle cells and platelets 8. Adhesion & aggregation of platelets, accumulation of ECM molecules (fibrous cap) 9. Atheroma (plaque) = lipids + necrotic core + fibrous cap Once the fibrous cap is broken down the plaque can rupture, causing thrombosis of the atheroma.

Question 108

Outline an approach for acute treatment of myocardial infarction.

Answer 108

1. **Morphine** – pain reduction 2. **Oxygen** – may not actually help if pulmonary function is normal, but won’t be harmful 3. **Antiplatelet** **drugs** (aspirin/clopidogrel) – inhibit platelet aggregation 4. **Nitrates** (Glycerol Trinitrate) – peripheral vasodilation

Question 109

Explain some common anticoagulants, their mechanism and adverse effects associated with them.

Answer 109

Question 110

Explain some common antiplatelet drugs, their mechanism and adverse effects associated with them.

Answer 110

Question 111

Explain some common fibrinolytics, their mechanism and adverse effects associated with them.

Answer 111

Question 112

List some ways in which a physician can be impaired.

Answer 112

1. Physical handicap/condition e.g. stroke, Alzheimer’s 2. Alcohol or drug dependency 3. Psychiatric condition e.g. OCD, depression, panic attacks 4. Temporary stress reaction 5. Declining competence due to age or illness

Question 113

Name some anterior and posterior relations of the kidney.

Answer 113

**Anterior Relations** * Liver * Duodenum * Jejunum * Colon * Stomach * Pancreas **Posterior Relations** * Diaphragm * Psoas Major * Quadratus Lumborum * Transversus abdominus (aponeurosis) * Subcostal nerves & vessels * Iliohypogastric & ilioinguinal nerves

Question 114

Outline the flow of blood from the abdominal aorta to a glomerulus.

Answer 114

1. **Abdominal Aorta** 2. Renal Arteries 3. Segmental Arteries 4. Interlobar Arteries 5. Arcuate Arteries 6. Interlobular Arteries 7. Afferent Arterioles 8. **Glomerulus**

Question 115

List some major functions of the kidney.

Answer 115

1. **Water balance**/plasma volume maintenance 2. **Regulation of ECF ion concentrations** - Na+, Cl-, K+, HCO3-, Ca2+, PO4-, H+ 3. **Acid-base balance** 4. **Excretion** of urea, uric acid, creatinine, drugs, pesticides 5. **Secretion** of erythropoietin & renin 6. **Conversion** of 25-hydroxyvitamin D to active form

Question 116

List the layers of the glomerular filter.

Answer 116

1. **Endothelium** – fenestrated, negatively charged endothelial cells 2. **Basement** **membrane** – type IV collagen, laminin, fibronectin, negatively charged proteoglycans 3. **Podocyte** **foot** **processes** (**pedicels**) – have a negative charge

Question 117

Describe the regulation of GFR.

Answer 117

**Autoregulation** - constriction/relaxation of afferent & efferent arterioles * **Myogenic**: ↑ afferent stretch = smooth muscle contraction = constriction of afferent arteriole = decreased GFR * **Tubuloglomerular**: Change in [Na+] detected by macula densa = release of vasoactive hormones (renin, endothelin, adenosine, bradykinin etc.) = constriction/dilation of afferent ± efferent arterioles change in GFR **Sympathetic Nerve Activation** * Adrenaline/noradrenaline constrict afferent arterioles = reduced renal bloodflow = reduced GFR **Renin-Angiotensin System – Angiotensin II** * Constricts efferent arteriole = ↑ glomerular pressure = decreased GFR * Causes peripheral vasoconstriction = ↑ TPR = ↑ MAP = ↑ GFR * ↑ Na+ and H2O reabsorption = ↑ blood volume = ↑ MAP = ↑ GFR * Stimulates aldosterone release (↑ Na+ and H2O reabsorption) **Atrial Natriuretic Peptide** * Atrial stretching (↑blood volume) = ↑ ANP * Dilates afferent arterioles = ↑ GFR * Inhibits renin-angiotension system = decreased Na+ and H2O reabsorption = decreased blood volume

Question 118

List nine effects of angiotensin II when binding to AT1 receptors.

Answer 118

1. Vasoconstriction (hypertension) 2. NaCl reabsorption, K+ secretion, H2O retention 3. Aldosterone Release (=NaCl reabsorption, K+ secretion, H2O retention) 4. ADH secretion (=↑H2O reabsorption in collecting duct) 5. Sympathetic Activation 6. Thirst 7. Cell Growth (hypertrophy/hyperplasia) 8. Oxidative Stress (activates NADPH oxidase – superoxide production) 9. Fibrosis (stimulates deposition of collagen)

Question 119

State the categories of hypertension and the blood pressures associated with them.

Answer 119

Question 120

List causes of primary and secondary hypertension.

Answer 120

**Primary Hypertension** (95% of cases) - precise aetiology unknown 1. Fetal factors (low birthweight) 2. Genetic factors (e.g. RAS defects) 3. Environmental factors - obesity, cholesterol **Secondary Hypertension** (5% of cases) - specific aetiology 1. Renal (80%) - renal artery stenosis, renin-secreting tumours, damage to the kidney, congenital ion channel defects 2. Endocrine - primary aldosteronism, phaeochromocytoma (↑catecholamines), cushing’s (↑cortisol), acromegaly (↑growth hormone), 3. Conn’s Syndrome (↑aldosterone) 4. Cardiovascular - coarctation of aorta, ↑ Cardiac output (↑blood volume) 5. Neurological - stress (↑SNS) 6. Drugs - NSAIDs, oral contraceptives, glucocorticoids, sympathomimetics 7. Pregnancy

Question 121

List seven risk factors for hypertension.

Answer 121

1. **Age** – over time systolic increases and diastolic decreases 2. **Sex** – higher prevalence in men 3. **Race** – African Americans especially 4. **Obesity** 5. **Atherosclerosis** 6. **Smoking** – nicotine 7. **High salt intake** 8. **High alcohol intake** 9. **Stress**

Question 122

Outline some different options for treatment of hypertension and the mechanism of action for each.

Answer 122

1. **α1-Adrenoceptors** - block action of noradrenaline, ↓peripheral resistance 2. **ACE Inhibitors** - block ACE, ↓effects of angiotensin II, ↑effects of bradykinin 3. **AT1 Receptor Antagonists** - block AT1 receptors, ↓ effects of angiotensin II 4. **β-Adrenoceptor Antagonists** - block effects of noradrenaline on β receptors (→↓TNFα) Ca2+ Channel Blockers - ↓ Ca2+ entry into cardiovascular muscle cells, ↓ constriction 5. **Diuretics** - ↓ reabsorption/ ↑secretion of water 6. **Endothelin Antagonists** - inhibit ETA/ETB receptors, ↓ effects of endothelin (vasoconstricts) 7. **Endopeptidase Inhibitors** - ↑ANP (↓breakdown by endopeptidase) → vascular relaxation

Question 123

Outline the movement of molecules at the level of the proximal convoluted tubule.

Answer 123

Question 124

Outline the movement of molecules at the levels of the thin descending and ascending limbs of the loop of Henle.

Answer 124

**Thin descending** * Permeable to H2O but not NaCl * H2O moves passively by countercurrent **Thin ascending** * Very low permeability to H2O * Na+ and Cl- move paracellularly

Question 125

Outline the movement of molecules at the level of the thick ascending limb of the loop of Henle.

Answer 125

* Na+/K+/Cl- reabsorption is secondary to Cl- active transport * Na+/K+/Cl- drive reabsorption of fluid and countercurrent * Paracellular absorption of Mg2+ & Ca2+ driven by electrical potential created by the movement of other ions

Question 126

Outline the movement of molecules at the level of the early distal tubule.

Answer 126

* Transport of NaCl (inhibited by thiazide diuretics) * Ca2+ reabsorption (stimulated by parathyroid hormone)

Question 127

Outline the movement of molecules at the level of the late distal tubule/cortical collecting duct.

Answer 127

Question 128

Outline the movement of molecules at the level of the medullary collecting duct.

Answer 128

* Permeability to H2O is controlled by ADH (vasopressin) by changing the number of surface AQP2 channels (aquaporins) * Passive movement of urea

Question 129

Outline four ways in which renal acid-base balance is achieved.

Answer 129

1. Active secretion of H+ by intercalated cells (late distal tubule/cortical collecting duct) 2. Reabsorption of HCO3- (proximal tubule (85%)/thick ascending limb) 3. The **Phosphate** **Buffer** **System** – phosphate in filtrate binds to excess H+, leading to excretion of the H+ as well as entry of a CO2 molecule from circulation into the tubular cell → generation of new HCO3- 4. The **Ammonia** **Buffer** **System** – two methods * In the proximal tubule glutamine (an amino acid) metabolised to ammonium (NH4+) and HCO3- - resulting in new HCO3- that reenters circulation * In the collecting duct, excess H+ binds to ammonia ions and is excreted as NH4+ - for every H+ molecule excreted a CO2 molecule enters the tubular cell from circulation and is used to make a new HCO3- molecule

Question 130

Explain nephrotic and nephritic syndromes.

Answer 130

**Nephrotic Syndrome** * Leakage of large amounts of protein due to increased glomerular permeability * → proteinuria, hypoalbuminaemia, hyperlipidaemia, lipiduria **Nephritic Syndrome** * Leakage of protein and red blood cells due to renal inflammation * → proteinuria, haematuria, azotaemia, oliguria, hypertension, oedema

Question 131

Outline some causes of renal renal failure?

Answer 131

Question 132

What is the clinical definition of renal failure?

Answer 132

* \>50% decrease in GFR (over the period of hours to days) * ± ↑ Nitrogenous wastes in body (BUN – blood urea nitrogen) * ± ↓ in urine output (oligouria/anuria)

Question 133

Describe the three phases of acute tubular necrosis.

Answer 133

1. **Oliguric phase** – tubular obstruction → NaCl & H2O retention, hyperkalaemia, metabolic acidosis 2. **Diuretic Phase** – sealing of tubulues but less reabsorption → loss of Na+, K+ (hypokalaemia), H2O 3. **Prolonged period of improving function** – gradual recovery, nocturia

Question 134

List some consequences of ARF.

Answer 134

1. Hyperkalaemia 2. Metabolic acidosis 3. Oedema 4. Hypertension 5. Uricaemia (azotaemia) 6. Secondary hyperparathyroidism 7. Anaemia (due to ↓ erythropoietin) 8. Depression of the immune system

Question 135

Name three sites of constriction of the ureters.

Answer 135

1. **Renal** **Pelvis** (pelvic-ureteric junction) 2. **Pelvic Brim** = near where ureters cross external iliac arteries anteriorly 3. **Uterovesical Junction** (where ureters enter bladder obliquely) = Act as a one way ‘flap’ - filling of bladder blocks off ureters

Question 136

Outline the nervous control of micturition.

Answer 136

Stretch receptors in the bladder wall stimulate the sacral plexus, which can stimulate the pontine micturition centre (pons) or directly stimulate pelvic splanchnic nerves **Detrusor muscle** * Pelvic splanchnic nerves (PSNS) stimulate contraction o Hypogastric nerves (SNS) cause some relaxation **Internal sphincter** * Maintained by hypogastric nerves (SNS) * Relaxation is stimulated by pelvis splanchnic nerves (PSNS) **External sphincter** * Maintained by the pudendal nerve (somatic) * Removal of somatic inhibition causes relaxation

Question 137

Outline three steps involved in an approach to maintaining patient concordance.

Answer 137

1. Elicit the patient’s views on medicines and taking drugs, and explore those views 2. Inform the patient of the pros and cons of taking or not taking the medicine, ensuring they understand this information 3. Involve the patient in treatment decisions.

Question 138

List some key features to focus on when assessing an ECG.

Answer 138

1. **Rate and rhythm** – heart rate, fibrillation 2. **Conduction intervals** – PR, QRS, QT 3. **The cardiac axis** 4. **The QRS complex** – especially for a pathological Q wave 5. **The ST segment and T wave** – ST elevation etc.