Concise Flashcards Sem 1

Question

Outline the process of lymphocyte production and maturation.

Answer 1

**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

Answer 2

**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)

Answer 3

**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)

Answer 4

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

Answer 5

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

Answer 6

Spiral valve/ valve of Hesler

Answer 7

* **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)

Answer 8

_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

Answer 9

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

Answer 10

**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

Answer 11

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)

Answer 12

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)

Answer 13

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

Answer 14

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

Answer 15

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

Answer 16

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

Answer 17

_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

Answer 18

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)

Answer 19

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)

Answer 20

* **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

Answer 21

**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

Answer 22

* **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

Answer 23

* **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

Answer 24

_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**

Answer 25

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

Answer 26

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

Answer 27

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

Answer 28

**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)

Answer 29

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

Answer 30

**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

Answer 31

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

Answer 32

_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

Answer 33

**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

Answer 34

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

Answer 35

**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

Answer 36

* **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

Answer 37

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

Answer 38

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

Answer 39

**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

Answer 40

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

Answer 41

**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

Answer 42

_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

Answer 43

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)

Answer 44

* **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’

Answer 45

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

Answer 46

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

Answer 47

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

Answer 48

_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

Answer 49

_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

Answer 50

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

Answer 51

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

Answer 52

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

Answer 53

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

Answer 54

* 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

Answer 55

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

Answer 56

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

Answer 57

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

Answer 58

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.

Answer 59

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

Answer 60

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

Answer 61

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

Answer 62

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

Answer 63

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

Answer 64

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

Answer 65

**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

Answer 66

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)

Answer 67

**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

Answer 68

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**

Answer 69

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

Answer 70

**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

Answer 71

* 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

Answer 72

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

Answer 73

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

Answer 74

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

Answer 75

**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

Answer 76

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

Answer 77

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

Answer 78

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

Answer 79

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

Answer 80

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

Answer 81

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.

Answer 82

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.