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Kitty - Past Papers & Practice Qs > Concise Flashcards Sem 1 > Flashcards

Concise Flashcards Sem 1

1
Q

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

A

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%
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2
Q

List four standard precautions.

A

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
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3
Q

Name the borders and contents of the femoral triangle.

A

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)
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4
Q

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

A
  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)
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5
Q

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

A

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
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6
Q

List the types of shock and summarise their pathogenesis.

A
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7
Q

List some physiological effects of alcohol.

(10)

A
  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
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8
Q

Outline a screening procedure for alcoholism.

A

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?
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9
Q

List 6 ethical duties required of doctors.

A

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
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10
Q

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

A
  • 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
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11
Q

Differentiate between civil and criminal law.

A
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12
Q

Describe the general Evidence Based Medicine (EBM) process.

A
  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
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13
Q

Name four processes involved in Medical medical self-regulation.

A
  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
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14
Q

Name four functions of the Medical Board of Australia.

A
  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
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15
Q

Name the layers of skin (in detail).

A

Layers of the Skin

  • Epidermis
    • Stratum corneum
    • Stratum lucidum (only thick skin)
    • Stratum granulosum
    • Stratum spinosum
    • Stratum basale
  • Dermis
    • Papillary dermis
    • Reticular dermis
  • Hypodermis
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16
Q

Summarise the nerve endings existing in the skin.

A
  • 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
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17
Q

Name the functions of skin (7).

A

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
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18
Q

Describe the four processes involved in the pathogenesis of acne.

A

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
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19
Q

Outline treatment options for acne.

A
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20
Q

Outline the mechanism of abcess formation.

A

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)
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21
Q

Name 7 virulence factors of Staphylococcus Aureus.

A

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
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22
Q

Outline the mechanisms of some major antibiotics.

A
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23
Q

Outline the three complement pathways.

A
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24
Q

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

A
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25
Q

Outline the process of lymphocyte production and maturation.

A
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26
Q

Outline the process of T lymphocyte-mediated killing.

A
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27
Q

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

A

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
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28
Q

Name 6 functions of antibodies

A

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)
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29
Q

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

A

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)

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30
Q

Describe four ways that antibodies develop diversity.

A
  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
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31
Q

Outline the pathogenesis of fever.

A
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32
Q

Outline the process of determining an APGAR score.

A
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33
Q

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

A
  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
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34
Q

What valve controls the cystic duct?

A

Spiral valve/ valve of Hesler

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35
Q

Explain the concept of zones within a liver acinus.

A
  • 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)
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36
Q

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

A
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37
Q

Outline the stages of viral infection (7).

A

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
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38
Q

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

A
  • Acyclovir – inhibits DNA polymerase
  • AZT – inhibits reverse transcriptase
  • Interferon-α – stimulates cells to inhibit viral translation
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39
Q

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

A
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40
Q

Describe some liver function tests and what abnormal levels indicate.

A
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41
Q

Outline the process of heme catabolism.

A
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42
Q

Outline the causes of jaundice.

A

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
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43
Q

Outline some of the clinical features of Down Syndrome.

A
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44
Q

Name some categories of notifiable diseases (8).

A
  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)
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45
Q

Name some retroperitoneal organs.

A

SAD PUCKER (retroperitoneal organs)

  • Suprarenals
  • Aorta & inferior vena cava
  • Duodenum (descending & horisontal)
  • Pancreas (except tail)
  • Ureters
  • Colon (ascending & descending)
  • Kidneys
  • (O)Esophagus
  • Rectum (middle 1/3)
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46
Q

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

A
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47
Q

Identify anterior and posterior relations of the stomach.

A

Posterior Relations

  • Omental bursa
  • Left kidney
  • Diaphragm, spleen,
  • left adrenal
  • Pancreas
  • Transverse mesocolon

Anterior Relations

  • Diaphragm (fundus)
  • Left lobe of liver
  • Anterior abdominal wall
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48
Q

Identify distinguishing features of the ileum and jejunum.

A
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49
Q

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

A
  1. Ascending colon - fixed
  2. Transverse colon - mobile
  3. Descending colon – fixed
  4. Sigmoid colon - mobile
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50
Q

Identify the two plexuses of the enteric nervous system.

A
  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
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51
Q

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

A

DOMES

  • Deranged Motility
  • Osmotic
  • Malabsorptive
  • Exudative
  • Secretory
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52
Q

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

A
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53
Q

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

A

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
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54
Q

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

A
  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)
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55
Q

Name the major causes of anaemia (9).

A
  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)
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56
Q

Explain some of the parameters used to assess anaemia.

A
57
Q

Name some principles of a balanced diet.

A
  • 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
58
Q

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

A

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
59
Q

Define the terms prevalence, indicence, epidemic and endemic.

A
  • 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
60
Q

Outline the blood supply, lymphatic drainage of the stomach.

A
  • 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
61
Q

List 4 features of granulomatous inflammation.

A

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
62
Q

Name 6 hormones that inhibit gastric secretion/motility.

A
  1. Somatostatin
  2. Prostaglandin E2
  3. Secretin
  4. Cholecystokinin (CCK)
  5. Gastric Inhibitory Peptide (GIP)
  6. Vasoactive Intestinal Peptide (VIP)
63
Q

Explain the stages of gastric secretion.

A
64
Q

Name 8 virulence factors of Helicobacter pylori.

A
  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
65
Q

Outline the treatment approach for peptic ulcers (4).

A
  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
66
Q

Explain the anabolic and catabolic pathways of appetite regulation.

A

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)
67
Q

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

A
68
Q

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

A
  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
69
Q

List the diagnostic criteria for anorexia nervosa and bulemia nervosa.

A

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
70
Q

List the four elements required for informed consent.

A
  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
71
Q

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

A

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
72
Q

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

A

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
73
Q

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

A
  • 2 CO2
  • 3 NADH molecules
  • 1 FADH2 molecule
  • 1 GTP molecule
74
Q

Identify some causes of hypoglycaemia.

A

1. Fasting - EXPLAIN

  • EXogenous drugs
    • Insulin, sulfonylureas
    • Alcohol
  • Pituitary insufficiency
  • Liver failure/inherited enzyme defect
  • Addison’s disease - ↓cortison
  • Islet cell tumours
  • Non-pancreatic neoplasms

2. Reactive

  • Drug-induced
  • Metabolic disease
  • Gastric surgery
75
Q

Name some relations of the pancreas.

A
  • 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
76
Q

Distinguish major features of Diabetes type I and II.

A
77
Q

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

A
78
Q

What is the clinical definition of DKA?

A

Blood glucose > 11 mmol/L

Venous pH < 7.3

Ketonaemia and ketonuria

79
Q

Explain the mechanisms behind some major oral hypoglycaemics.

A
  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
80
Q

List some causes of unconsciousness.

A

AEIOUTIPS

  • Alcohol/drugs
  • Endocrine/electrolytes
  • Insulin
  • Oxygen
  • Uraemia
  • Trauma
  • Infection/intercranial pressure
  • Poison/porphyrins
  • Seizure/stroke/space-occupying lesion/ sub-arachnoid haemorrhage
81
Q

Outline assessment of consciousness using the Glasgow coma scale.

A
82
Q

Explain the physiology of sound conduction (6 steps).

A
  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
83
Q

Distinguish between conductive and sensorineural hearing loss.

A
84
Q

Outline the branching of the airways.

A

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
85
Q

List some causes of tubal obstruction in the body.

A
86
Q

List 8 consequences of tubal obstruction.

A

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
87
Q

Describe the 6 classes of mutation leading to cystic fibrosis.

A
  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)
88
Q

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

A
89
Q

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

A
  • 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’
90
Q

Name some of the muscles involved in inspiration.

A

Principal

  1. External intercostals
  2. Interchondral part of internal intercostals
  3. Diaphragm

Accessory

  1. Sternocleidomastoid
  2. Scalenes
91
Q

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

A
  • Atmosphere: 160, 0.3
  • Alveoli: 100, 40
  • Arteries: 100, 40
  • Veins: 40, 45
92
Q

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

A
  1. reduced pH
  2. increased CO2
  3. increased temperature
  4. increased bisphosphoglycerate
93
Q

List some respiratory and non- respiratory causes of hypoxaemia.

A

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
94
Q

Identify some causes of asthma.

A

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
95
Q

Describe 6 airway changes involved in asthma.

A
  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
96
Q

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

A
97
Q

List the five clinical steps involved in smoking cessation.

A
  1. Ask
  2. Assess
  3. Advise
  4. Assist
  5. Arrange/follow up
98
Q

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

A
  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
99
Q

Outline the three shunts involved in foetal circulation.

A
  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
100
Q

List some social determinants of health.

A
  • 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
101
Q

List the layers of the heart.

A
  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
102
Q

Outline the transport of lipids.

A
103
Q

Outline the clotting cascade.

A
104
Q

Name the four steps in haemostasis.

A
  1. Vasoconstriction/Spasm
  2. Platelet Plug Formation
  3. Blood Coagulation – The Clotting Cascade
  4. Restoration of Normal Bloodflow
105
Q

Outline the fibrinolytic cascade.

A
106
Q

Outline three risk factors for thrombosis.

A
  1. Endothelial injury – atherosclerosis, hypertensive damage, MI
  2. Abnormal Bloodflow – stasis, turbulence, hyperviscosity
  3. Blood Hypercoagulability – primary (genetic), secondary (acquired changes in clotting factors)
107
Q

Outline the pathogenesis of atherosclerosis.

A
  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.

108
Q

Outline an approach for acute treatment of myocardial infarction.

A
  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
109
Q

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

A
110
Q

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

A
111
Q

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

A
112
Q

List some ways in which a physician can be impaired.

A
  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
113
Q

Name some anterior and posterior relations of the kidney.

A

Anterior Relations

  • Liver
  • Duodenum
  • Jejunum
  • Colon
  • Stomach
  • Pancreas

Posterior Relations

  • Diaphragm
  • Psoas Major
  • Quadratus Lumborum
  • Transversus abdominus (aponeurosis)
  • Subcostal nerves & vessels
  • Iliohypogastric & ilioinguinal nerves
114
Q

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

A
  1. Abdominal Aorta
  2. Renal Arteries
  3. Segmental Arteries
  4. Interlobar Arteries
  5. Arcuate Arteries
  6. Interlobular Arteries
  7. Afferent Arterioles
  8. Glomerulus
115
Q

List some major functions of the kidney.

A
  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
116
Q

List the layers of the glomerular filter.

A
  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
117
Q

Describe the regulation of GFR.

A

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
118
Q

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

A
  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)
119
Q

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

A
120
Q

List causes of primary and secondary hypertension.

A

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
121
Q

List seven risk factors for hypertension.

A
  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
122
Q

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

A
  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
123
Q

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

A
124
Q

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

A

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
125
Q

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

A
  • 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
126
Q

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

A
  • Transport of NaCl (inhibited by thiazide diuretics)
  • Ca2+ reabsorption (stimulated by parathyroid hormone)
127
Q

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

A
128
Q

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

A
  • Permeability to H2O is controlled by ADH (vasopressin) by changing the number of surface AQP2 channels (aquaporins)
  • Passive movement of urea
129
Q

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

A
  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
130
Q

Explain nephrotic and nephritic syndromes.

A

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
131
Q

Outline some causes of renal renal failure?

A
132
Q

What is the clinical definition of renal failure?

A
  • >50% decrease in GFR (over the period of hours to days)
  • ± ↑ Nitrogenous wastes in body (BUN – blood urea nitrogen)
  • ± ↓ in urine output (oligouria/anuria)
133
Q

Describe the three phases of acute tubular necrosis.

A
  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
134
Q

List some consequences of ARF.

A
  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
135
Q

Name three sites of constriction of the ureters.

A
  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
136
Q

Outline the nervous control of micturition.

A

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
137
Q

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

A
  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.
138
Q

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

A
  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.

Kitty - Past Papers & Practice Qs (12 decks)

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