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Phase 2a > HT Endocrine > Flashcards

HT Endocrine Flashcards

1
Q

What are the properties of peptide hormones? How do they work?

A
  • Made from short-chain amino acids (size is anything from few AAs to small protein) - Pre-Made and stored in cell, released and dissolved into blood when needed - Large, hydrophilic, charged molecules - cannot diffuse through a plasma membrane - Bind to receptors on cell membranes, triggering a second messenger to be released within cell - very quick - Examples: Insulin, growth hormone, TSH, ADH
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2
Q

What are the properties of steroid hormones? How do they work?

A
  • Synthesised from cholesterol - Not stored in cell, released as soon as they are Made - Not water soluble - must be bound to transport proteins to travel in blood - Lipid soluble - can cross plasma membrane and Bind to receptor inside cell - slow response - Examples: Testosterone, oestrogen, cortisol
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3
Q

Tell me about catecholamine hormones (amino acid derived)

A
  • Synthesised from the amino acid tyrosine - Acts same way as peptide hormone - Large, hydrophilic, charged molecules - cannot diffuse through a plasma membrane, so released via exocytosis - Examples: Adrenaline, thyroxine
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4
Q

Where is Broca’s area? What is its function?

A
  • Left frontal lobe, Brodmann‚Äòs area 44 and 45 - Language production
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5
Q

Where is Wernicke’s area? What is its function?

A
  • Left (usually) temporal lobe, Brodmann’s area 22- Perception of language
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6
Q

What are the layers of brain covering?

A
  • Skin - Bone - Dura mater - Arachnoid mater - (Subarachnoid space) - Pia mater
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7
Q

What is the function of the proximal convoluted tubule?

A

Reabsorption of: - some water and Na+ - some other ions - all glucose and amino acids

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8
Q

What is the function of the distal convoluted tubule?

A
  • Regulating acid-base balance - By secreting H+ and absorbing HCO3- - Also regulates Na+ level
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9
Q

What is the structure of the collecting duct in the kidney?

A

Principal cells: - Regulate Na+ reabsorption and K+ excretion - Respond to aldosterone and ADH Intercalated cells: - Exchange H+ for HCO3-

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10
Q

What is the structure of urothelium?

A
  • Complex stratified epithelium - Can stretch in 3 dimensions - Layer of umbrella cells - make it urine proof
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11
Q

Describe the drug metabolism of aspirin

A

Phase I: - Hydrolysis reaction: Aspirin + H2O —> Salcylic acid + Ethanoic acid Phase II: - Conjugated with glycine or glucuronic acid - Forms a range of ionised products which can be excreted

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12
Q

What is the metabolism reaction of alcohol

A

ADH alcohol dehydrogenase ALDH aldehyde dehydrogenase

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13
Q

What is the innervation of bladder contraction?

A
  • Autonomic parasympathetic (cholinergic) - S3-S5 nuclei - Drive detrusor contraction
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14
Q

What is the innervation of bladder relaxation?

A
  • Autonomic sympathetic (noradrenergic) - T10-L2 nuclei - Urethral contraction (smooth muscle component but remember the main part of the sphincter is skeletal muscle) - Inhibits detrusor contraction
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15
Q

What is the innervation of A-δ fibres (bladder stretch) and C fibres (bladder pain)?

A
  • Sensory Autonomic - S2-S4 nuclei
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16
Q

What are the cell types and their functions within the islets of langerhans in the pancreas?

A

Alpha cells - produce glucagon Beta cells - produce insulin and amylin Delta/D cells - produce somatostatin PP cells - produce pancreatic polypeptide

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17
Q

What are the classes of hormones?

A
  • Steroids - Peptides - Thyroid hormones - Catecholamines
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18
Q

Tell me about thyroid hormones üòé

A
  • released via proteolysis - T3 triiodothyronine, T4 thyroxine - Take a day to act - in blood bound to thyroglobulin binding protein (produced By liver)
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19
Q

What is the blood supply to the thyroid gland?

A
  • Superior Thyroid artery - off thyrocervical trunk (subclavian) - Inferior Thyroid artery - off external carotid artery
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20
Q

Where are the thyroid and parathyroid glands located?

A
  • Thyroid gland sits at C5-T1 - Two lobes connected by an isthmus - Parathyroid is 4 glands on the posterior surface of thyroid glands
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21
Q

What effect does parathyroid hormone have on the kidneys?

A
  • Increased conversion of 25-hydroxyvitamin D (inactive) to 1,25-dihydroxyvitamin D(active) - At the DCT: Increased Ca2+ reuptake and PO43- excretion
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22
Q

What effect does parathyroid hormone have on the gut?

A

Increased Ca2+ and PO43- absoroption

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23
Q

What hormones does the adrenal gland produce?

A

Adrenal cortex: - Zona glomerulosa - mineralocorticoids (eg: aldosterone) - Zona fasciculata - glucocorticoids (eg: cortisol) - Zona reticularis - adrenal androgens Adrenal medulla: - Catecholamines (eg: adrenaline)

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24
Q

Pathophysiology of T2DM

A
  • Peripheral Insulin resistance with partial Insulin deficiency - Decreased GLUT4 expression - impaired Insulin secretion - Lipid and beta amyloid deposits in pancreas, progressive b cell damage
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25
Q

Epidemiology of T2DM

A
  • Presents later on in life (usually 30+ years) - Males > females - People of Asian, African and Afro-Carribean ethnicity are 2-4x more likely to develop T2DM than white people
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26
Q

Clinical presentation of T2DM

A
  • Obese hypertensive older patient - Polydipsia - Nocturia - Polyuria - Glycosuria - Recurrent thrush
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27
Q

Diagnosis of T2DM

A
  • same as T1DM - Prediabetes exists this time
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28
Q

Risk factors for T2DM

A
  • Genetic link (stronger than T1DM) - Obesity - Alcohol excess - Hypertension - Gestational diabetes - PCOS - Drugs: corticosteroids, thiazides
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29
Q

Last line of treatment for T2DM if all else fails

A

Insulin treatment

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30
Q

Treatment for T2DM

A

Initial: Biguanide (metformin) Second line: Carry on Metformin and add either: - DPP-4 inhibitor - Pioglitazone - Sulfonylurea - SGLT-2 inhibitor

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31
Q

Epidemiology of Diabetic Ketoacidosis

A

4% of T1DM patients develop each year

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32
Q

Risk factors for DKA

A
  • Poorly managed/undiagnosed T1DM - Infection/illness - Characteristic in patients around 20 years old
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33
Q

Pathophysiology of DKA

A
  • Absolute immune deficiency unrestrained lipolysis and gluconeogenesis and Decreased Peripheral glucose uptake - Not all glucose from gluconeogenesis is usable so converted to ketone bodies, which is acidic
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34
Q

Describe Kussmaul’s breathing

A

Deep and rapid breathing in acidosis to expel acidic carbon dioxide

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35
Q

Signs of DKA

A
  • Kussmaul’s breathing - Pear drop breath - Reduced tissue turgar (hypotension + tachycardia)
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36
Q

How to investigate DKA

A
  • Ketones > 3mmol/L - RPG > 11.1mmol/L (hyperglycemic) - pH < 7.3 or HCO3- < 15mmol - Urine dipstick glyosuria/ketonuria
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37
Q

What are common differentials of DKA?

A
  • HHS - Lactic acidosis - identical presentation, normal serum glucose and Ketones - Starvation ketosis - physiologically appropriate lipolysis
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38
Q

Treatment for DKA (in order)

A
  • ABCDE - IV fluids FIRST 0.9% saline - IV insulin 0.1units/kg/hour - once glucose level <14mmol add 10% glucose - Restore electrolytes, eg: K+
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39
Q

Lateral corticospinal tract

A
  • Supplies limbs - Fine motor movement - Decussates at medulla
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40
Q

Ventral corticospinal tracts

A
  • Supplies trunk (proximal muscles) - Decussates at level of effector muscle - Also motor movement
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41
Q

Corticobulbar tract

A

Head and neck via cranial nerves

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42
Q

Symptoms of HHS

A
  • Generalised weakness and leg cramps - Confusion, lethargy, hallucinations, headaches - Visual disturbance - Polyuria and Polydipsia - Nausea, vomiting and abdo pain (more common in DKA)
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43
Q

Epidemiology of HHS

A
  • Less than 1% of diabetes admissions - 5-15% mortality Risk factors: - Infection - MI - Poor medication compliance
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44
Q

Pathophysiology of HHS

A
  • Rise in counter-regulatory hormones (glucagon, Ad, cortisol, GH) - Causes hyperglycaemia ans hyperosmolality - Electrolytes in blood overflow into urine -> excessive loss of water and electrolytes
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45
Q

Characteristics of HHS

A
  • Marked hyperglycaemia - hyperosmolality - Profound dehydration - Electrolyte abnormalities
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46
Q

Diagnosis of HHS

A

Diagnostic: - Hyperglycaemia ‚â•30mmol/L without a metabolic acidosis or significant ketonaemia - Hyperosmolality ‚â•320mOsmol/kg - Hypovolaemia Other tests: - Urine dipstick: heavy glycosuria - U+E: low total body K+, high serum K+

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47
Q

How can HHS be differentiated from Diabetic ketoacidosis?

A

DKA - T1DM - Patients younger and leaner - Ketoacidosis - Develops over hours to a day HHS - T2DM - No ketoacidosis - Significantly higher mortality rate - Develops over a longer time - days to a week

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48
Q

Treatment of HHS

A
  • IV fluid 0.9% saline - IV insulin only if there is ketonaemia or IV fluids aren’t working - LMWH to anticoagulate patient as they have thicker blood - Electrolyte loss (K+)
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49
Q

What are complications of HHS treatment with insulin?

A
  • Insulin-related hypoglycaemia - Hypokalaemia
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50
Q

What structures are in the cavernous sinus?

A

(OTOMCAT) - Oculomotor nerve - Trochlear nerve - Ophthalmic division of trigeminal nerve - Maxillary division of trigeminal nerve - Carotid artery - Abducens nerve

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51
Q

DCML tract

A
  • Ascending (sensory) - Dorsal root -> medulla, then decussates - Fine touch, vibration and proprioception
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52
Q

Spinothalamic tract

A
  • Ascending (sensory) - Decussates at spine 1-2 levels above dorsal entry - Pain, temperature, crude touch - Anterior - trunk - Posterior - limbs
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53
Q

Brown sequard syndrome

A
  • Ipsilateral DCML loss - decussate at medulla - Ipsilateral corticospinal loss - decussate at medulla - Contralateral spinothalamic loss - decussate at spinal cord (1-2 levels above)
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54
Q

Blood supply to the pituitary gland

A
  • Anterior - Superior hypophyseal artery - Posterior - Inferior hypophyseal artery the hypothalamophyseal portal system is a branch of the internal carotid artery
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55
Q

Steps of acute inflammation

A
  • Increased vessel calibre - inflammation cytokines (bradykinin, prostacyclin, NO) mediate vasodilation - fluid exudate - vessels become leaky, fluid forced out of vessel - Cellular exudate - abundant in neutrophils
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56
Q

5 cardinal signs of acute inflammation

A
  • Rubor (redness due to dilation of small vessels) - Dolor (pain) - Calor (heat) - Tumor (swelling from oedema or a physical mass) - loss of function
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57
Q

Causes of acute inflammation

A
  • Microbial infections - Hypersensitivity reactions - physical agents - Chemicals - Bacterial toxins - Tissue necrosis
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58
Q

Neutrophil action in acute inflammation

A
  • Margination - migrate to edge of blood vessel (plasmatic zone) due to increase in plasma viscocity and slow flow - Adhesion - selectins Bind to neutrophil, cause rolling along the blood vessel margin - Emigration + diapedesis - movement out of blood vessel through or inbetween endothelium onto basal lamina and then vessel wall - Chemotaxis - site of inflammation
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59
Q

Neutrophil action at the site of inflammation

A
  • Phagocytosis - Phagolysosome + Bacterial killing - Macrophages clear debris
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60
Q

Outcomes of acute inflammation

A
  • Resolution - normal - Supporation - pus formation - Organisation - granulation tissue + fibrosis - Progression - excessive recurrent inflammation -> becomes chronic and fibrotic tissue
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61
Q

Chronic inflammation

A
  • Subsequent and prolonged response to Tissue injury - Lymphocytes, Macrophages and plasma cells - Longer onset, long lasting effects - Autoimmune diseases
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62
Q

Causes of chronic inflammation

A
  • resistance of infective agent - Endogenous + materials - Autoimmune conditions - Primary granulomatous diseases - Transplant rejection
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63
Q

Macroscopic appearance of chronic inflammation

A
  • Chronic ulcer - Chronic abscess cavity - granulomatous inflammation - fibrosis
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64
Q

Microscopic appearance of chronic inflammation

A
  • Lymphocytes, plasma cells and Macrophages - exudate is Not a common feature - Evidence of continuing destruction - Possible Tissue necrosis
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65
Q

Cellular cooperation in chronic inflammation

A
  • B lymphocytes - transform into plasma cells and produce antibodies - T lymphocytes - responsible for cell-mediated immunity - Macrophages - respond to chemotactic stimuli, produce cytokines (interferon alpha and beta, IL1, IL6, IL8, TNF-alpha)
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66
Q

What are granulomas?

A
  • An aggregate of epithelioid histocytes (macrophages) - Granuloma + eosinophil -> parasite - Secrete ACE as a blood marker
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67
Q

Types of granulomas

A
  • Central necrosis - TB (identified by Ziel-Neelsen stain) - No central necrosis - sarcoidosis, leprosy, vasculitis, Crohn’s disease
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68
Q

What is thrombosis?

A

Solidification of blood constituents (mostly platelets) forming in vessels

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69
Q

Platelets

A
  • NO nucleus, arise from megakaryocytes - Contain alpha granules (Adhesion) and dense granules (aggregation) - Contain lysosomes - Activated, releasing their granules when they come into contact with collagen - Activation forms thrombus in intact vessels
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70
Q

Thrombosis formation (primary platelet plug)

A
  • Platelet aggregation, starts the coagulation cascade - Positive feedback loops
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71
Q

Causes of thrombosis (Virchow’s triangle, typically 2 out of these 3)

A
  • Endothelial injury (trauma, surgery, MI, smoking) - Hypercoagulability (sepsis, atherosclerosis, COCP, preggomalignancy) - Decreased blood flow (AF, immobility)
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72
Q

Arterial thrombosis

A
  • By atherogenesis and plaque rupture - High pressure, low pulse - Thin cool Skin, intermittent claudication - Mainly Made of platelets - so treat with antiplatelet (aspirin)
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73
Q

Venous thrombosis

A
  • Caused By venous stasis - low pressure, High pulse - Rubor, tumour and pain - Mainly fibrin - so treated By anticoagulants (DOACs, warfarin)
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74
Q

Fate of thrombi

A
  • Resolution (dissolves and clears, normal/best case scenario) - Organisation (leaves scar tissue, slight narrowing of vessel lumen) - Recanalisation (intimal cells may proliferate, capillaries may grow into the thrombus and fuse to form larger vessels) -
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75
Q

Formation of the secondary platelet plug (coagulation cascade)

A

Prothrombin -> thrombin Fibrinogen -> fibrin

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76
Q

What is an embolism

A

A mass of material in the vascular system able to block in a vessel and block its lumen

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77
Q

Arterial vs venous embolism

A

Arterial - Lodges in systemic circulation (from left heart) - eg: AF thrombus lodges in carotid artery -> ischaemic stroke Venous - Lodges in pulmonary circulation (from right heart) - eg: DVT thrombus embolises and lodges in pulmonary artery -> pulmonary embolism

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78
Q

Ischaemia

A
  • the reduction in blood flow to a Tissue or part of the body Caused By constriction or blockage of the blood vessels supplying it - effects can be reversible - Brief attack - Cardiomyocytes and cerebral neurons are most vulnerable
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79
Q

Infarction

A
  • the necrosis of part of the whole of an organ that occurs when the artery supplying it becomes obstructed- usually macroscopic - Reperfusion injury damage to Tissue during reoxygenation
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80
Q

What organs are susceptible to infarcts?

A
  • most organs as they only have a single artery supplying them - liver, brain and lungs are Less susceptible as they have a dual supply
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81
Q

What is atherosclerosis?

A
  • Fibrolipid plaques forming in the intima and media of systemic arteries - more in High pressure arteries, eg: aorta and bifurcations
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82
Q

What is in an atherosclerotic plaque?

A
  • Lipids (cholesterol) - Smooth muscle - Macrophages (+foam cells) - Platelets - Fibroblasts
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83
Q

What are foam cells?

A

Macrophages that phagocytose LDLs

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84
Q

Atherosclerosis formation

A

NAME?

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85
Q

Risk factors for atherosclerosis

A
  • Smoking - High bp - Hyperlipidemia - Increasing age - Male - Poorly controlled diabetes mellitus (all risk factors for MI!!)
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86
Q

Complications of atherosclerosis

A
  • cerebral infarction - carotid atheroma, leading to TIAs and cerebral infarcts - MI - Aortic aneurysm - Peripheral vascular disease - Gangrene - Cardiac failure - Ischaemic collitis in colon
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87
Q

Preventative measures for atherosclerosis

A
  • smoking cessation - blood pressure control - Weight reduction - low dose aspirin - Statins - control diabetes
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88
Q

What is apoptosis?

A
  • Non-inflammatory, controlled cell death in single cells - cells shrink, organelles retained, CSM intact - Chromatin unaltered, fragmented for easy Phagocytosis
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89
Q

What is necrosis?

A
  • Induces inflammation and repair, traumatic cell death - cells burst, organelles splurge, CSM damaged - Chromatin altered, cell is f*cked
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90
Q

Intrinsic apoptosis mechanism

A
  • Bax is a protein, inhibited by BCl-2 - It acts on mitochondrial membrane to promote cytochrome C reusase - This activates caspases
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91
Q

Extrinsic apoptosis mechanism

A

Fas-L or TNF-L binds to CSM receptors which activate caspases

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92
Q

Cytotoxic apopstosis mechanism

A
  • CD8+ binding releases Granzyme B from CD8+ cells - Granzyme B -> Perforin -> Caspases
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93
Q

Types of necrosis

A

Coagulative, liquifactive, caseous and gangrene

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94
Q

Coagulative necrosis

A
  • most common type - can occur in most organs - Caused By ischaemia
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95
Q

Liquefactive necrosis

A

Occurs in the brain due to its lack of substantial supporting stroma

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96
Q

Caseous necrosis

A
  • Causes a cheese pattern - eg: TB
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97
Q

Gangrene

A
  • necrosis from rotting of the Tissue - Affected Tissue appears black due to deposition of iron sulphide from degraded haemoglobin
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98
Q

What is inflammation?

A

Acute/chronic tissue injury response

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99
Q

What are polymorphs?

A
  • What neutrophils are referred to as sometimes - Because they have a varying number of lobulated nuclei
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100
Q

What is hypertrophy?

A
  • increase in cell size without cell division - eg: skeletal muscle
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101
Q

What is hyperplasia?

A
  • increase in cell number By mitosis - eg: Bone marrow at High alititudes, prostate at older age
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102
Q

What is atrophy?

A
  • Decrease in tissue/organ size caused by a decrease in the number or size of constituent cells - eg: brain in Alzheimer’s, muscular atrophy in ALS
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103
Q

What is metaplasia?

A
  • The change in differentiation of a cell from one fully-differentiated cell type to another - eg: GORD (squamous -> columnar epithelia)
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104
Q

What is dysplasia?

A

Morphological changes seen in cells in the progression to becoming cancer

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105
Q

What is carcinogenesis?

A

Transformation of normal cells to neoplastic (malignant) cells through permanent genetic alterations or mutations

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106
Q

What is a neoplasm?

A

An autonomous, abnormal and persistent growth

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107
Q

What is a tumour?

A

Any abnormal swelling; neoplasm, inflammation, hypertrophy, hyperplasm

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108
Q

What can a neoplasm arise from?

A
  • Nucleated cells - So can’t arise from erythrocytes but can arise from their precursor
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109
Q

Properties of benign tumours

A
  • Non-invasive - Localised - slow growth rate, low mitotic activity - Close resemblance to normal Tissue - Well circumscribed - Rare necrosis and ulceration - growth on mucosal surfaces - Often exophytic (outward growth)
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110
Q

Properties of malignant tumours

A
  • invasive - Rapid growth rate, High mitotic activity - Poorly defined + irregular border - Hyperchromatic and pleomorphic nuclei - common necrosis and ulceration - growth on mucosal surfaces and Skin - Often endophytic (inward growth)
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111
Q

Complications of benign tumours

A
  • Hormone secreting (eg: prolactinoma) - Pressure on local structures (eg: pituitary -> optic chiasm) - Obstruct flow - Transformation to malignant neoplasm - Anxiety
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112
Q

Complications of malignant tumours

A
  • all of the issues of benign tumours + - Destroy surrounding Tissue - Metastasise (spread around the body) - blood loss from ulcers - pain - Paraneoplastic (eg: SCLC, SIADH) - form Secondary tumours
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113
Q

Benign epithelial neoplasms

A
  • Papilloma - Non-glandular, Non-secretory, eg: squamous cell Papilloma - Adenoma - glandular, secretory, eg: colonic Adenoma
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114
Q

Malignant epithelial neoplasms (carcinomas)

A

eg: urothelial carcinoma glandular epithelium -> adenocarcinoma

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115
Q

Benign connective tissue neoplasm

A
  • Lipoma - adipocytes - Chondroma - cartilage - Osteoma - Bone - Angioma - vascular - Rhabdomyoma - striated muscle (Rare) - Leiomyoma - smooth muscle (more common) - Neuroma - nerves
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116
Q

Malignant connective tissue neoplasms

A

Same as benign ones, but followed by ‘sarcoma’ instead of ‘myoma’

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117
Q

What is a tumour called where the cell origin is unknown?

A

Anaplastic

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118
Q

Lymphoid tumours (always malignant)

A
  • Leukemia, lymphoma - Need to be treated By systemic chemotherapy
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119
Q

Other tumours

A
  • Melanoma (melanocyte malignancy) - Mesothelioma (mesothelial malignancy - typically pleural) - Teratoma - cancer of all 3 embryonic germ layers - Blastoma - embryonal tumours
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120
Q

Eponymously named tumours

A
  • Burkitt’s lymphoma (B cell malignany cause by EBV) - Kaposi sarcoma (vascular endothelial malignancy, HIV associated) - Ewing’s sarcoma (bone malignancy)
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121
Q

Tumour differentiation grading

A
  • Graded based on similarity to parent cell 1. >75% cells resemble parent - well differentiated 2. 10-75% 3. <10% cells resemble parent - poorly differentiated
122
Q

Characteristics of the neoplastic cell

A
  • Autocrine growth stimulation (overexpression of GF and mutation of tumour suppressor genes, eg: P53, and underexpression of growth inhibitors) - Evasion of apoptosis - Telomerase - prevents shortening of telomeres with each replication
123
Q

Classes of carcinogens

A
  • Chemical - eg: paints, dyes, rubber, soot - Viruses - eg: EBV, HPV - Ionising and Non-Ionising radiation - eg: UVA and UVB, Ionising radiation - hormones, parasites, mycotoxics - eg: High oestrogen, anabolic Steroids - Misc - eg: asbestos, arsenic
124
Q

Host factors for cancer

A
  • Race - Diet - age - Gender - Inheritance - Premalignant lesions - Transplacental exposure
125
Q

Metastasis pathway

A
  1. Detachment of tumour cell 2. Invasion of surrounding connective tissue 3. Intravasation into blood vessels 4. Evasion of host defence mechanisms 5. Adherance to endothelium at a remote location 6. Extravasation to distant site 7. Angiogenesis - growth of own blood supply
126
Q

Methods of cancer spread

A
  • Haematogenous - via blood, Bone, breast, lung, liver - Lymphatic - Secondary formation in lymph nodes - Transcolemic - via exudative fluid accumulation, spread through pleural, pericardial, peritoneal effusions
127
Q

Method of spread for sarcomas

A

Mostly haematogenous

128
Q

Method of spread for carcinomas

A
  • Mostly Lymphatic - Exceptions: follicular Thyroid, choriocarcinoma, RCC, HCC
129
Q

Tumour staging

A
  • spread determined By histopthological and clinical examination - TNM: Primary tumour, lymph node, metastases - Different for leukemias, lymphomas and CNS cancers
130
Q

Screening in the UK

A
  • Cervical cancer (Cervical swab test) - breast cancer (mammogram) - Colorectal cancer (fecal occult) - Heel prick test at birth for sickle cell, CF and hypothyroid
131
Q

Mutation involved in colorectal cancer

A
  • FAP (familial adenamatous polyposis) - HNPCC (lynch syndrome)
132
Q

FAP

A
  • Autosomal dominant - Mutated APC (adenomatous polyposis coli) gene, millions of colorectal adenomas inevitable - Adenocarcinoma by 35 years old - Overexpression of x-MYC and point mutation in KRAS
133
Q

HNPCC

A
  • Autosomal dominant - Mutated MSH gene - Involved in DNA mismatch repair
134
Q

Which tumours are most likely to metastasise via bone?

A

Breast Lung/lymphoma Thyroid Kidney Prostate …and multiple myeloma

135
Q

Primary lymphoid organs

A
  • Bone marrow - origin of all immune cells, b cell maturation site - Thymus - T cell maturation site, thymic tolerance
136
Q

Secondary lymphoid organs

A
  • lymph nodes - site of DC, b and T cell interactions - Spleen - RBC recycling, encapsulated Bacterial cell killing
137
Q

Tertiary lymphoid organs

A
  • Pathological - Germinal centres of rapidly proliferating Lymphocytes
138
Q

Innate immunity

A
  • Non-specific - Rapid - Already active (little Activation needed) - NO memory - short duration - killing usually via complement Activation - mediated By neutrophils and Macrophages
139
Q

Adaptive immunity

A
  • specific - slow - Needs Activation - have memory - killing usually antibody mediated - main cells are T, b and plasma cells - long lasting
140
Q

Examples of physical barriers

A
  • Skin - Mucus - Cilia
141
Q

Examples of chemical barriers

A
  • Lysozyme in tears - Stomach acid
142
Q

Compliment pathways

A
  • Classical - Lectin - Alternate
143
Q

Compliment system destroys foreign bodies by…

A
  • Direct lysis - Membrane attack complex formation - Opsonisation - Increased phagocytosis via protein C3b - Inflammation - Macrophage chemotaxis via proteins C3a and C5a
144
Q

Innate cells - neutrophils

A
  • Key mediator of acute inflammation - IL8 chemokine - 70% of all leukocytes - Act in hours-days - Express CD66 receptor (common for all granulocytes)
145
Q

Innate cells - macrophages

A
  • Act over months-years (typically chronic) - Phagocytosis, antigen presenting and cytokine secreting (TNF-a, IL1 and IL12) - Express CD14+ and CD40+ - Can be circulating or resident (eg: Kuppfer cells, alveolar macrophages) - Clear apoptotic debris
146
Q

Innate cells: eosinophils

A
  • Release major basic protein - Seen in parasitic infections
147
Q

Innate cells: basophils

A
  • Circulate mast cells - Secrete serotonin and heparin - Important in asthma, anaphylaxis, atopic dermatitis and hay fever
148
Q

Innate cells: mast cells

A
  • Important in parastic infections and allergic reactions - Activate type 1 hypersensitivity: IgE crosslinking -> degranulation -> histamine release - Fixed at tissues at mucosal surfaces
149
Q

Innate cells: natural killer cells

A
  • In blood and tissues - Express CD16+ - Antibody-dependent cellular cytotoxicity - Recognise self and non-self by the presence of MHC-I on cell surfaces - Activation -> degranulation -> perforin -> perforates viral infected cells
150
Q

Non-cellular components of innate immunity

A

Physical and chemical barriers

151
Q

Receptors on innate cells

A
  • Toll like receptors (TLRs) and nod like receptors - respond to PAMPs and DAMPs
152
Q

Which TLRs are intracellular?

A

3, 7, 8, 9 (rest are extracellular)

153
Q

What are antigen presenting cells?

A
  • the interface between innate and adaptive immunity - all present exogenous antigens in the presence of MHCII - best cells for this are dendritic cells - (Macrophages and b-cells Also do this)
154
Q

What do dendritic cells do?

A
  • Present foreign antigens to T helper cells - Stimulates further T helper proliferation - Stimulates B cell production -> antibodies
155
Q

What is formed when a dendritic cell and T helper cell communicate?

A

Immune synapse

156
Q

3 conditions that must be met for antigen presenting cells to function

A
  • receptor binding - Co-stimulation (other molecules Bind after Primary receptor binding) - cytokine Release
157
Q

Adaptive cells: T cells

A
  • Mature in the Thymus - thymic tolerance selects best T cells - T cell never encountering antigen (Not matured in Thymus yet) na√Øve T cell
158
Q

Process of thymic tolerance

A
  • Positive selection - T cells tested to see if they recognise major histocompatability complexes 1 and 2 (selected FOR) - Negative selection - T cells tested to see if they produce an immunological response against MHCs (selected AGAINST) - Allocation
159
Q

Allocation in thymic tolerance

A
  • If interact with MHC1 -> CD8+ cells (cytotoxic, kill) - If interact with MHC2 -> CD4+ cells (helper, increase immunity response by activating cells)
160
Q

Adaptive cells: B cells

A
  • maturation and production in the Bone marrow - Any b cells with autoimmunity apoptose
161
Q

Activation of B cells

A
  • APC and interactions between MHC-II activates T helper 2 cells - T helper 2 cell releases IL4 (B cell proliferation) and IL5 (B cell differentiation into plasma cell -> immunoglobulins) - IGs act against specific pathogen present - Somatic hypermutation
162
Q

What do IL4 and IL5 promote class switching to?

A

IL4 - IgA IL5 - IgE

163
Q

IgG

A
  • Most abundant in blood - Highly specific - Key in secondary response - 4 subtypes - Can cross the placenta
164
Q

IgA

A
  • most abundant in total body - Found on mucosal linings, colostrum and breast milk (a dimer)
165
Q

IgM

A
  • FIRST Ig released in adaptive response - b cell mediated - a pentamer
166
Q

IgE

A
  • Least abundant in body - Activates mast cell + basophil degranulation in type 1 hypersensitivity (anaphylaxis)
167
Q

IgD

A

Unknown function, irrelevant

168
Q

Major histocompatability complex

A
  • Also known as human leukocyte antigen (HLA) - On chromosome 6 - Interact with T cells - Confer susceptibility to inherited autoimmune diseases
169
Q

Type 1 hypersensitivity

A
  • Anaphylactic - antigen reacts with IgE bound to mast cells - vasodilation, Increased permeability, bronchoconstriction, facial flush, puritis, swollen tongue and face - eg: atopy: asthma, eczema, hay fever
170
Q

Type 2 hypersensitivity

A
  • Antibody-antigen complex formation üë¥üèª Goodpasture’s Rheumatic fever AHA Myasthenia gravis Pernicious anaemia Anti-TSH (Graves’)
171
Q

Type 3 hypersensitivity

A
  • Antibody-antigen complex deposition üíÉüèª Haemolytic uraemic syndrome and hypersensitivity pneumonitis IgA nephropathy Post-strep glomerulonephritis SLE
172
Q

Type 4 hypersensitivity

A
  • Delayed - T-cell mediated and activated by antigen presenting cells GBS MS üê± Contact dermatitis + coeliac Allopurinol drug reaction Tuberculin skin test and T1DM
173
Q

Assessing vitals in anaphylaxis

A

A - airways - hoarse voice, stridor B - breathing - SpO2 < 94% C - circulation - are they pale, cold, clammy? low BP D - disability - confused, comatose, movemet E - exposure

174
Q

What is immune tolerance?

A
  • Physiological - Central - thymic tolerance - Peripheral - If T/B faulty cell evade central tolerance, they’re dealt with in secondary lymphoid organs
175
Q

What is autoimmunity?

A
  • Phathological response vs self - faulty immune tolerance - Molecularmimickery
176
Q

Organ specific autoimmunity

A
  • T1DM - endocrine pancrease b cells - MS - oligodendrocytes of CNS - Pernicious anaemia - parietal cells of Stomach - Myesthemia gravis
177
Q

Non-organ specific autoimmunity

A
  • Affects DNA, eg: SLE - Affects cell antigens - RBCs -> autoimmune haemolytic anaemia - Platelets - > immune thrombocytopenic purpura - Rheumatoid arthritis
178
Q

Immunodeficiency can be…

A
  • Inherited (defects in T cells), eg: IgA deficiency (north Europe), SCID (death within 2 years) - Acquired, eg: HIV
179
Q

Patterns of immunodeficiency

A
  • Decrease in T helper cells in HIV, PCP pneumonia - B cell deficiency - Complement deficiency (SLE) - Hyposplenism - lack of/decreased function of the spleen ->
180
Q

What are the Pfizer and Biotech Moderna COVID-19 vaccines made from?

A

mRNA

181
Q

What are vaccinations?

A

A form of active immunity

182
Q

Forms of vaccines

A
  • Live attenuated (genetically modified) organism, eg: MMR, BCG, Polio - DNA antigens - Subunit/toxoid vaccines, eg: tetanus, diphteria, cholera - Recombinant vector, eg: Hep b - whole inactivated pathogen, eg: influenza
183
Q

Active immunity natural vs artificial

A

Natural - Body encounters pathogen + produces memory cell after infection Artificial - Vaccine mimics encountering pathogen + stimulates Ig production

184
Q

Passive immunity natural vs artificial

A

Natural - Maternal Igs passed onto feeding baby in breast milk/colostrum Artificial - Antivenom, injection of Ig from another organism

185
Q

Advantages and disadvantages of live attentuated pathogens

A

Advantages: - Full natural immune response - Prolonged protection - Often only single immunisation Disadvantages: - Immunocompromised patients may become infected - Can have outbreak in places with poor sanitation

186
Q

Advantages and disadvantages of whole inactivated pathogens

A

Advantages: - No risk of infection - Storage less critical - Good immune response Disadvantages: - Just activates humoral response (not T cells) - Not full transient infection - Boosters required

187
Q

Advantages and disadvantages of subunit/toxoid vaccines

A

Advantages: - Safe (only parts of pathogen are used) - No risk of infection - Easier to store and preserve Disadvantages: - Less powerful immune response - Repeated vaccinations and edjuvants - Consider genetic heterogeneity of population and choice of antigen

188
Q

Advantages and disadvantages of DNA antigen vaccine

A

Advantages: - Safe, even in immunocompromised patients - No complex storage or transport - Simple drug delivery Disadvantages: - Mild response during boosting - No transient infection

189
Q

Advantages and disadvantages of recombinant vector vaccines

A

Advantages: - Ideal stimulus to immune system - Immunological memory - Flexible Disadvantages: - Can cause illness in compromised individuals - Immune response can regate effectiveness - Requires refridgeration for transport

190
Q

Types of drug administration

A

Systemic - Enteral (GI tract: PO and PR) - Par-enteral (non-GI tract) Local

191
Q

Examples of parenteral drug administration (not via GI tract)

A
  • Intravenous - Intramuscular - Subcutaneous - Inhalers - Sublingual
192
Q

Examples of local drug administration

A
  • Topical - Intranasal - Eye drops - Inhalation - Transdermal
193
Q

What is pharmacodynamics?

A

Action of the drug on the body

194
Q

What is pharmacokinetics?

A

Action of the body on the drug

195
Q

What is an agonist?

A
  • Full affinity - Full efficacy - Mimics endogenous substance eg: Salbutamol is a beta 2 agonist
196
Q

What is an antagonist?

A
  • Full affinity - NO efficacy - Therefore Decrease the Activation of the receptor - can be reversible or irreversible (if covalent bond forms) eg: propanolol is a beta blocker
197
Q

Types of receptor ligands

A
  • Agonists (including partial) - Antagonists - Allosteric modulators
198
Q

What is bioavailability?

A
  • How much of a drug reaches systemic circulation unaltered - IV drugs have a 100% bioavailability as they go straight into systemic circulation
199
Q

What does a competitive antagonist do?

A
  • Binds to the active site - Decreases efficacy reversibly - affinity is unchanged - Ligand concentration is rate limiting eg: naloxone
200
Q

What does a non-competitive antagonist do?

A
  • Binds away from the active site, changing its shape - Decreases efficacy irreversibly - affinity is reduced - Ligand concentration is Not the rate limiting step eg: ketamine
201
Q

Ways drugs cross membranes

A
  • Passive diffusion - Facilitated diffusion - active transport - Endocytosis
202
Q

Factors of pharmacokinetics

A
  • Absorption - Distribution - Metabolism - Elimination
203
Q

First pass metabolism

A
  • The gut and liver metabolise drugs given orally before reaching circulation - Phase 1 and 2 detoxification by the liver - Aims to slightly increase hydrophilicity - By microsomal enzymes, eg: CYP450
204
Q

What does drug distribution depend on?

A

NAME?

205
Q

What drugs can the kidney excrete?

A
  • water soluble Drugs - Not Lipid soluble Drugs
206
Q

How does the liver metabolise drugs to help the kidney?

A
  • Phase 1: Mildly increases hydrophilicity via microsomal enzyme cytochrome p450 - Phase 2: Majorly increases hydrophilicity by conjugation, making the drug polar, eg: acetylation, glucoronidation - Drug becomes water soluble
207
Q

What are inducer drugs

A
  • increase cytochrome P450 activity and speed up Metabolism of other Drugs - May result in sub-therapeutic dose
208
Q

What are inhibitor drugs?

A
  • Decrease cytochrome P450 activity, reduce Metabolism of other Drugs - May result in toxicity - eg: erythromycin, grape juice
209
Q

Examples of inducers

A

PCARBS Phenytoin Carbamazepine Alcohol (chronic use) Rifampicin Barbiturates (St John’s Wort) Sulfonylureas and smoking

210
Q

Examples of inhibitors

A

ODEVICES Omeprazole Disulfiram Erythromycin Valproate Isoniazid Ciprofloxacin Ethanol (acute use) Sulphonamides and SSRIs

211
Q

First order elimination of drugs

A
  • Catalysed By enzymes - rate of Metabolism directly proportional to drug concentration
212
Q

Zero order elimination of drugs

A
  • enzymes saturated By High drug doses - rate of Metabolism is constant - eg: ethanol, phenytoin
213
Q

Allosteric modulators

A
  • increase/Decrease normal Ligand binding - eg: benzodiazepine
214
Q

Non-selective vs selective beta blockers

A
  • Non-selective binds to every single beta adrenergic receptor (1 and 2) - CONTRAINDICATIONS - Selective binds only to a specific subtype of beta adrenergic receptor (eg: cardioselective) - Usually we just say more or less selective rather than categoris
215
Q

Enzymes as drug targets

A

NSAIDS - Inhibit Cox-1 - Prevent arachidonic acid - Decrease prostaglandin production - Risk of GI bleeds due to ulcers as prostaglandins maintain stomach mucosa ACE inhibitors - Inhibit conversion of Angiotensin I -> II - Antihypertensive - Many side effects including hyperkalemia and dry cough

216
Q

Transporters as drug targets

A
  • Mostly ATP dependent - Proton pump inhibitors (eg: omeprazole) cause irreversible inhibition of H+, K+ and ATPase pumps, decreasing pH - Diuretics - Selective serotonin reuptake inhibitors - Tricyclic/tetracyclic antidepressants
217
Q

How does local anaesthesia work

A

Blocks Na+ voltage gated channels

218
Q

Specific vs selective drugs

A
  • specific - act on certain targets - selective - act on subtype of target
219
Q

Neurotransmitter in between synapses in cholinergic pharmacology

A

Always acetylcholine acting on nicotine

220
Q

Ach binding at the nmj

A
  • Autonomic sympathetic nervous system: Noradrenaline working on noradrenergic receptors - Autonomic parasympathetic nervous system: Muscarinic acetylcholine receptors - Somatic nervous system: Acetylcholinergic nicotinic receptors
221
Q

Drugs at the neuromuscular junction

A
  • Botolinum toxin (botox) - Curare (nAch-R antagonist) - Ach-ase inhibitors
222
Q

How does botox work?

A
  • Binds to presynaptic vesicles - Ach Release inhibited - Paralysis
223
Q

How do Ach-ase inhibitors work?

A
  • Inhibit the breakdown of Ach - Increased concentration at the neuromuscular juntion
224
Q

Overstimulation of Ach at the neurmuscular junction

A

Cholinergic crisis Salivation Lacrimation Urination Defacation GI distress Emesis Anything that understimulates Ach does the opposite

225
Q

Parasympathetic (Ach) responses

A
  • Rest + digest - Pupil constricts - Lower heart rate - Bronchoconstritction - Increased GI motility and secretion - detrusor muscle contracts - Penis points (erect)
226
Q

Sympathetic (NAd) response

A
  • Fight or flight - Pupil dilates - Increased heart rate - Bronchodilation - Decreased GI motility and secretion - detrusor muscle relaxes - Penis shoots (ejaculation)
227
Q

Adrenaline formation

A

Tyrosine -> DOPA -> Dopamine -> Noradrenaline -> Adrenaline

228
Q

NAd alpha 1 and 2 receptors

A
  • Vessels + sphincters - Agonism causes: - Vasoconstriction - Bladder contraction - Pupil dilation - (eg: tamsulosin alpha blocker for benign prostatic hyperplasia)
229
Q

NAd beta 1 receptors

A
  • heart - Agonism Causes Increased force of heart contraction - Higher blood pressure - Renin Release
230
Q

NAd beta 2 receptors

A
  • lungs - Agonism Causes Bronchodilation
231
Q

Agonism and antagonism in beta 2 receptors

A

Agonists: Short and long acting beta 2 agonists for asthma Antagonists: Non-selective beta blockers

232
Q

Drug for community acquired pneumonia

A

Antibiotics such as amoxicillin/clarythromycin

233
Q

Drug for HAP

A

Co-amoxiclav (3x daily, 500 or 125mg for 5 days)

234
Q

Drugs for TB (ripe) and their side effects

A

Rifampicin - 6 months - red urine and tears, hep, drug interactions Isoniazid - 6 months - hep, peripheral neuropathy Pyramizinamide - 2 months - hep, arthralgia, rash Ethambutol - 2 months - optic neuritis Give first 2 for 12 months if in CNS

235
Q

What should you take with isoniazid

A

Pyramidine to prevent: - B6 deficiency - Siderobastic anaemia - Peripheral neuropathy

236
Q

Drug for cellulitis

A

High dose oral antibiotic If MRSA, give vancomycin

237
Q

Side effect of trimthoprim

A

Can cause birth defects in the first trimester of pregnancy

238
Q

Treatment for pyelonephritis

A
  • Analgesia: Paracetamol - Antibiotics: Ciprofloxacin or Co-amoxiclav (if pregnant, give cefalexin) - Refer to hospital if there are signs of sepsis
239
Q

Treatment for chlamydia

A
  • FIRST line: doxycycline - if CI or Not tolerated: azithromycin - if CI: erythromycin…or ofloxacin but this is CI in pregnancy - Sexual intercourse should be avoided until treatment is complete - Partner must Also be treated
240
Q

Treatment for gonnorrhoea

A
  • IM ceftriaxone 1g - Refer to GUM clinic
241
Q

Treatment for early syphilis

A
  • Single deep intramuscular dose of benzathine benzylpenicillin - Refer to GUM clinic - Notify all partners in the last 3 months
242
Q

Drug for H.Pylori🧢

A

Clarythromycin Amoxicillin PPI For 7 days

243
Q

Drug for gastroenteritis

A
  • Campylobacter -> clarythromycin - Amoebiasis -> metronidazole and diloxanide - Giardiasis -> tinidazole
244
Q

Drug for C.Difficile

A
  • Vancomycin - 125mg - 4x a day - for 10 days
245
Q

Drug for bacterial meningitis in hospital

A
  • Ceftriaxone (3rd gen cephalosporin) - Cefuroxime if prgenant or under 3 months old - Amoxicillin if listeria suspected - Steroids simultaneously (dexamethasone) within 12 hrs
246
Q

Drug for bacterial meningitis in community

A

Parenteral benzylpenicillin (IV or IM) and then refer to hospital urgently Dosage: - Children < 1: 300mg - Children 1-9: 600mg - Adults and children 10+: 1200mg

247
Q

Drug for infective endocarditis

A

Antibiotics

248
Q

Types of pain

A
  • Acute (nociceptive) - Cancer - Neuropathic (nerve pain) - Chronic non-cancer (3+ months)
249
Q

Possible categories for adverse drug reaction reporting:

A

Augmented - is the pain predictable/common? Bizarre - is there a chance of allergy? Chronic - has patient been using the drug for a long time? Delayed - has patient used drug in the past? End of use - is the patient withdrawing from the drug?

250
Q

Things that affect drug absorption

A
  • Acidity (eg: PPI), ionised drugs can‚Äôt cross phospholipid bilayer - Motility (eg: erythromycin) - Solubility
251
Q

Types of opioids

A
  • Naturally ocurring from the poppy - morphine + codeine - Modification - diamorphine (heroin), oxycodone, dihydrocodeine - Synthetic opioids - eg: pethidine
252
Q

What do opioids act on?

A
  • CNS + GI tract receptors - Resp centres of the brain (pontine)
253
Q

Side effects of opioids

A
  • Addiction - Constipation - Nausea and vomiting - Respiratory distress/depression
254
Q

Tolerance vs dependance

A
  • tolerance - Physiological, body has gotten used to a certain amount of drug, desensitisation - Dependance - Physcological, craving euphora
255
Q

Treatment for opioid induced respiratory depression

A
  • naloxone (competitive opioid inhibitor) - IV is fastest route
256
Q

Types of anticoagulants

A
  • warfarin - Direct oral anticoagulation - Thrombolytics - LMWH (low molecular Weight heparin)- Antiplatelets (aspirin, clopidogrel)
257
Q

What to give a patient bleeding on Warfarin?

A

Vitamin K

258
Q

How to NSAIDs decrease inflammation?

A

By inhibiting Cox2

259
Q

Side effects of ACE inhibitors

A
  • High bradykinin accumulation in lungs Causes dry caugh (switch to ARB) - Dilutes afferent arteriole/glomerulus, can cause AKI due to low GFR
260
Q

Side effects of PPIs

A

Prolonged use can increase fracture risk

261
Q

Dopamine agonists and antagonists

A
  • Agonists, used in prolactinoma, acromegaly and early in Parkinson’s - Antagonists often for nausea and vomiting (eg: metoclopramide, antiemetic) + for psychiatric disorders (eg: haloperidol)
262
Q

Where are DA receptors mostly found?

A

Nucleus accumbens in brain

263
Q

GABA

A
  • Main inhibitory CNS neurotransmitter - Agonists - benzodiazepines (eg: lorazepan and diazepan) - Anxiety, sleep disorders, alcohol withdrawal, status epilepticus,
264
Q

H1 and H2 antagonists

A
  • H1: For allergy (T1 IgE anaphylaxis), eg: loratidine - H2: 2nd line for GORD/high acid reflux after PPI, eg: ranitidine, cimetidine
265
Q

Glutamate

A

Main excitatory CNS neurotransmittor

266
Q

Drug factors that influence drug interactions

A
  • Solubility - Narrow therapeutic index:
267
Q

Factors that affect drug excretion

A
  • acids cleared faster if urine is weakly basic - Bases clear faster if urine is weakly acidic
268
Q

Side effects of beta blockers

A
  • low blood pressure - slow HR - Symptoms of shock
269
Q

What can ankle swelling be caused by?

A

Calcium channel blockers (eg: amlodipine) OR heart failure

270
Q

Steroid side effects (glucocorticoids)

A

CUSHINGOID MAP Cataracts/glaucoma Ulcers Striae Hypertension Infection risk increase Necrosis of bone Growth restriction Osteoporosis ICP high DMT2 Myopathy Adipose hypertrophy Pancreatitis Sleep problems

271
Q

Thiazides

A
  • eg: bendroflumethiazide and indapemide - Inhibits Na-Cl channel cotransporter in distal convoluted tubule - Increased Cl-, Na+ and water excreted
272
Q

Spironolactone

A
  • Inhibits ENaC channel in collecting duct (aldosterone antagonist) - Increased Na+ and water excreted - Increased K+ retention
273
Q

Mechanism of warfarin

A

Antivitamin K because in inhibits Vitamin K epoxide reductase

274
Q

Thrombolytics

A
  • “Clot buster” - eg: alteplase, Activated Tissue plasminogen, activates plasmin to degrade fibrin
275
Q

Hospital autopsy

A
  • Less than 10% in the UK - Requires medical certificate of cause of death (MCCD) - Used for audit, teaching, research and governance
276
Q

Medico-legal autopsy

A
  • > 90% in the UK - Coronial autopsy - death is not due to unlawful action - Forensic autopsy - unlawful (eg: murder)
277
Q

What percentage of deaths are referred to the coroner?

A
  • About 40% - But they only choose to investigate about 10%
278
Q

Deaths referred to coroner

A
  • Presumed natural - Presumed iatrogenic - Presumed unnatural
279
Q

Presumed natural death

A
  • Not seen by a doctor in the last 14 days - Unknown cause
280
Q

Presumed iatrogenic death

A
  • Peri/postoperative deaths - Anaesthetic deaths - Abortions - Complications of therapy
281
Q

Presumed unnatural death

A
  • Accidents - Industrial death - Suicide - Unlawful killing - Neglect - Custody deaths
282
Q

Who carries out an autopsy?

A

A doctor (pathologist)

283
Q

Who can refer to autopsy

A
  • Doctors - Registrar of BDM (statuatory duty to Refer) - Relatives - Police - Anatomical pathology technicians
284
Q

What 4 questions do coronial autopsies aim to answer?

A
  • Who was the deceased? - when did they die? - Where did they die? - How did they come About their death?
285
Q

Steps of autopsy

A
  • external examination - Evisceration - internal examination
286
Q

Autopsy external examination

A
  • Identification: formal identifiers, Gender, age, body habitus, jewellery, body modifications, clothing - disease and treatment - Injuries
287
Q

Autopsy evisceration

A
  • Y-shaped incision - Open all body cavities - Examine all organs in situ - Remove thoracic and abdominal organs - Remove brain
288
Q

Autopsy internal examination

A
  • heart and great vessels - lungs trachea, bronchi - liver, gallbladder, pancreas - Spleen, Thymus and lymph nodes - Genitourinaty tract - endocrine organs - CNS
289
Q

Lifespan of neutrophil polymorphs

A

2-3 days

290
Q

Cellular sequence of acute inflammation

A
  • injury or Infection - neutrophils arrive and phagocytose and Release enzymes - Marophages arrive and phagocytose - Either Resolution with clearance of inflammation or Progression to Chronic inflammation
291
Q

Examples of acute inflammation

A
  • acute appendicitis - Frostbite - Streptococcal sore throat - Lobar pneumonia
292
Q

Treating inflammation

A
  • Ice/cold - Antihistamines - aspirin/ibuprofen - Inhibit prostaglandins - corticosteroids - upregulate inhibitors of inflammation and downregulate Chemical mediators of inflammation
293
Q

What is the acute mediator of inflammation?

A

Histamine

294
Q

Ischaemia vs infarction

A

Ischaemia - reduction in blood flow Infarction - reduction in blood flow with subsequent cell death

295
Q

Endothelial damage theory for atherosclerosis

A
  • Endothelial cells are delicate - Easily damaged By cigarette smoke, shesring forces as arterial divisions, Hyperlipidemia, glycosylation products
296
Q

When does apoptosis take place?

A
  • Development - removal of cells during Development, eg: interdigital webs - cell turnover - removal of cells during normal turnover, eg: cells in the intestinal villi at the tips are replaces By cells from below
297
Q

Apoptosis in HIV

A
  • can induce apoptosis in CD4 helper cells - Reduces their numbers enormously to produce an immunodeficient state
298
Q

Examples of necrosis

A
  • infarction due to lack of blood supply - Frostbite - Toxic venom from reptiles and insects - Pancreatitis - Avascular necrosis of Bone- cuts off blood supply
299
Q

Why do we get deafer as we get older?

A

Hair cells in cochlea can’t divide

300
Q

Basal cell carcinoma

A
  • the Skin only invades locally - can be cured By complete local excision
301
Q

What is adjuvant therapy?

A

Extra treatment given after surgical excision Eg: radiotherapy in breast cancer

302
Q

Example of chronic inflammatory process from the start

A

Infectous mononucleosis

Phase 2a (7 decks)

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