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Haroon Phase 2A > ICS > Flashcards

ICS Flashcards

1
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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2
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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3
Q

Causes of acute inflammation

A

Microbial infections - Hypersensitivity reactions - physical agents - Chemicals - Bacterial toxins - Tissue necrosis

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4
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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5
Q

Neutrophil action at the site of inflammation

A

Phagocytosis - Phagolysosome + Bacterial killing - Macrophages clear debris

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6
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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7
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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8
Q

Causes of chronic inflammation

A

Resistance of infective agent - Endogenous + materials - Autoimmune conditions - Primary granulomatous diseases - Transplant rejection

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9
Q

Macroscopic appearance of chronic inflammation

A

Chronic ulcer - Chronic abscess cavity - granulomatous inflammation - fibrosis

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10
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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11
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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12
Q

What are granulomas?

A
  • An aggregate of epithelioid histocytes (macrophages) - Granuloma + eosinophil -> parasite - Secrete ACE as a blood marker
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13
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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14
Q

What is thrombosis?

A

Solidification of blood constituents (mostly platelets) forming in vessels

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15
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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16
Q

Thrombosis formation (primary platelet plug)

A

Platelet aggregation, starts the coagulation cascade - Positive feedback loops

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17
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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18
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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19
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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20
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) - Embolism (fragments of the thrombus break off into circulation)
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21
Q

Formation of the secondary platelet plug (coagulation cascade)

A

Prothrombin -> thrombin Fibrinogen -> fibrin

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22
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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23
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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24
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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25
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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26
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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27
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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28
Q

What is in an atherosclerotic plaque?

A
  • Lipids (cholesterol) - Smooth muscle - Macrophages (+foam cells) - Platelets - Fibroblasts
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29
Q

What are foam cells?

A

Macrophages that phagocytose LDLs

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30
Q

Atherosclerosis formation

A
  • Macrophages form foam cells from lipids in arterial wall - fatty streak formation (platelets) > intermediate lesion - Plaque protrudes into artery lumen and disrupts laminar flow - medial thinning and platelet aggregation - Secondary platelet plug forms fibrin mesh over itself and traps red blood cells - Fibroblasts form smooth muscle ‘fibrous cap’ over this - Continuous formation of secondary platelet plug, this is a stable atheroma - plaque stabilisation/( fibrous cap formation)
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31
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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32
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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33
Q

Preventative measures for atherosclerosis

A

smoking cessation - blood pressure control - Weight reduction - low dose aspirin - Statins - control diabetes

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34
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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35
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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36
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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37
Q

Extrinsic apoptosis mechanism

A

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

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38
Q

Cytotoxic apopstosis mechanism

A
  • CD8+ binding releases Granzyme B from CD8+ cells - Granzyme B -> Perforin -> Caspases
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39
Q

Types of necrosis

A

Coagulative, liquifactive, caseous and gangrene

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40
Q

Coagulative necrosis

A

most common type - can occur in most organs - Caused by ischaemia

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41
Q

Liquefactive necrosis

A

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

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42
Q

Caseous necrosis

A

Causes a cheese pattern - eg: TB

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43
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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44
Q

What is inflammation?

A

Acute/chronic tissue injury response

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45
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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46
Q

What is hypertrophy?

A

increase in cell size without cell division - eg: skeletal muscle

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47
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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48
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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49
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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50
Q

What is dysplasia?

A

Morphological changes seen in cells in the progression to becoming cancer

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51
Q

What is carcinogenesis?

A

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

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52
Q

What is a neoplasm?

A

An autonomous, abnormal and persistent growth

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53
Q

What is a tumour?

A

Any abnormal swelling; neoplasm, inflammation, hypertrophy, hyperplasm

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54
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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55
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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56
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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57
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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58
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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59
Q

Benign epithelial neoplasms

A

Papilloma - Non-glandular, Non-secretory, eg: squamous cell Papilloma - Adenoma - glandular, secretory, eg: colonic Adenoma

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60
Q

Malignant epithelial neoplasms (carcinomas)

A

eg: urothelial carcinoma glandular epithelium -> adenocarcinoma

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61
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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62
Q

Malignant connective tissue neoplasms

A

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

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63
Q

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

A

Anaplastic

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64
Q

Lymphoid tumours (always malignant)

A

Leukemia, lymphoma - Need to be treated by systemic chemotherapy

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65
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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66
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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67
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
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68
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

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69
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

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70
Q

Host factors for cancer

A

Race - Diet - age - Gender - Inheritance - Premalignant lesions - Transplacental exposure

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71
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
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72
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

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73
Q

Method of spread for sarcomas

A

Mostly haematogenous

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74
Q

Method of spread for carcinomas

A

Mostly Lymphatic - Exceptions: follicular thyroid, choriocarcinoma, RCC, HCC

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75
Q

Tumour staging

A

spread determined by histopthological and clinical examination - TNM: Primary tumour, lymph node, metastases - Different for leukemias, lymphomas and CNS cancers

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76
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

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77
Q

Mutation involved in colorectal cancer

A

FAP (familial adenamatous polyposis) - HNPCC (lynch syndrome)

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78
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
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79
Q

HNPCC

A

Autosomal dominant - Mutated MSH gene - Involved in DNA mismatch repair

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80
Q

Which tumours are most likely to metastasise via bone?

A

Breast Lung/lymphoma Thyroid Kidney Prostate …and multiple myeloma

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81
Q

Haematopoesis chart

A

img

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82
Q

Primary lymphoid organs

A

bone marrow - origin of all immune cells, B cell maturation site - Thymus - T cell maturation site, thymic tolerance

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83
Q

Secondary lymphoid organs

A

lymph nodes - site of DC, B and T cell interactions - Spleen - RBC recycling, encapsulated Bacterial cell killing

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84
Q

Tertiary lymphoid organs

A

Pathological - Germinal centres of rapidly proliferating Lymphocytes

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85
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

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86
Q

Adaptive immunity

A

specific - slow - Needs Activation - have memory - killing Usually antibody mediated - Main cells are T, B and plasma cells - long lasting

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87
Q

Examples of physical barriers

A

skin - Mucus - Cilia

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88
Q

Examples of chemical barriers

A

Lysozyme in tears - Stomach acid

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89
Q

Compliment pathways

A

Classical - Lectin - Alternate

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90
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
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91
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)
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92
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
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93
Q

Innate cells: eosinophils

A

Release major basic protein - Seen in parasitic infections

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94
Q

Innate cells: basophils

A

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

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95
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
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96
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
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97
Q

Non-cellular components of innate immunity

A

Physical and chemical barriers

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98
Q

Receptors on innate cells

A

Toll like receptors (TLRs) and nod like receptors - respond to PAMPs and DAMPs

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99
Q

Which TLRs are intracellular?

A

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

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100
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)

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101
Q

What do dendritic cells do?

A
  • Present foreign antigens to T helper cells - Stimulates further T helper proliferation - Stimulates B cell production -> antibodies
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102
Q

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

A

Immune synapse

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103
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

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104
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) = naïve T cell

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105
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
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106
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)
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107
Q

Adaptive cells: B cells

A

maturation and production in the bone marrow - Any B cells with autoimmunity apoptose

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108
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 and class switching mutate IGs to target different variants
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109
Q

What do IL4 and IL5 promote class switching to?

A

IL4 - IgA IL5 - IgE

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110
Q

IgG

A
  • Most abundant in blood - Highly specific - Key in secondary response - 4 subtypes - Can cross the placenta
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111
Q

IgA

A

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

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112
Q

IgM

A

First Ig released in adaptive response - B cell mediated - a pentamer

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113
Q

IgE

A
  • Least abundant in body - Activates mast cell + basophil degranulation in type 1 hypersensitivity (anaphylaxis)
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114
Q

IgD

A

Unknown function, irrelevant

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115
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
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116
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

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117
Q

Type 2 hypersensitivity

A
  • Antibody-antigen complex formation 👴🏻 Goodpasture’s Rheumatic fever AHA Myasthenia gravis Pernicious anaemia Anti-TSH (Graves’)
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118
Q

Type 3 hypersensitivity

A
  • Antibody-antigen complex deposition 💃🏻 Haemolytic uraemic syndrome and hypersensitivity pneumonitis IgA nephropathy Post-strep glomerulonephritis SLE
119
Q

Type 4 hypersensitivity

A
  • Delayed - T-cell mediated and activated by antigen presenting cells GBS MS 🐱 Contact dermatitis + coeliac Allopurinol drug reaction Tuberculin skin test and T1DM
120
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

121
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
122
Q

What is autoimmunity?

A

Phathological response vs self - faulty immune tolerance - Molecularmimickery

123
Q

Organ specific autoimmunity

A

T1DM - endocrine pancrease B cells - MS - oligodendrocytes of CNS - Pernicious anaemia - parietal cells of Stomach - Myesthemia gravis

124
Q

Non-organ specific autoimmunity

A
  • Affects DNA, eg: SLE - Affects cell antigens - RBCs -> autoimmune haemolytic anaemia - Platelets - > immune thrombocytopenic purpura - Rheumatoid arthritis
125
Q

Immunodeficiency can be…

A
  • Inherited (defects in T cells), eg: IgA deficiency (north Europe), SCID (death within 2 years) - Acquired, eg: HIV
126
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 ->
127
Q

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

A

mRNA

128
Q

What are vaccinations?

A

A form of active immunity

129
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

130
Q

Active immunity natural vs artificial

A

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

131
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

132
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

133
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

134
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

135
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

136
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

137
Q

Types of drug administration

A

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

138
Q

Examples of parenteral drug administration (not via GI tract)

A

Intravenous - Intramuscular - Subcutaneous - Inhalers - Sublingual

139
Q

Examples of local drug administration

A

Topical - Intranasal - Eye drops - Inhalation - Transdermal

140
Q

What is pharmacodynamics?

A

Action of the drug on the body

141
Q

What is pharmacokinetics?

A

Action of the body on the drug

142
Q

What is an agonist?

A
  • Full affinity - Full efficacy - Mimics endogenous substance eg: Salbutamol is a beta 2 agonist
143
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

144
Q

Types of receptor ligands

A

Agonists (including partial) - Antagonists - Allosteric modulators

145
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
146
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

147
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

148
Q

Ways drugs cross membranes

A

Passive diffusion - Facilitated diffusion - active transport - Endocytosis

149
Q

Factors of pharmacokinetics

A

Absorption - Distribution - Metabolism - Elimination

150
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
151
Q

What does drug distribution depend on?

A
  • Blood flow to area - Permeability of capillaries - Protein binding (albumin=slower) - Lipochilicity/lipophobicity - Volume of distribution
152
Q

What drugs can the kidney excrete?

A

Water soluble drugs - not lipid soluble drugs

153
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
154
Q

What are inducer drugs

A

increase cytochrome P450 activity and speed up Metabolism of other drugs - May result in sub-therapeutic dose

155
Q

What are inhibitor drugs?

A

Decrease cytochrome P450 activity, reduce Metabolism of other drugs - May result in toxicity - eg: erythromycin, grape juice

156
Q

Examples of inducers

A

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

157
Q

Examples of inhibitors

A

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

158
Q

First order elimination of drugs

A

Catalysed by enzymes - rate of Metabolism directly proportional to drug concentration

159
Q

Zero order elimination of drugs

A

enzymes saturated by High drug doses - rate of Metabolism is constant - eg: ethanol, phenytoin

160
Q

First order vs zero order drug elimination

A

img

161
Q

Allosteric modulators

A

increase/Decrease normal Ligand binding - eg: benzodiazepine

162
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 categorising them in this way (eg: atenolol is a less selective B1 blocker)
163
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

164
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
165
Q

How does local anaesthesia work

A

Blocks Na+ voltage gated channels

166
Q

Specific vs selective drugs

A

specific - Act on certain targets - selective - Act on subtype of target

167
Q

Neurotransmitter in between synapses in cholinergic pharmacology

A

Always acetylcholine acting on nicotine

168
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

169
Q

Drugs at the neuromuscular junction

A
  • Botolinum toxin (botox) - Curare (nAch-R antagonist) - Ach-ase inhibitors
170
Q

How does botox work?

A

Binds to presynaptic vesicles - Ach Release inhibited - Paralysis

171
Q

How do Ach-ase inhibitors work?

A

Inhibit the breakdown of Ach - Increased concentration at the neuromuscular juntion

172
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

173
Q

Parasympathetic (Ach) responses

A

Rest + digest - Pupil constricts - Lower heart rate - Bronchoconstritction - Increased GI motility and secretion - Detrusor muscle contracts - Penis points (erect)

174
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)

175
Q

Adrenaline formation

A

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

176
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)
177
Q

NAd beta 1 receptors

A

heart - Agonism Causes Increased force of heart contraction - Higher blood pressure - Renin Release

178
Q

NAd beta 2 receptors

A

lungs - Agonism Causes Bronchodilation

179
Q

Agonism and antagonism in beta 2 receptors

A

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

180
Q

Drug for community acquired pneumonia

A

Antibiotics such as amoxicillin/clarythromycin

181
Q

Drug for HAP

A

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

182
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

183
Q

What should you take with isoniazid

A

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

184
Q

Drug for cellulitis

A

High dose oral antibiotic If MRSA, give vancomycin

185
Q

Side effect of trimthoprim

A

Can cause birth defects in the first trimester of pregnancy

186
Q

Drug for H.Pylori🧢

A

Clarythromycin Amoxicillin PPI For 7 days

187
Q

Drug for gastroenteritis

A
  • Campylobacter -> clarythromycin - Amoebiasis -> metronidazole and diloxanide - Giardiasis -> tinidazole
188
Q

Drug for C.Difficile

A
  • Vancomycin - 125mg - 4x a day - for 10 days
189
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

190
Q

Drug for infective endocarditis

A

Antibiotics

191
Q

Types of pain

A
  • Acute (nociceptive) - Cancer - Neuropathic (nerve pain) - Chronic non-cancer (3+ months)
192
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?

193
Q

Things that affect drug absorption

A

Acidity (eg: PPI), ionised drugs can’t cross phospholipid bilayer - motility (eg: erythromycin) - Solubility

194
Q

Types of opioids

A

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

195
Q

What do opioids act on?

A

CNS + GI tract receptors - Resp centres of the brain (pontine)

196
Q

Side effects of opioids

A

Addiction - Constipation - Nausea and vomiting - Respiratory distress/depression

197
Q

Tolerance vs dependance

A

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

198
Q

Treatment for opioid induced respiratory depression

A

naloxone (competitive opioid inhibitor) - IV is fastest route

199
Q

Types of anticoagulants

A

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

200
Q

What to give a patient bleeding on Warfarin?

A

Vitamin K

201
Q

How to NSAIDs decrease inflammation?

A

By inhibiting Cox2

202
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

203
Q

Side effects of PPIs

A

Prolonged use can increase fracture risk

204
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)
205
Q

Where are DA receptors mostly found?

A

Nucleus accumbens in brain

206
Q

GABA

A
  • Main inhibitory CNS neurotransmitter - Agonists - benzodiazepines (eg: lorazepan and diazepan) - Anxiety, sleep disorders, alcohol withdrawal, status epilepticus,
207
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
208
Q

Glutamate

A

Main excitatory CNS neurotransmittor

209
Q

Drug factors that influence drug interactions

A
  • Solubility - Narrow therapeutic index:
210
Q

Factors that affect drug excretion

A

Acids cleared faster if urine is weakly basic - Bases clear faster if urine is weakly acidic

211
Q

Side effects of beta blockers

A

low blood pressure - slow HR - Symptoms of shock

212
Q

What can ankle swelling be caused by?

A

Calcium channel blockers (eg: amlodipine) OR heart failure

213
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

214
Q

Thiazides

A
  • eg: bendroflumethiazide and indapemide - Inhibits Na-Cl channel cotransporter in distal convoluted tubule - Increased Cl-, Na+ and water excreted
215
Q

Spironolactone

A

Inhibits ENaC channel in collecting duct (aldosterone antagonist) - Increased Na+ and Water excreted - Increased K+ retention

216
Q

Mechanism of warfarin

A

Antivitamin K because in inhibits Vitamin K epoxide reductase

217
Q

Thrombolytics

A

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

218
Q

Lifespan of neutrophil polymorphs

A

2-3 days

219
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

220
Q

Examples of acute inflammation

A

acute appendicitis - Frostbite - Streptococcal sore throat - Lobar pneumonia

221
Q

Treating inflammation

A

Ice/cold - Antihistamines - aspirin/ibuprofen - Inhibit prostaglandins - Corticosteroids - upregulate inhibitors of inflammation and downregulate Chemical mediators of inflammation

222
Q

What is the acute mediator of inflammation?

A

Histamine

223
Q

Ischaemia vs infarction

A

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

224
Q

Endothelial damage theory for atherosclerosis

A

Endothelial cells are delicate - Easily damaged by cigarette smoke, shesring forces as arterial divisions, Hyperlipidemia, glycosylation products

225
Q

p53 DNA damage pathway

A

img

226
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

227
Q

Apoptosis in HIV

A

can induce apoptosis in CD4 helper cells - Reduces their numbers enormously to produce An immunodeficient state

228
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

229
Q

Why do we get deafer as we get older?

A

Hair cells in cochlea can’t divide

230
Q

Basal cell carcinoma

A

the skin only invades locally - can be cured by complete local excision

231
Q

What is adjuvant therapy?

A

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

232
Q

Example of chronic inflammatory process from the start

A

Infectous mononucleosis

233
Q

Metaplasia in smoking

A

Cilliated bronchial epithelium with mucocillary escalator -> squamous epithelium

234
Q

What is oncogenesis?

A

The transformation of normal cells to benign or malignant tumours through permanent genetic alterations or mutations

235
Q

Carcinogen definitions

A

Carcinogenic = cancer causing Oncogenesis = tumour causing Mutagenic = act on DNA

236
Q

Types of carcinoma

A

In situ and invasive

237
Q

Angiogenesis promoters

A

vascular Endothelial growth factor - basic fibroblast growth factor

238
Q

Angiogenesis inhibitors

A

Angiostatin - Endostatin - Vasculoatatin

239
Q

Tumours that are most likely to metastasise to the lung

A

Sarcomas, any common cancers

240
Q

Tumours that are most likely to metastasise to the liver

A

GI tract tumours - Carcinoid tumours lf intestine - Pancreatic - breast - Bronchial

241
Q

Cons of conventional chemotherapy

A

not selective for tumour cells - targets other cells, causing hair Loss, diarrhoea and myelosuppresion

242
Q

What tumours is chemotherapy good for?

A

Fast dividing ones: - Germ cell tumours of testis - Acute leukemia - Lymphomas - Embryonal paediatric tumours - Choriocarcinoma

243
Q

What is targeted chemotherapy?

A

Exploits some difference between cancer cells and normal cells to target drugs to the cancer cells - More effective - less side effects

244
Q

Arterial ulcers

A

Punched out holes - little exudate - tips of toes + lateral maleolus - Pale cool skin - low distal pulse - Peripheral vascular disease

245
Q

Venous ulcers

A

less demarcated - Lots of exudate - medial malleolus + inner calf - Warm erythematous skin - Deep vein thrombosis

246
Q

Additive/summative drug interaction

A

Total effect is the sum of the two drugs put together

247
Q

Synergy drug interaction

A

Taking the two drugs together increases the effect

248
Q

Antagonist drug interaction

A

Reduces the effect of the agonist

249
Q

Potentiation drug reaction

A

Effect of one drug is increased but the other one isn’t

250
Q

Where are most drugs metabolised and excreted?

A

Metabolised: liver Excreted: kidneys

251
Q

Example of drug interaction that affects absorption

A

morphine Decreases motility in the GI system, decreasing Absorption

252
Q

What happens if you add a drugs that is higher protein binding than the original drug?

A

The original drug won’t work (competitive inhibition)

253
Q

Morphine metabolism

A

Metabolised into morphine-6-glucoronide by CYP450 - cleared out by the kidney - Adding phenytoin makes the transfer More effective, causing a morphine overdose (enzyme induction)

254
Q

What does metronidazole do?

A

Decreases effect of CYP450 - effect duration of morphine is Longer as it’s being Metabolised slower - this is enzyme inhibition

255
Q

What is INR in pharmacology?

A

International normalised ratio - High INR = too much water or drug induced = enzyme inhibition

256
Q

Types of receptors

A

Ligand-gated ion channels - nicotinic Ach receptors - G protein coupled receptors (most common) - beta-adrenoreceptors - Kinase-linked receptors - for growth factors - Cystolic/nuclear receptors - steroid Hormones

257
Q

What is a receptor?

A

A component of a cell that interacts with a specific ligand and initiates a change of biochemical events leading to the ligands observed effects

258
Q

Exogenous vs endogenous ligands

A

Exogenous - drugs Endogenous -hormones, neurotransmitters etc

259
Q

What are the only polysaccharide vaccines?

A

Pneumococcal disease - Meningococcal disease - Samonella typhi

260
Q

Which vaccines are administered as live attentuated in the UK?

A

BCG - MMR

261
Q

Classical PAMPs

A

Flagellin - Lipopolysaccharide - Peptidoglycan - Liparabinomannan of mycobacteria

262
Q

What immunoglobulins are involved in inactivated vaccines?

A

IgM followed by IgG

263
Q

Codeine

A

Needs to be converted to morphine to work - 10% of people don’t have cytochrome CYP2D6 that converts it - 10% of people have too much of the enzyme - Don’t give it to kids or breastfeeding mothers

264
Q

Oral bioavailibility of opioids

A
  • 50% - 5mg diamorphine = 10mg morphine = 100mg pethidine - Give double amount of oral morphine compared to IM
265
Q

Opioid withdrawal

A
  • Starts within 24 hours - Lasts about 72 hours
266
Q

Patient risk factors for adverse drug reactions

A
  • Gender (F>M) - Elderly - Neonates - Polypharmacy - Genetic predisposition - Hypersensitivity - Hepatic/renal impairments - Adherance problems
267
Q

Drug risk factors for adverse drug reactions

A

Steep dose-response curve - low therapeutic index - Commonly Causes ADRs

268
Q

Augmented ARD

A

Extension of Primary effect (eg: bradycardia and propanolol, hypoglycaemia and insulin) - Secondary effect (eg: bronchospasm with propanolol) - High morbidity, low mortality - Excludes drug abuse and overdose

269
Q

Bizzare ARD

A
  • Not predictable or related to pharmacology - Not dose dependant - Can’t be readily reversed - Can be allergy or hypersensitivity - Low morbidity, high mortality
270
Q

Continuous ARD

A

Uncommon - related to cumulative dose - Time related - eg: steroids and osteoporosis, analgeis nephropathy, colonic dysfunction due to laxatives

271
Q

Delayed ARD

A

Uncommon - Usually dose related - Shows itself some Time after use of drug

272
Q

Ending of drug use ARD

A

Uncommon - occurs soon after drug withdrawn - eg: opiate withdrawal, adrenocortical insufficiency due to glucocorticoud withdrawal, withdrawal seizures when anticonvulsants are stopped

273
Q

Failure ARDs

A

common - dose related - Often Caused by drug interactions - eg: oral contraceptive pill, warfarin

274
Q

What to report on an MHRA yellow card

A

all suspected reactions to herbal medicines and black triangle drugs - all serious suspected reactions for established drugs, vaccines, contrast media and drug interactions

275
Q

Affinity vs efficacy vs potency

A

affinity - How Well a Ligand Binds to its Receptor - efficacy - How Well a Ligand successfully activates its Receptor - Potency - relative strength of the drug, How Well it Causes a response in the body

276
Q

What is the EC50?

A

The dose required to pertain 50% of a response

277
Q

What is a therapeutic range?

A

Upper and Lower bounds of safe doses of a drug. - Narrower range = Need More care in dispensing

278
Q

Treatment for cardiogenic shock

A

Dobutamine - Increases force and rate of Cardiac contraction

279
Q

When to give opioids?

A

in Chronic severe pain relief - Mostly cancer pain

280
Q

Stages of atherogenesis

A
  1. Endothelial demage 2. Fatty streaks 3. Intermediate lesions 4. Fibrous plaques/advanced lesions 5. Plaque erosion 6. Plaque rupture
281
Q

TLRs and their targets

A

TLR2: Gram positive bacteria and mycobacteria (inc fungi)TLR4: Gram negative bacteria and lipopolysaccharides TLR5: Bacteria and flagellin TLR7: Single-strand RNA TLR9: Non-methylated DNA

282
Q

Risk factors for morphine metabolism

A

Elderly - not eating or drinking - reduced kidney function - do renal profile to assess metabolic function before prescribing

283
Q

What is the mechanism of action for erythromycin?

A

Inhibits protein syntesis by binding to ribosomal 50s subunit

284
Q

Cell wall and nucleic acid synthesis (MEMORISE)

A

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285
Q

Risk factors for developing tuberculosis

A
  • HIV - Born in high prevalance area - Close contact with TB positive person - Children under 5 - History of TB - Immunosippression - Homelessness - Prison - Excessive alcohol - IVDU - Smokers - Co-morbidities - Diabetes - End stage CKD receiving RRT - Malignancy
286
Q

Which cell type is the primary receptor for HIV?

A

CD4+ Retroviral therapy targets within this cell type: - Fusion/entry inhibitors - Reverse transcriptase inhibitors - Integrase inhibitors - Protease inhibitors

287
Q

Mechanism of ACh release

A

Action potential arrives at presynaptic terminal - Ach is Release into synapse and Binds to postsynaptic Receptor - Broken down by AChesterase into acetate and choline - choline reuptaken by presynaptic terminal - Binds with Acetyl CoA to form new Ach

288
Q

What are the three classes of enzyme inhibitors?

A

reversible - irreversible - Partially reversible

289
Q

Side effects of acetylcholinesterase inhibitors

A

Nausea - diarrhoea - Dizziness - bradycardia - Insomnia - Headaches - muscle cramps (link to parasympathetic Activation)

290
Q

What blood markers are secreted in sarcoidosis?

A

ACE and calcium

291
Q

Cells that regenerate

A

Hepatocytes - Pneumocytes - all blood cells - gut epithelium - skin epithelium - Osteocytes

292
Q

Mechanism of aspirin

A
  • Irreversibly inhibits Cox-2 - Prevents the breakdown of arachidonic acid into prostaglandin H2 (non-selective for Cox-1 and Cox-2)
293
Q

Furosemide

A
  • Loop diuretic - Inhibits Na-K-Cl channels in ascending loop of Henlé - Increases ion and water excretion and inhibits their absorption in PCT

Haroon Phase 2A (14 decks)

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