Intro To Clinical Sciences Flashcards

Question

What are 8 host factors for cancer risk?

Answer 1

Ethnicity Age Sex Sexual behaviours Diet/exercise Premalignant conditions (eg polyps) Inherited predisposition Trans-placental carcinogenesis

Answer 2

The time between exposure to a carcinogen and the time the cancer “begins”

Answer 3

Initial lesion Fatty streak Plaque progression If it is unstable the plaque may then rupture

Answer 4

Fibroblasts

Answer 5

May be due to a myobacterial infection such as TB or leprosy Seen in chron’s and sarcoidosis

Answer 6

Neutrophil polymorphs Macrophages Lymphocytes Fibroblasts

Answer 7

Neutrophil polymorph

Answer 8

Macrophages

Answer 9

Lymphocyte

Answer 10

- Injury/infection - neutrophils arrive, phagocytose and release enzymes - macrophages arrive and phagocytose - resolution with clearance/ progress to chronic

Answer 11

= neutrophil-mediated Acute appendicitis Frostbite Streotococcal sore throat

Answer 12

= macrophage/lymphocyte mediated Either progresses from acute of starts as ‘chronic’ Starts with macrophages and lymphocytes then usually fibroblasts If there is no tissue damage then it can be resolved but often ends up with repair and formation of scar tissue

Answer 13

Ice- stops capillaries from being flooded with blood and fluid escaping Antihistamine- histamine is a chemical mediator of acute inflammation Ibuprofen- inhibits prostaglandin sythetase Steroids- upregulate inhibitors of inflammation, downregulates mediators

Answer 14

Basal cell carcinoma

Answer 15

Liposarcoma Those that do are breast, lung, prostate, renal cell and thyroid

Answer 16

Rhabdomyosarcoma

Answer 17

Carcinoma in situ

Answer 18

adenocarcinoma

Answer 19

Growth related to overall body growth

Answer 20

Anaplastic carcinoma of the thyroid

Answer 21

Cause of death not known Presumed iatrogenic Anaesthetic deaths Abortion Complications of therapy Presumed unnatural Suicide (by legal diagnosis) Unlawful killing Neglect Custody deaths War Industrial deaths

Answer 22

Programmed cell death in normal cell turnover

Answer 23

P53 protein detects DNA damage and triggers apoptosis if appt. Enzymes are released which auto digest the cell (many of these enzymes = caspases)

Answer 24

Cancer- cells often don’t apoptose, sometimes due to mutation in p53 gene so can no longer detect damage HIV- HIV can induce apoptosis (in CD4 helper cells)

Answer 25

Wholesale destruction of large numbers of cells by some external factor

Answer 26

1. Infarction due to loss of blood supply 2. Frostbite 3. Toxic venom from reptiles and insects 4. Pacreatitis

Answer 27

Increase in size of an organ due to increase in the size of its constituent cells

Answer 28

Increase in size of an organ due to increase in the number of its constituent cells

Answer 29

Hypertrophy= in organs where cells cannot divide Hyperplasia= in organs where cells can divide Mixed hypertrophy/hyperplasia occurs in organs where cells can divide

Answer 30

Smooth muscle cells of the uterus during pregnancy

Answer 31

Decrease in size of an organ due to decrease in size and/or number of its constituent cells

Answer 32

Change in cell differentiation from one fully-differentiated type to another fully-differentiated type (usually caused by consistent change in environment)

Answer 33

Barrett’s oesophagus Oesophageal squamous epithelium to glandular epithelium in continued acid reflux from the stomach

Answer 34

=abnormal growth Morphological change that may be seen in cells in the progression on to development of cancer (neoplasia)

Answer 35

Bronchial epithelium in cigarette smokers- metaplasia from ciliated to squamous

Answer 36

Sclerotic (increases BMD) Lytic (reduced BMD)

Answer 37

Colon Stomach Pancreas Carcinoid tumours of intestine

Answer 38

Because the metastases become lodged in the small pulmonary vessels The lungs act like a filter for tumours

Answer 39

Because tumours cannot grow above ~2mm when they have no blood supply If we can find a way to stop angiogenesis- we can find a way to stop tumours growing?

Answer 40

Adhesion receptors Collagenases Cell motility

Answer 41

These are produced to help the cancer metabolise collagen and the basement membrane

Answer 42

Appendicities

Answer 43

Infection mononucleosis = mono = glandular fever

Answer 44

Benign prostate enlargement

Answer 45

Renal infarction = necrosis

Answer 46

Brain in dementia

Answer 47

Laminar flow= cells travels in the centre of vessels not touching the sides Endothelial cells lining vessels are not ‘sticky’ until they are damaged

Answer 48

The formation of a solid mass from blood constituents in an intact vessel in a living person

Answer 49

Change in vessel wall Change in blood constituents Change in blood flow

Answer 50

Mass of material in the vascular system able to become lodged within a vessel and block it

Answer 51

Most commonly a thrombus Sometimes air, cholesterol crystals, tumours and fat

Answer 52

Reduction in blood flow to a tissue without any other complications

Answer 53

Reduction in blood flow to a tissue that is so reduced it can no loner support the mere maintenance of cells in the tissue so they die

Answer 54

Present at birth- can be inherited or environmental

Answer 55

Myocardial cells Neurones

Answer 56

Resolution= initiating factor removed and tissue left undamaged or able to regenerate Repair= initiating factor is still present and tissue left damaged or unable to regenerate

Answer 57

Primary intention- when wound edges are clean, surgically incised, without much loss of cell/tissue and wounds have opposed edges Secondary intention- wound edges are not clean, margins are irregular, and not surgically incised

Answer 58

Resolution

Answer 59

Accumulation of fibrolipid plaques in systemic arteries

Answer 60

Hypertension Hyperlipidaemia Cigarette smoking Poorly-controlled diabetes

Answer 61

Endothelial cells are delicate- can be damaged by smoking, lipids, oxidative agents etc. Damage leads to endothelial ulceration, microthrombi, eventual development of established atherosclerotic plaques.

Answer 62

- Damage to endothelium- becomes permeable to LDLs - LDLs deposit in tunica intima and become oxidised- now they can’t leave - Oxidised LDLs activate endothelial expressions for WBCs so monocytes are taken into intima - Monocytes -> macrophages + LDL = FOAM - FOAM release lipids when they die= plaque

Answer 63

Enzyme Ligand Transporter Channel

Answer 64

Exogenous (drugs) Endogenous (hormones, neurotransmitter)

Answer 65

Ligand-gated ion channels (nicotine, ACh) G protein coupled receptors, GCPR (beta-andrenoceptors) Kinase-linked receptors (growth factors) Cytosolic/nuclear receptors (steroid)

Answer 66

Regulated by factors that control their ability to bind to and hydrolyze GTP to GDP

Answer 67

M3R: Gq protein, PLC couple, IP3/DAG 2nd mes. B2-AR: Gs protein, AC couple, cyclic AMP 2nd mes.

Answer 68

Kinases are enzymes which catalyse the transfer of phosphate groups between proteins- substrate gains phophate from ATP Receptors are activated when the binding of an extracellular ligand causes enzymatic activity on the intracellular side

Answer 69

By modifying gene transcription

Answer 70

The ability of a drug-receptor complex to produce a maximum functional response

Answer 71

The response given by a drug at a given dose

Answer 72

How ‘much’ it works- ie. Does it give a 100% response at a given dose

Answer 73

When two drugs have opposing effects. In competitive they bind to the same site In non-competitive the antagonist binds to an allosteric site.

Answer 74

Receptor-related: affinity and efficacy Tissue related: receptor number and signal amplification

Answer 75

How well the ligand binds to the receptor

Answer 76

How well the ligand activated the receptor

Answer 77

Agonists have both affinity and efficacy- some more than others. Antagonists have affinity and ZERO efficacy

Answer 78

An irreversible antagonist- once bound to the receptor, it will not com off

Answer 79

When a response is seen when not all receptors have been stimulated so there are spare receptors even though a response is seen

Answer 80

In allergies where there is too much histamine In Parkinson’s where there is too little dopamine

Answer 81

Agonists activate a receptor when bound Antagonists reduce the effect of a receptor when bound

Answer 82

When a drug that binds to the same receptor as an agonist induces a response opposite to that of the agonist.

Answer 83

When there is a reduction in the effect of the agonist over time often when there are continuously high concentrations

Answer 84

The rapid desensitisation to a drug which is uncoupled, internalised and degraded

Answer 85

Isoprenaline is a non-selective B-adrenoceptor agonist. Salbutamol is selective- will only activate the receptors in the lungs where as Iso is non-specific

Answer 86

How two drugs interact independent of the body- so the way they interact has nothing to do with any body systems or environments.

Answer 87

The effect a drug has on the body (Not always the primary effect)

Answer 88

What the body does to the drug. How a drug is absorbed, distributed, metabolised and excreted.

Answer 89

Summation/additive Synergism Antagonism/blockade Potentiation

Answer 90

When two drugs work together to do the same thing and have an effect equal to the sum of their individual effects.

Answer 91

When two drugs work together to produce a response greater than the sum of both individual responses

Answer 92

When one drug antagonises/blocks the effect of another so 1+1=0

Answer 93

When one drug makes the effect of another more potent without changing itself.

Answer 94

A- absorption D- distribution M- metabolism E- excretion Most drugs are hepatically metabolised and renally excreted

Answer 95

How available a drug is over time (use area under graph of blood concentration x time) Fraction of an administered drug that reaches the systemic circulation

Answer 96

Because all drugs exist in an equilibrium of their ionised and unionised states- where the unionised drugs can move into cells though the bilayer. PH affects the equilibrium and therefore how much drug can pas into the cells

Answer 97

How some drugs up or down regulate the enzymatic change of a drug into its active form therefore up or down regulating the active drug

Answer 98

Warfarin (in context of protein binding and enzyme inhibition/induction) And any that may induce acute kidney injury (ace inhibitors, NSAIDs, furosemide and gentimicin)

Answer 99

Nicotinic and muscuarinic

Answer 100

Block the rate limiting step in the cholesterol pathway- reduces levels of “bad cholesterol”

Answer 101

Carbidopa inhibitor for DDC (L-dopa -> dopamine) Tolcapone inhibitor for COMT (L-dopa -> 3-methyl DOPA) both in periphery and in CNS Selegiline inhibitor for MAO-B (dopamine -> DOPAC)

Answer 102

Uniporters= use energy from ATP to pull molecules in Symporters= use the movement in of molecules to pull in another molecule against a concentration gradient Antiporters = one substance moves against its gradient using energy from a second substance moving with its gradient

Answer 103

It inhibits trasport in NKCC (sodium potassium chlorine cotransported). = a diuretic so inhibits

Answer 104

Heart failure

Answer 105

Nerve failure and arrhythmia

Answer 106

Has two sets of three independent proteins- multiple genes code for different sub-units

Answer 107

ENaC= epithelial sodium channels

Answer 108

Often at excitable cells such as muscle and neurones

Answer 109

They are normally found closed, but are activated at depolarised membrane potentials- Ca2+ enters the cell and the Ca-sensitive K channels are opened …

Answer 110

Voltage gated calcium channels- inhibits contraction of cardiac muscle Causes vasodilation to lower blood pressure

Answer 111

Lidocaine= anaesthetic It blocks transmission of action potential to voltage gated sodium channels

Answer 112

Closed Open Inactivated

Answer 113

Regulation of insulin in the pancreas- increased glucose leads to block of these channels and opening of Ca2+ channels so insulin release is triggered

Answer 114

On voltage gated K channels- block them so insulin is secreted So used to treat type 2 diabetes

Answer 115

On the Na/K ATPase- mainly in the myocardium Used for atrial fibrillation and heart failure Inhibition causes an increase in intracellular Na so there is decreased activity in Na-Ca exchanger and hence less Ca in intracellularly Slows down action potential therefore slows down heart rate

Answer 116

This is the proton pump of the stomach and is responsible for the acidification of the stomach so inhibition of this inhibits acid secretion

Answer 117

Proton pumps in the stomach to lower stomach pH

Answer 118

Nerve gases (sarin) Insecticides Pesticides

Answer 119

Omeprazole (proton pump inhibitor) Ramiprill (ACE inhibitor) Aspirin (COX inhibitor) Paracetamol (COX inhibitor) Simvastatin (statin)

Answer 120

Compound foreign to an organism’s normal biochemistry eg any drug or poison

Answer 121

Primarily membrane associated monoocidase proteins in the mitochondria/ER They are major enzymes of drug metabolism Most drugs undergo deactivation by CYPs, some are activated to their active compounds

Answer 122

Morphine Codeine

Answer 123

Diamorphine Oxycodone Dihydrocodeine

Answer 124

Pethidine Fentanyl Alfentanil Remifentail

Answer 125

Synthetic partial agonist: buprenorphine Antagonists: naloxone

Answer 126

5mg 50% of oral is metabolised by liver

Answer 127

Paranteral (not oral)- IM, IV, subcutaneous IV patient controlled analgesia Epidural/CSF Trans-dermal patches for lipid soluble drugs eg fentanyl

Answer 128

Diamorphine

Answer 129

Diamorphine

Answer 130

Inhibit the release of pain transmitters at the spinal cord and midbrain giving euphoria- changes the emotional perception of pain Act on g-protein coupled receptors via second messenger

Answer 131

They act on the descending inhibition of pain- part of fight or flight These were never designed for sustained activation (which opioids provide) and sustained activation leads to tolerance and addiction

Answer 132

Mu (MOP) Delta (DOP) Kappa (KOP) Nociceptin (NOP)

Answer 133

MOP agonists cause depression instead of euphoria

Answer 134

Tolerance is the down regulation of receptors that occurs with prolonged use of a drug- where you then need a higher dose to achieve the same effect Dependence is the psychological effects- craving, euphoria etc

Answer 135

Starts within 24 hours and lasts around 72

Answer 136

Respiratory depression Sedation Nausea and vomiting Constipation Itching Immune suppression Endocrine effects

Answer 137

ABC (+ 999) Naloxone IV- titration to effect- 1ml in 10ml saline- don’t give it all at once

Answer 138

Combination of opioid-induced central respiratory depression (reduced respiratory drive), decreased level of consciousness and upper airway obstruction due to decrease in supraglottic airway tone.

Answer 139

For treatment of chronic non-cancer pain

Answer 140

Codeine is metabolised by CYP2D6 It’s activity is decreased n=in 10-15% of Caucasian population and absent in a further 10%- in these people codeine will have a reduced or absent effect CYP2D6 is overactive in 5% of this population so these may be at risk of respiratory depression with codeiene

Answer 141

To morphine 6 glucuronide which is more potent than morphine and is renally excreted

Answer 142

A weak opioid agonist- slightly stronger than codeine Is metabolised by CYP2D6 to o-desmethyl tramadol to be active- therefore won’t be effective in about 10% of people

Answer 143

It has effects as a serotonin and nor-epinephrine reuptake inhibitor It interacts with SSRIs, tricyclic antidepressants and MAOIs

Answer 144

= allergy Antigen reacts with IgE bound to mast cell Eg. Anaphylaxis

Answer 145

IgG or IgM binds to antigen on cell surface Antibody mediated immune response Eg. Pernicious anaemia, rheumatic fever

Answer 146

Free antigen and antibody combine (IgG, IgA) to form immune complex Eg. Systemic lupus erythematosus

Answer 147

=T-cell mediated =Delayed type hypersensitivity Cell dependant (Th1/cytotoxic T cells/macrophages) Divided into 3 subgroups: damage caused activation of macrophages, activation of TH2 cells and directly by cytotoxic T cells Eg. Tuberculosis

Answer 148

1: allergy, asthma, anaphylaxis 2: some drug allergies eg penicillin 3: serum sickness, contact dermititis 4: chronic asthma, contact dermititis

Answer 149

Skin: swelling, itching and red Airways: excessive mucus production, bronchoconstriction GI: abdominal bloating, vomiting, diarrhoea Anaphylaxis: airways, breathing, circulation etc.

Answer 150

Abnormal responses to harmless foreign materials

Answer 151

Anaphylaxis Allergic asthma Allergic rhinitis (hay fever) Atopic dermatitis Oral allergy syndrome (food allergy) Angiodema (not idiopathic one)

Answer 152

Cytokines Chemokines Lipids

Answer 153

Mast cells Eosinophils Basophils

Answer 154

0.3-100 micrograms/ml

Answer 155

Eosinophils respond in parasitic infections. They have an antagonistic action to basophils and have IgE receptors Basophils are involved in inflammatory reactions= the circulating form of MAST cells. They also have receptors for IgE and release histamine

Answer 156

Produced by a specific cell lineage in marrow Characterised by a requirement for c-kit protein (systemic mastocytosis= caused by c-kit mutations)

Answer 157

FceRI = high affinity FceRII= low affinity CD23= low affinity

Answer 158

B cells, T cells, monocytes, eosinophils, platelets and neutrophils Their functions are to regulate IgE synthesis, trigger cytokines release by monocytes and to present antigens

Answer 159

Eosinophils Mast cells Basophils

Answer 160

They have preformed compounds: Histamine (arteriolar dilation, capillary leakage and cholinergic reflex bronchoconstriction) Chemotactic factors (cytokines) Proteases (tryptase, chymase) Proteoglycans (chondroitin sulphate and heparin) Most of these factors lead to eosinophil attraction and activation

Answer 161

Within minutes they release lipid derived mediators: Leukotrienes (endothelial contraction with vascular leakage), prostaglandin D2 (inducer of smooth muscle contraction), platelet activating factor (increased platelet aggregation). Within hours they release cytokines IL-8, IL-5, IL-4, IL-14 and RANTES

Answer 162

Cold/mechanical deformation (Asthma?) Aspirin Tartrazine NO2 Latex

Answer 163

Indirect because they act via IgE Allergens such as latex, venom, foods, drugs, dander- for these prior sensitisation is required Bacterial viral antigens

Answer 164

Lymphocytes (th2) Dendritic cells (for antigen presentation) Neurons (cholinergic/andrenergic)

Answer 165

Complex inflammatory disease of the bronchi Commonly triggered by allergens Can involve eosinophil influx to the lungs Often involves IgE

Answer 166

A hereditary predisposition to the development of immediate hypersensitivity reactions against common environmental antigens

Answer 167

Non-Th2 cell mechanism CD8 T cells control eosinophil responses Similar to type 4 hypersensitivuty

Answer 168

= immunotherapy Increasing doses of antigen sub-lingually or sub-cutaenously There are risks of moderate and life-threatening reactions

Answer 169

Can we supress Th2? Can we deliver suppressive cytokines? We can use anti-DC23 antibodies to decrease IgE levels

Answer 170

Xolair (selectively binds to IgE) = inhibits the binding of IgE to FceRI It is very costly, slightly increases cancer incidence

Answer 171

Avoid allergens Desensitisation to allergens Prevent IgE production Prevent IgE interaction with receptor Prevent mast cell activation Inhibit mast cell products

Answer 172

IL-5 antibody= mepolizumab IL-5 receptor antibody= reslizumab, benralizumab Anti IL-4/IL-13 = depilumab

Answer 173

Mast cell stabilisers Beta2 agonists (increase cAMP) Glucocorticoids (inhibit gene transcription) Calcium channel blockers Signalling inhibitors

Answer 174

Histamine receptor agonists Leukotriene antagonists Tryptase inhibitors (prevent airway smooth muscle activation) Protease-activated receptor 2 agonists (PAR-2 agonists)

Answer 175

Drug discovery Preclinical development Clinical development

Answer 176

Vincristine

Answer 177

Chimeric antibody (infliximab) Fusion protein (etanercept) Human antibody (adalimumab)

Answer 178

It is a monoclonal antibody from mice against TNF alpha Initially used for chron’s disease now for rheumatoid arthritis also Given by IV infusion every 6-8 weeks

Answer 179

HUman Monoclonal antibody In Rheumatoid Arthritis

Answer 180

Unwanted or harmful reaction following administration of a drug or combination of drugs under normal conditions of use and is suspected to be related to the drug

Answer 181

Side effects can be beneficial but adverse drug reaction are ALWAYS negative

Answer 182

Toxic effects (when beyond the therapeutic range) Collateral effects (when within the therapeutic range) Hyper-susceptibility effects (when below the therapeutic range)

Answer 183

If dose is too high If excretion is impaired

Answer 184

More common in women More common at extreme ages (old and young) Polypharmacy Genetic predisposition Hypersensitivity Hepatic/renal impairment Adherence problems

Answer 185

Low therapeutic index (easy to reach toxic range) Steep dose-response curve

Answer 186

Pharmaceutical variation Receptor abnormality Abnormal biological system that is unmasked by the drug Abnormalities in drug metabolism Immunilogical Drug-drug interactions Multifactorial

Answer 187

Rapid reactions (eg due to quick histamine release with rapid administration of vancomycin) First dose reactions Early reactions Intermediate reactions Late reaction (maybe when drug is stopped) Delayed reactions (thalidomide in pregnancy)

Answer 188

Type A = Augmented pharmacological Type B = Bizarre or idiosyncratic Type C = Chronic Type D = Delayed Type E = End of treatment Type F = Failure of therapy

Answer 189

= augmented Predictable, dose dependent, common Excludes drug abuse and overdose

Answer 190

= bizarre Not predictable, not dose dependent Eg. Anaphylaxis from penicillin Less common but more often serious Can be allergy or hypersensitivity

Answer 191

= chronic Eg. Osteoporosis from long term steroids Uncommon and related to cumulative dose

Answer 192

= delayed Eg malignancies after immunosuppression Usually dose related and uncommon

Answer 193

= end of treatment May occur after abrupt drug withdrawal eg. Opiate withdrawal syndrome

Answer 194

= failure Eg. Getting pregnant on the pill because taking other antibiotics

Answer 195

Dose relatedness Timing patient Susceptibility

Answer 196

Symptoms soon after new drug is started Symptoms after dosage increase Symptoms disappear when drug is stopped Symptoms reappear when drug is restarted

Answer 197

Antibiotics Anti-neoplastics Cardiovascular drugs Hypoglycaemics NSAIDs CNS drugs

Answer 198

A scheme to report ADRs These only need to be suspected It is voluntary

Answer 199

All suspected reactions for herbal medicine All suspected reactions for black triangle drugs (undergoing observation even though they’re on the market) All serious suspected reactions for established drugs, vaccines and drug interactions

Answer 200

Used to indicate medicine that are undergoing additional monitoring

Answer 201

Suspected drug(s) Suspected reaction(s) Patient details Reporter details

Answer 202

Immediate- urticarial (rash), anaphylaxis Delayed- hepatitis, other rashes

Answer 203

Had a prior exposure IgE antibodies formed after exposure IgE becomes attaches to mast cells Re-exposure causes mast cell degranulation and release of substances such as histamine

Answer 204

Due to direct mast cell degranulation No prior exposure necessary Clinically identical to immune anaphylaxis

Answer 205

Immediate rapid onset after exposure to drug (80-90%) Swelling of lipids, face, oedema HYPOtension Cardiac arrest

Answer 206

Basic life support Stop drug if possible Adrenaline (Intramuscular- epi-pen is 300mcg, hospital is 500mcg) High flow oxygen Antihistamines if rash

Answer 207

Causes vasoconstriction Stimulates beta1-adrenoceptors Reduces oedema Bronchodilates Attenuates further release of mediators from mast cells and basophils by nincrease c-AMP so release of inflammatory mediators is reduced

Answer 208

Does not correlate with pharmacological properties of the drug No linear relation to dose Reaction similar to other allergens Disappearance on cessation and reappearance on re-exposure Only occurs in a minority of patients on the drug

Answer 209

Serum mast cell tryptase. Peaks an hour after reaction and lasts around 6 hours

Answer 210

Has beta-adrenergic receptor activity. Stimulation of beta1-adrenergic receptors causes positive ionotropic and chonotropic effects on the heart (increased force and rate). Stimulation of beta2-adrenergic receptors reduce oedema and bronchodilates

Answer 211

Histamine 1 receptors mediate vasodilation, hypotension and flushing. Histamine 2 receptors increase atrial and ventricular contractility, atrial chronotrophy and coronary artery vasodilation.

Answer 212

Because the spleen removes RBCs

Answer 213

Non-specific defence system that you were born with

Answer 214

Acquired defence to destroy/prevent growth of pathogens

Answer 215

Neutrophils Natural killer cells Macrophages Mast cells Eosinophils Basophils

Answer 216

Most abundant WBC, phagocytic and involved in inflammation

Answer 217

(When monocytes migrate from blood to tissue they become macrophages) Phagocytic, antigen presenting and secrete cytokines

Answer 218

Involved in allergies

Answer 219

Involved in parasitic infections

Answer 220

Involved in anaphylaxis and asthma (IgE binds to allergen which then binds to mast cells causing them to release products incl histamines)

Answer 221

Release Lytic granules that kill cells infected with virus

Answer 222

Dendritic cells§

Answer 223

T cells: T helper cells and cytotoxic T cells B cells

Answer 224

T helper cells: CD4 Cytotoxic T cells: CD8

Answer 225

Express CD4 Activate B cells and cytotoxic T cells

Answer 226

Express CD8 Release perforin that cause cells to lyse

Answer 227

The mature B cell marker (protein on B cells) Monoclonal antibodies targed CD20 Used to measure levels of B cells which may be elevated in certain B cell leukaemias

Answer 228

Neutralise toxins Opsonisation of pathogens (attract phagocytes to them) Destroy pathogens

Answer 229

IgA IgM IgG IgE

Answer 230

It is the most abundant antibody in the blood and is highly specific It has 4 subclasses It can cross the placenta

Answer 231

It is bound to mast cells and basophils by FceR. Important in allergy and parasite infections.

Answer 232

IgG levels increase in second exposure IgM levels experience the same increase as in the first exposure. (Should be IgMore but it’s not!)

Answer 233

Active: immunity produced by the host immune system Passive: immunity produced with no host participation

Answer 234

1. Vascular component (dilation of vessels and increased vascular permeability) 2. Exudative component (leakage of protein rich fluid) 3. Neutrophil polymorph (recruited to tissue)

Answer 235

1. Migration (increased plasma viscosity and slowing flow causes neutrophils to migrate to plasmatic zone) 2. Adhesion (adhesion of neutrophils to endothelium within venules) 3. Emigration (neutrophils pass through endothelial cells to the basal lamina and then vessel wall) Diapedesis (some RBCs may also escape from vessels = passive transport)

Answer 236

Microbial infection (bacteria, virus) Hypersensitivity reactions Physical agents (trauma, heat) Chemicals Bacterial toxins Tissue necrosis

Answer 237

Rubor (Redness due to small vessel dilation) Calor (heat peripherally) Tumour (swelling due to oedema or mass) Dolor (=pain) Loss of function (due to ischaemia?)

Answer 238

1. Resolution 2. Suppuration (formation of pus -> scarring) 3. Organisation (Replacement by granulation tissue) 4. Progression to chronic

Answer 239

Cholinergic= relating to acetylcholine (ACh) and its receptor Adrenergic= relating to (nor)adrenaline and their receptors

Answer 240

Organism which colonises (lives in) the host but causes no disease in normal circumastances (If these move to somewhere they don’t belong they can then cause disease eg UTI)

Answer 241

Microbe that only causes disease if host defence are compromised- normally don’t cause disease

Answer 242

The degree to which a given organism is pathogenic

Answer 243

Gram positive = purple Gram negative = red

Answer 244

Pili/fimbriae

Answer 245

Mycobacteria

Answer 246

Ziehl-Neelsen stain

Answer 247

Gram positives have: capsule, large peptidoglycan layer then an inner membrane Gram negatives: capsule, lipopolysaccharide layer (endotoxin), outer membrane, lipoproteins, small peptidoglycan layer then inner membrane

Answer 248

Less than an hour

Answer 249

20-30 mins

Answer 250

Component of the outer membrane of bacteria eg a lipopolysaccharide in gram negative bacteria

Answer 251

Secreted proteins of gram positive and gram negative bacteria

Answer 252

Spores formed inside a bacteria that are highly resistant to temperature and water

Answer 253

Composition: protein Action: specific Effect from heat: labile Antigenicity: strong (bc protein) Producer: gram positive and gram negative

Answer 254

Composition: lipipolysaccharide Action: non-specific Effect from heat: stable Antigenicity: weak Producer: only gram negative

Answer 255

Conjugation

Answer 256

Mutations (deletion, insertion, substitution) Gene transfer (by transformation, transduction and conjugation)

Answer 257

The ability of an antigen or foreign species to bind to something

Answer 258

Streptococci Staphylococci

Answer 259

Staphylococci tend to group in clusters Streptococci tend to group in chains

Answer 260

Infection in bone

Answer 261

Do they contain a coagulase (blood clotting) enzyme or not

Answer 262

Staphylococcus aureus= coagulase positive Staphylococcus epidermis= coagulase negative

Answer 263

Aerosol and touch

Answer 264

Methicillin resistant staphylococcus aureus

Answer 265

Pyogenic- via pus (wound infections, abscesses, pneumonia) Toxin mediated (food poisoning, toxic shock)

Answer 266

They are opportunistic (only really affect immunocompromised or prosthetics or by going to a place they don’t belong)

Answer 267

S. Epidermis= pusy skin S. Saprophyticus= acute cystitis

Answer 268

Alpha- partial haemolysis on blood agar- green Beta- complete lysis on blood agar- blue Negative/gamma- no lysis

Answer 269

Using Lancefield microbead agglutination test Group A= s. Pyogenes Group B= s.agalactiae

Answer 270

Respiratory (tonsillitis) Skin and soft tissue (wound infections, cellulitis) Scarlet fever Complications incl rheumatic fever, glomerulonephritis

Answer 271

Dental caries and abscesses Infective endocarditis

Answer 272

Listeria monocytogenes (only causes infection in immunocompromised eg pregnant) Bacillus anthracis (forms spores) Corynebacterium diphtheriae (prevented by vaccine, leads to cvrs issues)

Answer 273

C. Tetani = tetanus (from infected wounds -> muscle contractions and spasms) C. Botulinum = botulism (from contaminated canned food -> paralysis) C. Difficile = antibiotic associate diarrhoea -> pseudomembranous colitis (attacks gut enterocytes)

Answer 274

Spore forming Produce toxins

Answer 275

Gram negative have an inner and outer layer

Answer 276

LPS= the outer leaflet of the outer membrane on gram negatives. It comprises: -lipid A= toxic portion -core antigen -somatic antigen (highly antigenic)

Answer 277

Any product/strategy that contributes to pathogenicity 1. Colonisation factors (adhesins, invasins, nutrient aquisition, defence against host) 2. Toxins (effectors)

Answer 278

= enterobacteria Rods, mostly motile Grow aerobically but can become anaerobic if necessary (eg large intestine = anaerobic)

Answer 279

Selectively for testing enterobacteria To see if they can use lactose for energy/food or not

Answer 280

Shigella flexneri cannot use lactose and is not motile Escherichia coli (E. coli) can use lactose and is motile Salmonella enterica cannot use lactose but is motile

Answer 281

E.coli- via faeces or catherisation

Answer 282

Wound infections UTIs Gastroenteritis Travellers’ diarrhoea Bacteraemia (sometimes -> sepsis) Meningitis sometimes in infants but rare

Answer 283

There may be several ‘pathovars’ The core genome exists and can acquire pathogenic genes/accessory genes that cause pathogenicity

Answer 284

Shigella = “e.coli + virulence plasmid”

Answer 285

Dysenteriae (most severe) Flexneri Boydii Sonnei (least severe)

Answer 286

Frequent passage of stools Pus and blood, cramps and fever Spread person-to-person or though contaminated food and water

Answer 287

Induce their own uptake from M cells on the gut. Induce apoptosis of macrophages which then release shigella when they die = inflammation and distraction of gut tissue

Answer 288

S. Enterica = responsible for salmonellosis S. Bongori= rare, from contact with reptiles

Answer 289

Gastroenteritis (food poising from milk, poultry and eggs) (localised infection) Enteric fever or typhoid fever (not localised= systemic) (from poor quality drinking water) Bacteraemia

Answer 290

Invasion of gut epithelium Transcytosed to basolateral membrane Enters submucosa macrophages Intracellular survival/replication

Answer 291

= pathogenic enterobacteria Has surface motility= swarming Is elongated & Produces urease so urine pH increases, calcium phosphate precipitates making bladder/kidney stones

Answer 292

Evnironmental Opportunistic- often seen in immunocompromised/elderly/neonates Normally exists in gastrointestinal tract- here it is benign but can cause infections if goes elsewhere such as UTI, neurone, sepsis etc This is multi drug resistance

Answer 293

Infection from an animal

Answer 294

Facultative anaerobe Curved rods with single polar flagellum Causes cholera- most severe diarrhoeal disease Contamination of drinking waster due to flooding/poor sanitation Faecal-oral route not person-to-person Causes production of very watery stool “rice water stool” = loss of fluids and electrolytes

Answer 295

Free-living motile and rod shaped Opportunistic Resistant to many antibiotics and some disinfectants

Answer 296

1. Localised (burn/surgical wounds, UTIs keratitis- these are GREEN fluorescent) 2. Systematic (bacteraemia -> sepsis) occurs in neutropenic patients- with low blood count 3. ICU patients on ventilators/intubated (= ventilator acquired pneumonia) All of these are opportunistic

Answer 297

Exclusively human parasites Carried in the nasal pharynx- non capsulated strains Opportunistic infections include: Meningitis Bronchopneumonia Epiglottitism (caused by invasive strains with a capsule), sinusitis and otitis media Bacteraemia (caused by invasive strains with a capsule) Pneumonia in compromised patients (CF, COPD)

Answer 298

Heating a blood agar it gives a brown colour = chocolate agar

Answer 299

Causes 1-3% of pneumonias It is severe- has a 15-20% mortality Affects the immunocompromised Infection from man-made aquatic environments

Answer 300

Pertussis= whooping cough Short, sometimes oval, rods Fastidious (complex nutritional needs to hard to grow in lab) Low contagious dose- aerosol transmission Humans are the only known reservoir Non-invasive (localised)

Answer 301

Non-flaggellated diplococci (called this because they go round in pairs) Two major species: n.meningitidis and n.gonorrhoeae Humans are the only known resevoir

Answer 302

= meningococcus Carried asymptomatically by 5-10% of population Person-to-person often when over populated groups of young people

Answer 303

= gonococcus Causes gonorrhoea- second most common STD worldwide Person-to-person Can be asymptomatic (10% of men, 50% of women) Can lead to various itises

Answer 304

Spiral rods Two common species: jejuni and coli Unipolar or bipolar flagella Most common cause of food poisoning (lives in guts of certain animals so if not cooked properly or pasteurised) Symptoms incl mild to severe diarrhoea

Answer 305

Spiral shaped, polar flagella tuft Before this was discovered- we thought the stomach was sterile but this was found in about 50% of stomachs Can cause gastritis and peptic ulcer disease Can cause cancer (gastric adenocarcinoma)

Answer 306

Non-motile rods Most abundant bacteria in large intestine Opportunistic (eg through ulcers) Most common cause of anaerobic infections Main one is B.Fragilis (least common but causes most infections)

Answer 307

Very small non-motile Not rod shaped or spiral shaped! Obligate intracellular parasites Many live asymptomatically Can only be detected by PCR or by seeing if the person has antibodies- though they could have had these for years

Answer 308

Unique growth cycle with 2 developmental stages: 1. Elementary Bodies (rigid) which enter cells through endocytosis. They then differentiate into… 2. Reticulate bodies (fragile) which replicate and acquire nutrients from host cell

Answer 309

C. Trachomatis C. Pneumoniae C. Psittaci

Answer 310

There are 3 strains: Trachoma biovar (can lead to blindness, through eye-to-eye transmission) Genital tract biovar (most common STD= what we know as chlamydia) (infects epithelial cells and can ascend to uterus and ovaries) (can cause conjunctivitis from hand-to-eye transmission) Lympho granuloma venereum biovar

Answer 311

1. Fresh culture must be used 2. Dilute cells and form a thin film over the slide 3. Pass slide over a Bunsen burner to make it warm (not hot!) 4. Stain cells with crystal violet then rinse with water after 30-40 secs 5. Add grams iodine and leave for 1 minute before rinsing 6. Decolorise the cells with iodine or ethanol (dropwise with slide tilted) then wash off excess 7. Cover cells with safronin and then rinse with water before drying

Answer 312

Helical Isoahedral Complex Non-enveloped Enveloped

Answer 313

Infectious, obligate intracellular parasite comprising genetic material (DNA OR RNA surrounded by a protein coat and/or membrane

Answer 314

1. Attachment to a specific receptor 2. Cell entry: uncoating of virion within cell 3. Host cell interaction + replication (migration of genome to nucleus and transcription to mRNA using host materials, translation of mRNA produces structural proteins, viral genome and non-structural proteins such as enzymes) 4. Assembly of virion (= complete infectious viral particle) 5. Release of new virus particles

Answer 315

1. Direct distraction of host cells 2. Modification of host cell 3. Over-reactivity of immune system 4. Damage through cell proliferation 5. Evasion of host defences (at cellular level and at molecular level)

Answer 316

By direct destruction of host cells Causes lysis of Neurons -> paralysis

Answer 317

By modification of host cells Causes atrophies in villi and flatten epithelial cells to decrease small intestine surface area so fewer nutrients are absorbed Causes hyperosmotic state Causes profuse diarrhoea

Answer 318

By over-reactivity of immune system Produces cytotoxic response which leads to jaundice, fever etc

Answer 319

By over-activity of immune system

Answer 320

Causes cervical cancer By damage though cell proliferation (Viral expression of HPV proteins + viral DNA is integrated into host chromosomes leads to dysplasia and neoplasia)

Answer 321

1. Direct distraction of host cells (poliovirus) 2. Modification of host cell (rotavirus) 3. Over-reactivity of immune system (hep B) 4. Damage through cell proliferation (papilloma) 5. Evasion of host defences (cellular level =herpesviridae) (molecular level = HIV, influenza)

Answer 322

At a molecular level -> antigenic variability, prevention of host cell apoptosis, down regulation of proteins, interference with host cell antigen processing pathways eg. HIV

Answer 323

Ask about their lochia (bleeding after birth) Ask about contraception Ask about support/partner Ask about mental health Ask about domestic abuse Check for baby genital mutilation Ask any other concerns Do baby check

Answer 324

Red reflex (using ophthalmoscope) Hip dysplasia Check ears (too low -> down’s) Check testicular descention Check heart

Answer 325

Fetal anatomy scan Screening for down’s Sickle cell and thalassaemia Screening for infectious diseases

Answer 326

Physical external inspection Hearing test Newborn blood spot = CF, PKU, sickle cell etc Physical examination = cardiac, hip dysplasia, eyes, testes

Answer 327

Physical = heart, hips, cataract, testes Includes = weight, head circumference, appearance, tone/movement/posture, head and eyes

Answer 328

Height Weight Vision Hearing

Answer 329

General development Growth, eating and activity Tooth brushing/dental appointments Behaviour Sleep Safety Vaccinations

Answer 330

(Antigens are provided directly to us) Mostly cross-placental Sometimes via transfusion of blood/serum

Answer 331

Made from inactivated virus Attenuated live organism Secreted products Constituents of cell walls Recombinant components

Answer 332

Primary vaccine failure= person doesn’t develop immunity Secondary= initially responds but protection wanes over time

Answer 333

Diptheria Polio Tetanus Pertussis (= whooping cough) Haemophilus influenza type B Meningococcal disease (-> meningitis, sepsis)

Answer 334

Breathing very quickly (infants should breath at 30-50- more when they’re younger) Prominent ribs and sub costal recession because diaphragm is trying so hard

Answer 335

Attacks the nerves causing poliomyelitis (damage to myelin) When the nerves are damaged, the muscles begin to waste = muscle atrophy

Answer 336

They’re very dangerous/harmful Very infectious and vaccine preventable If they need specific control measures

Answer 337

Blood CSF Joints Lower resp tract Pleural fluid Peritoneal cavity

Answer 338

Gastrointestinal tract Skin Bladder Oral cavity Vagina Urethra

Answer 339

“Sandpaper rash” = rash feels rough “Strawberry tongue” Think of risk settings and co-inections

Answer 340

Relating to adrenaline or noradrenaline and their receptors

Answer 341

Relating to acetylcholine and its receptors

Answer 342

Somatic= single neuron, innervates skeletal muscles, leads to excitation Autonomic= tow neuron chain- two neurones separated by autonomic ganglion, smooth muscle & cardiac muscles & glands, leads to either excitation or inhibition

Answer 343

Preganglionic= ACh acts on NICOTINIC receptors Postganglionic= ACh acts on MUSCARINIC receptors (parasympathetic) and NORADRENALINE acts on Alpha and Beta receptors (sympathetic)

Answer 344

Sometimes ACh is released at sympathetic post-ganglion if terminals (eg in sweat glands) Nitric oxide is released from parasympathetic postganglionic termini in blood vessels

Answer 345

M1: brain M2: heart M3: all organs with parasympathetic innervation M4: mainly CNS M5: mainly CNS All found outside the cell and will activate intracellular processes though G-proteins

Answer 346

On the heart sino-atrial node (pacemaker) Activation decreases the heart rate On the atrio-ventricular node Decreases conduction velocity (slows down heart) Induces AV node block (PR interval increases)

Answer 347

In the resp system: Acivation produces mucus and smooth muscle contraction (leading to bronchoconstriction) In the GI tract: Increases saliva production and gut motility Stimulates biliary secretion In the skin- only in places were SYMPathetic system releases ACh Activation causes sweating In the urinary system: Activation causes contraction of detrusor muscle and relaxation of internal urethral sphincter so urination In the eye: Causes myosis (pupil constriction) Causes increased drainage of aqueous humours and secretion of tears

Answer 348

Acivation produces mucus and smooth muscle contraction (leading to bronchoconstriction)

Answer 349

Increases saliva production and gut motility Stimulates biliary secretion

Answer 350

Only in places where there is sympathetic release of ACh Causes sweating

Answer 351

Contraction of detrusor muscle Relaxation of internal urethral sphincter = urination

Answer 352

Myosis (constriction of pupils) Increased drainage of aqueous humours Secretion of tears

Answer 353

Myosis and blurred vision Hypersalivation Bronchoconstriction Bradycardia/ heart block Diarrhoea Polyuria (too much urine) Hyperhidrosis (excessive sweating)

Answer 354

They are M3 agonists (= do what M3 does) They increase drainage of aqueous humour, reduce ocular pressure and treat closed angle glaucoma (which occur when fluid is trapped) Also can treat dry mouth

Answer 355

Hyoscine is an M3 ANTAgonist It is used in palliative care to treat respiratory secretions and symptoms of bowel obstruction

Answer 356

Tiotropium Glycopyrronium Umeclidinium Aclidinium Can result in bronchodilation Also antagonise other M3 receptors therefore cause dry mouth, urinary retention and can worsen glaucoma

Answer 357

Solifenacin = treatment for overactive bladder Mebeverine = treatment for irritable bowel syndrome (by slowing contractility)

Answer 358

Skeletal muscle weakness

Answer 359

Disease where ACh receptor antibodies are present and bind to ACh receptors (at neuromuscular junction) Causes skeletal muscle weakness so fatigue on attempts at repeated movement It can be treated by anti-cholinersterses which block the breakdown of ACh so there is more available at the NM junction

Answer 360

A group of chemicals= neurotransmitters One of them is noradrenaline Important in stress response

Answer 361

Noradrenaline is released from sympathetic nerve fibre ends Adrenaline is released from adrenal glands

Answer 362

It is the precursor of Nora/adrenaline (Chemical precursor- they have similar structures apart from presence of one more group)

Answer 363

Alpha 1 Alpha 2 Beta 1 Beta 2 Beta 3

Answer 364

Contracts smooth muscle (pupils and blood vessels)

Answer 365

Mixed effects on smooth muscle

Answer 366

Chronotropic and ionotropic effects on heart

Answer 367

Effects heart rate

Answer 368

Effects strength/ power of heart beat

Answer 369

Relax smooth muscle (in premature labour and asthma)

Answer 370

Enhance lipolysis Relax detrusor muscle of bladder

Answer 371

Increases intracellular Ca2+

Answer 372

Inhibition of cAMP generation

Answer 373

Lower blood pressure by blocking alpha 1 Treating phaeochromocytoma (catecholamines secreting tumours) Blocking alpha 1 receptors in the prostate for benign prostatic hypertrophy

Answer 374

Reduce heart rate Reduce stroke volume Reduce myocardial oxygen demand eg. In post-myocardial infarction

Answer 375

Main targets: Heart Kidney Fat cells Activation leads to: Tachycardia Increased stroke volume Renin release Lipolysis and hyperglycaemia

Answer 376

Bronchi: bronchodilation Bladder wall: inhibiting micturition Uterus: inhibition of labour Skeletal muscle: increase contraction speed (-> tremor) Pancreas: insulin and glucagon secretion

Answer 377

It increases heart rate and myocardial contractility but bypasses the beta-adrenergic receptor site therefore acts irrespective of the presence of beta-receptor blockers

Answer 378

Beta 2 adrenergic receptors

Answer 379

Chronic ulcer Chronic abscess cavit Granulomatous inflammation Fibrosis

Answer 380

Primary -> chronic Primary granulomatous disease Transplant rejection Primary chronic inflammation (due to autoimmune conditions, endo/exogenous materials or resistance to infective agents)

Answer 381

Neutrophils Monocytes

Answer 382

Lymphocytes Macrophages Plasma cells

Answer 383

Redness Heat Swelling Pain Loss of funtion

Answer 384

Neutrophil extravasation (leakage from vein into tissues)

Answer 385

Cellular infiltrate of lymphocytes, macrophages and plasma cells Possible granulomas?

Answer 386

Microbial infections Hypersensitivity Tissue necrosis Chemicals Physical agents Bacterial toxins

Answer 387

Resistance of infective agent Endogenous/exogenous materials Autoimmune conditions Primary granulomatous diseases (Above are all for primary chronic inflammation) Transplant rejection Progression from acute

Answer 388

Arterial thrombi are cold, painful and pale. They are commonly caused by atheroma and can cause a myocardial infarction and/or stroke Venous thrombi are tender, red and swollen and are commonly caused by stasis across valves. They can cause DVTs and pulmonary embolisms

Answer 389

Arterial emboli travel downstream to the heart/brain/peripheries (causing attack/stroke/gangrene) Gangrene= tissue dies cos of no blood Venous emboli travel to the vena cava and cause pulmonary embolisms. The size of the emboli will determine its impact

Answer 390

Hypertrophy (increase in size of cells) Hyperplasia (increase in number of cells) Atrophy (decrease in cell side and/or number) Metaplasia (change from one fully differentiated type of cell to another) Dysplasia (morphological change seen in progression to cancer)

Answer 391

Apoptosis = programmed death Necrosis = unprogrammed (due to adverse event incl infarction, burn, trauma) (followed by acute inflammation)

Answer 392

Malignant = endophytic Benign = exophytic

Answer 393

Grade 1 = well differentiated (closely resembles parent tissue) Grade 2 = moderately differentiated Grade 3 = poorly differentiated

Answer 394

Within each of the following there are stages: T= primary tumour N= lymph node status M= metastatic status

Answer 395

T1: less than 3cm T2: greater than 3cm T3: any size tumour but is near airway or has spread locally to chest wall/diaphragm T4: any size tumour but is located within airway or invited local structure incl heart/esophagus

Answer 396

N0: no lymph nodes are affected N1: tumour spread to nearby nodes on the same side of the body N2: tumour has spread to nodes further away but on the same side N3: cancer cells present in the lymph nodes on the other side of the tumour- or in nodes near the collar/neck

Answer 397

M0: mo metastases M1: metastases

Answer 398

VZV= one virus causes 2 diseases: Chicken pox= primary infection Shingles (herpes zoster)= secondary reactivation

Answer 399

At day 0 (There is 1 to 3 week incubation period before the rash starts on day 0)

Answer 400

Immunocompromised/patients who have had transplants Adults Pregnant women Smokers

Answer 401

Macula to papule to vesicle to postule to crust

Answer 402

Smallpox affects peripheries Chickenpox affects central parts of the body

Answer 403

Age of the patient Onset of the rash Any contacts Immune suppressed? Pregnant?

Answer 404

Dehydration Haemorrhagic change Cerebellar ataxia (common) = poor muscle control Encephalitis (may present as confusion) Varicella pneumonia (= chicken pox specific pneumonia) Bacteria empyema (pockets of pus collected inside body cavities) Skin and soft tissue infection Deep sepsis? Congenital varicella syndrome (in babies of pregnant mothers)

Answer 405

It occurs in 10-15% of cases of chickenpox in pregnancy Usually is asymptomatic but if there are manifestations they will have shingles in their first year of life It can cause severe defects including skin scarring, limb hypoplasia (poorly developed limbs), visceral and ocular lesions and microcephalic/growth retardation

Answer 406

The ability of a virus to lie dormant (not doing anything) within a body. It is important because they can ‘wake up’ when/if the body goes though a period of lower immunity eg. Chemotherapy For example- chicknpox virus can be dormant then come back and travel along the same sensory nerve to the same patch of skin it once was in- and come back as shingles. (Therefore a rash on one side of the body at a place supplied by one nerve root is commonly shingles).

Answer 407

Chickenpox develops slowly and has distinctive stages where lesions look different whereas shingles comes on rapidly and therefore you cannot visualise the stages of development. Shingles is most common in the elderly compared to chickenpox in children.

Answer 408

More present in the thoracic region and less frequently in the cervical, lumbar and sacral dermatomes. 10-20% of cases are opthalmic (dangerous affects opthalmic division of trigeminal nerve) Very painful as nerve is irritated.

Answer 409

There’s bleeding in to the skin The rash will not blanch under pressure (disappear)

Answer 410

Enterovirsus (rash on hand, foot and mouth) Parovirus (red cheeks- doesn’t normally make children majorly ill) (interacts with bone marrow and cause anaemia Vesicular rashes (such as herpes- causing rash on the boundary between lip and skin) Mucositis (shedding epithelium from inside of mouth= left a place for bugs to enter)

Answer 411

Atypical lymphocytes (larger, sticking to red blood cells)

Answer 412

When it comes back in patients with immunodeficiency (who have become immunosupressed) When it comes back, it is very different from the first infection. Causes a ‘pizza pan retina’ which is sight affecting (inflammation looks like soft cheese and blood looks like tomato)

Answer 413

=CCDC Cough Coryza (inflammation of mucosal membrane incl in nose) Diarrhoea Control (immune control- report it!)

Answer 414

Eukaryotes Single called with a nucleas = one celled animals

Answer 415

Flagellates: have tails Amoebae: use finger like projections to pull themselves along Microsporidia: tiny and not very mobile Sporozoa: one called non-motile Ciliates: have cillia that push them along

Answer 416

African tyrpanosomiasis American tyrpanosomiasis Leishmaniasis Trichomonas vaginalis Gardiasis

Answer 417

= sleeping sickness Chancre (hard ulcer/sore) Flu like symptoms CNS involvement: sleepy, confusion, personality change Coma and death! Diagnosed by blood film

Answer 418

= Chagas’ disease Transmitted by triatomine bug (faeces entering via bite) Causes acute flu like symptoms Causes chronic cardiomyopathy, megaoesophagus, megacolon

Answer 419

Spread by bite of sandfly More than 20 human species 3 clinical species: - cutaneous (not too troublesome- only a bad bite and maybe a scar) - mucocutaneous (effects nose and pharynx- destructive lesions= social rejection) - visceral (massive splenomegaly, hepatomegaly, high fatality without treatment, fever, weight loss and anaemia)

Answer 420

Sexually transmitted Asymptomatic/ dysuria (painful/difficult urination), yellow frothy discharge = treated with metronidazole

Answer 421

Diarrhoea Cramps, bloating, flatulance Recent travel Trophozoites/cysts seen in stool Treated with metronidazole!

Answer 422

Foeco-oral spread Caused dysentery (bloody diarrhoea), colitis, liver and lung abscesses Trophozites/cysts can be seen in stool Treated with metronidazole!!!

Answer 423

Cryptosporidiosis Toxoplasmosis

Answer 424

Waterborne Causes diarrhoea (watery with no blood) Vomiting, fever and weight loss Oocytes seen in stool Usually seen in the severe immunocompromised

Answer 425

Contaminated food and water (with feline/cat faeces) Only really causes issues with pregnant women or reactivation from immune compromising. In these cases may cause toxoplasma encephalitis and/or chorioretinitis (may affect vision)

Answer 426

Fever Recent travel

Answer 427

PLASMODIUM FALCIPARUM = most prevalent and most deadly Plasmodium ovale Plasmodium vivax Plasmodium malariae Plasmodium knowlesi

Answer 428

FEVER Chills/headache/vomiting/diarrhoea Anaemia, jaundice, hepatosplenomegaly “Black water fever” = dark dark urine because haemoglobin escapes

Answer 429

Mosquito stage Human liver stage Human blood stages

Answer 430

Agents produced by micro-organisms that kill or inhibit the growth of bacterias in high-dilution = work by binding to a target site on a bacteria

Answer 431

Intolerance/allergy/anaphylaxis Side effects Age Renal and liver function Pregnancy and breast feeding Drug interactions Risk of clostridium difficile (where normal GI flora is taken over by clostridium difficile- causes diarrhoea and GI issues)

Answer 432

On the cell wall (peptidoglycan)

Answer 433

Penicillin V Benzylpenicillinn Flucloxacillin Amoxicillin +cephalopsporins

Answer 434

Cephalexin Cefuroxime Cetriaxone Ceftotaxime

Answer 435

For gram-positives They have a thick cell wall- so we need a “cell wall weapon” Eg. Strep, staphylo

Answer 436

Flucloxacillin

Answer 437

Oral penicillin V IV benzylpencillin

Answer 438

Oral (PO) amoxicillin IV benzylpencillin

Answer 439

Methicillin-resistant staphylococcus aureus

Answer 440

Vancomycin Teicoplanin They are ‘cell wall weapon’ antibiotics Used when someone has a penicillin allergy

Answer 441

For gram-positives ONLY For those that are resistent to beta-lactase eg. MRSA or when there is allergy to penicillin

Answer 442

They are antibiotics that interfere with protein synthesis Treat gram-positives and atypical pneumonia pathogens Used in penicillin allergy and severe pneumonia

Answer 443

Antibiotics interfere with protein synthesis Eg. Clinamycin Act on gram-positives Used in cellulitis (if allergic to penicillin) and in necrotising faciilitis?????

Answer 444

GI infections UTIs Diarrhoea causing infections

Answer 445

Antibiotic that acts on protein synthesis = act on gram negatives and staphs Treat UTIs and infective endocarditis

Answer 446

It needs to be used to treat the most at risk/ most sick people Treats resistant gram negatives in immunocompromised Has a broad activity

Answer 447

Antibiotics that act on DNA synthesis Act on gram negatives much more than gram positives Used when there is a penicillin allergy to treat UTIs and intra-abdominal infections

Answer 448

Both treat UTIs Both are broad but trimethoprim is mainly used for gram negatives

Answer 449

They also have beta-lactamase inhibitors So inhibit the proteins made by gram negatives

Answer 450

=augentim Treats staph.aureus, streps, enterococci, gram negatives and anearobes Is used to treat aspiration pneumonia, severe community-acquired pneumonia or more resistant urinary pathogens

Answer 451

Antibiotics that treat gram positives and negatives (but not pseudomonas, anaerobes and enterococci) Used in some surgical prophylaxis, abdominal infections and non-severe penicillin allergy

Answer 452

Carbapenemase producing enterobacteriaiseae = resistant to antibiotics (Carbapenems are one of the broadest spectrum antibiotics available)

Answer 453

“Vomiting bug” High attack rates among lose contacts (low infecting dose) Has short lived immunity only Is relatively resistant to conventional cleaning- alcohol gel isn’t really enough = very common in hospitals

Answer 454

A stomach bug that lays dormant in the stomach but when it ‘awakes’ it releases toxins that cause a toxic megacolon = prolonged hospital stays Must wash hands thoroughly- alcohol gel isn’t really enough

Answer 455

= Caused by patients’ own bacterial flora Commonly happens from cannulas The infection can spread down the line of cannulas/trachiostomy

Answer 456

Good nutrition and hydration Antisepsis/skin prep Good theatre practice Remove lines and catheters as soon as clinically possible Change from IV to oral treatment as soon as possible

Answer 457

Mosquito has a blood meal and ingests gametocytes of malaria- these mature and fuse in the gut (They fuse to form a macrogametocyte, then an ookinete, then an oocyte) The oocytes release sporozoites into salivary glands which are injected into the human host next time the mosquito feeds

Answer 458

Mosquito injects sporozoites into the human host- they migrate to liver cells and proliferate here These injected cells= schizont cells Schizont bursts and ruptures into the blood stream so the schizont offspring enter the blood

Answer 459

The schizont offspring enter the blood (after bursting into the blood stream) and enter a cycle of infecting red blood cells, proliferating in them and bursting out of them. Not all cells enter this cycle- some become gematocytes and get eaten by mosquitos to continue the life cycle.

Answer 460

It causes obstructed microcirculation When RBCs are infected by this type of malaria, they display to macrophages that they have a pathogen inside them and they become sticky The infected RBCs stick to the endothelium where they roll on it, stick (in situ rosetting) and eventually cause vascular occlusion

Answer 461

P.ovale and p.vivax The hypozoites don’t all initially escape- some remain and cause a relapse months or years later

Answer 462

By interfering with any of the following bacterial processes: Cell wall synthesis Nuclei acid synthesis Protein synthesis

Answer 463

Beta-lactams

Answer 464

Beta lactams (incl penicillin and cephalosporins) Carbapenems Monobactams Glycopeptides

Answer 465

Disrupt peptidoglycan (cell wall) production by binding covalently and irreversibly to the penicillin binding proteins = cell wall is disrupted= lysis =hypo-osmosis environment= bacteria destroyed

Answer 466

Gram negatives have an additional lipopolysaccharide layer that decreases antibiotic penetration

Answer 467

Metronidazole Rifampicin Fluroquinolones

Answer 468

By inhibition DNA gyrase (catalyses supercooling of double stranded DNA in bacteria) By inhibition of DNA polymerase (eg. Rifampin)

Answer 469

By affecting the ribosomes: Either the 50S subunit or the 30S subunit

Answer 470

Directly: destroy phagocytes or the cells in which bacteria replicate Indirectly: inflammation (eg. Necrotic cells), immune pathology By releasing toxins: exotoxins (proteins) and endotoxins (gram negative) Diarrhoea- by bacteria damaging the gut by trying to ‘clear’ the gut

Answer 471

Bectericidal= kills bacteria Becteriostatic= suppresses growth/multiplication of bacteria

Answer 472

Minimum inhibitory concentration (Lowest conc where bacterial growth is inhibited)

Answer 473

The ability to bind to enough target sites so that enough damage is done The ability to remain at the binding site for long enough so that enough damage is done = concentration and time

Answer 474

It is about ensuring medicines deliver a value (financially and to the patient) Ensuing safety and reducing wastage Avoiding taking unnecessary medicines

Answer 475

= no longer compliance (as this removes the patient’s opinion or desire) Adherence acknowledges the doctor’s “orders” and the patient’s beliefs

Answer 476

Not taking Taking incorrect dose Taking more or less often Stopping prematurely Modifying treatment to accommodate for other things Continuing with behaviours against medical advice (eg smoking, diet)

Answer 477

Practical barriers (unintentional) eg. Misunderstanding, problems using the treatment, inability to pay and forgetting Intentional/motivational barriers incl patient beliefs and personal preferences

Answer 478

90% of people with HIV to be diagnosed 90% of people diagnosed to be on ART (antiretroviral therapy) 90% of those on ART to have viral supression

Answer 479

Sexual Vertical Blood

Answer 480

Undetectable = Untransmittable

Answer 481

= pre-exposure prophylaxis of HIV

Answer 482

When a clinician has indicated that a person needs testing Routine screening in high prevalence locations Antenatal screening Screening in high risk groups Patient initiated requests for screening

Answer 483

Point of care tests for HIV = finger prick blood = immediate result = lower sensitivity and specificity (produces false positives and false negatives) = lower incubation period

Answer 484

Viruses that use reverse transcriptase to make a DNA copy of themselves to be incorporated into the host genome

Answer 485

Viral envelope has a high affinity for CD4 Attaches to CD4 and enters the cell via a chemokine receptor (CCR5 on first infection and CXCR4 later) Uses reverse transcriptase to produce DNA which enters the nucleus New viral contents is made by the cell

Answer 486

Integrase inhibitors

Answer 487

In general, when the CD4 count is higher, there are infections such as vaginal/oral candidiasis, skin disease, fatigue and pneumonia As the CD4 count reduces, there are infections such as herpes, leukoplakia, thrush, lymphoma and CMV (herpes)

Answer 488

HIV is integrated into the DNA of infected CD4-expressing cells (mostly helper T cells) The number of infected cells in the blood does not correlate to the extent of immune supression Immune system is constantly activated by HIV which drives pathogenesis

Answer 489

Very vigorous but with no demonstrable protective immunity (though rare exceptions) Excessive immune activation which actually favours viral replication Ongoing viral replication + immunological impairment leads to clinical signs of immunodeficiency

Answer 490

Issues of adherence and side effects and resistance They seem to develop ‘old age’ related illnesses at a young age such as Cv disease, lung disease etc

Answer 491

There always persists a resevoir of infected cells- these will start to replicate again within weeks of cessation of therapy

Answer 492

The idea is to wake up the latent virus (which remains as a reservoir during treatment) the immediately after, overwhelm with ART to try and wipe out the viral reservoir

Answer 493

HIV viral load CD4 count

Answer 494

Reactivation of varicella voster virus at the dorsal roots (chicken pox-> shingles) Oral thrush Oral hairy leukoplakia (white areas on the tongue which cannot be scraped off - from EBV) Molluscum contagiosum (pox virus popular in kids but rare in adults and normally due to HIV)

Answer 495

Fungal pneumonia (pneumocystis jirovecci) where oxygen levels drop during/after exercise Does not cause illness unless there is immunodeficiency Can be treated by co-trimoxazole (weird because this is an antibiotic

Answer 496

From 500-1500 cells/mm^3

Answer 497

They have AIDS TB in HIV = AIDS defining

Answer 498

= highly active anti-retroviral therapy You usually give 3 antiretroviral drugs (two NRTIs and one other) which act on different point of the replication cycle

Answer 499

Endo= glands secrete into the blood Exo= grands secrete through a duct to the site of action

Answer 500

Hormone action on adjacent cells

Answer 501

Hormone action on the same cells as where they’re secreted

Answer 502

Water soluble hormones travel unbound and bind to surface receptors on cells Fat soluble hormones are protein-bound anddiffuse into cells

Answer 503

Peptides Amines Iodothryonines Cholesterol derrivatives and steroids

Answer 504

Steroid hormones are synthesised on demand, peptides and monoamine hormones are stored in vesicles

Answer 505

Vary in length, in linear or ring structures Stored in secretory granules, are hydrophilic They are released in pulses or bursts and cleared by tissue or circulating enzymes

Answer 506

Synthesis from preprohormone to prohormone Packaging from prohormone to hormone (stored as hormone and secreted as hormone)

Answer 507

Thyroid hormones

Answer 508

= thyroid hormones Protein bound Conjugation of iodothyrosines give rise to T3 and T4

Answer 509

Vit D Adrenocorticoids and gonadal steroids

Answer 510

Fat soluble Enters cell directly into the nucleus to stimulate mRNA production Transported via vitamin D binding protein

Answer 511

Enter cell passing to nucleus to induce a response (altered into the active metabolite and bind to a cytoplasmic receptor)

Answer 512

Diffuse through membrane Bind to receptor Receptor-hormone complex enters nucleus Receptor-hormone complex binds to GRE This binding initiates transcription of gene to mRNA mRNA directs protein synthesis

Answer 513

Humoral stimuli= release caused by altered levels in blood Neural stimuli= release caused by neural input Hormonal stimuli= release caused by another hormone

Answer 514

Hormone metabolism (removal) Hormone receptor induction (so therefore hormone can now work) Hormone receptor down regulation (so now hormone can’t work) Synergism (combined effects of two hormones is bigger than the sum) Antagonism

Answer 515

Oxytocin ADH

Answer 516

Hypothalamic neurons synthesise oxytocin and ADH, they are transported down the axons of the hypothalamic-hypophyseal tract to the posterior pituitary

Answer 517

Increased by: High osmolality and low blood volume Nausea, vomiting, stress and exersice Reduced by Caffeine, alcohol

Answer 518

TSH ACTH FSH LH GHRH PRL These all stimulate the release of hormones from the hypothalamus

Answer 519

Tumour mess effects (vision loss from optic chaism, headaches etc) Hormone excess Hormone deficiency

Answer 520

Accelerate food metabolism Increases protein synthesis Stimulation of carb metabolism Enhances fat metabolism Increases ventilation rate Increases cardiac output and heart rate Brain development Increased growth rate

Answer 521

Switches off the appetite People who are leptin deficient are often very obese, hyperinsulinaemic

Answer 522

Stimulate appetite and growth hormone release High levels in blood during fasting

Answer 523

Pale skin Central obesity

Answer 524

Secreted in response to food Inhibits gastric motility Reduces appetite

Answer 525

Olfactory Gustatory Cognitive Visual

Answer 526

CCK GLP (glucose dependent glucagon) Insulin PYY (leptin in the long term)

Answer 527

A drug administered by mucosal absorption

Answer 528

Time and concentration (Time dependant antibiotics need to be given regularly at shorter intervals) (Concentration dependant antibiotics need to be given in larger doses at less regular intervals)

Answer 529

Change the antibiotic target (stop from binding from binding to itself and make bind to something else) Destroy antibiotic (by some enzyme process) Prevent antibiotic access (by modifying number/size/selectivity of membrane channels) Remove antibiotic from bacteria (pump out once it’s already in)

Answer 530

Flucloxacillin (methicillin) can no longer bind to staphylococcus aureus because the target has changed shape

Answer 531

Intrinsic= naturally resistant (so all sub populations will be equally resistant) Acquired= due to spontaneous gene mutation or horizontal gene transfer (3 ways)

Answer 532

Transduction (mediated by bacteriophages which parakeet the DNA from one to another) Conjugation (a sex pills forms between two cells and a plasmid is transferred) = most concerning Transformation (take up free DNA from the environment and incorporate it into their chromosome)

Answer 533

MRSA (methicillin/Flucloxacillin resistant staphylococcus aureus) =bacteriophage mediated transduction VRA (vancomycin resistant enterococci) = plasmid mediated

Answer 534

ESBL (extended spectrum beta lactamase) = hydrolyse oxyimino sites of different antibiotics

Answer 535

HIV exposed uninfected infants

Answer 536

Heart muscle abnormalities (in 20%) Chronic lung disease (in 30%) Growth stunting (30-50%)

Answer 537

There are multiple variants of HIV-1 There are multiple routes of aquisition

Answer 538

Viral load should immediately drop DC4 count should slowly rise again but in some people it never does/does very late or slowly

Answer 539

PCP = pneumocystis pneumonia Fungal pneumonia

Answer 540

Being lipid soluble means that a drug can cross the blood brain barrier more quickly Being protein bound means there will be a lower concentration of the drug in the plasma making a slower delivery

Answer 541

Morphine is metabolised in the liver to morphine-6-glucoronide which is more potent than morphine It is excreted in the kidney

Answer 542

Double orally compared to IM This is because morphine is is taken into the liver immediately after enteric absorption and metabolised into an inactive compound before entering circulation

Answer 543

From the liver (sometimes kidney) from the breakdown of glucose or from gluconeogenesis

Answer 544

Glucose enters via GLUT2 Glucose is phosphorylated by glucokinase (generating ATP which closes KATP channels so the membrane is depolarised) Calcium then comes in to the cell Calcium stimulates the secretion of insulin

Answer 545

Insulin stimulates insulin receptor …signalling cascade… GLUT4 transporters travel to the membrane enabling glucose to enter the cell

Answer 546

Acute hyperglycaemia leads to acute metabolic emergencies: diabetic ketoacidosis (and hyperosmolar coma rare and only in type 2) Chronic hyperglycaemia leading to tissue complications Side effects of treatment (hyPOglycaemia)

Answer 547

Diabetic retinopathy

Answer 548

Cardiovascular disease

Answer 549

Diabetic neuropathy

Answer 550

Diabetic nephropathy (-> end stage renal disease)

Answer 551

Type 1 Type 2 (incl gestational and medication induced) MODY (maturity inset diabetes of youth)= monogenic diabetes Pancreatic diabetes (caused by recurrent pancreatitis causing damage to beta cells) Endocrine diabetes (secondary to excessive secretion of growth hormone in acromegaly, or steroids in cushing’s) Malnutrition related diabetes

Answer 552

Alongside symptoms: Random plasma glucose > 11mmol/l Fasting plasma glucose >7mmol/l (normal is less than 4) No symptoms: GTT (glucose tolerance test) Measure HbA1c > 48mmol/mol (measures how much glucose is attached to haemoglobin)

Answer 553

Insulin deficiency disease characterised by loss of beta cells due to autoimmune destruction

Answer 554

Beta cells are lost because they express antigens of HLA histocompatability system- may be in response to environment? We don’t know? This activates a chronic cell mediated immune process leading to chronic insulin deficiency

Answer 555

Genes + environment lead to 2 main defects: Impaired insulin secretion Insulin resistance!!! In some order: insulin demand is very high because it is not working, leads to progressive hyperglycaemia and high free fatty acids

Answer 556

Type 2 diabetes has a history of years of impaired glucose tolerance before clinical symptoms show, they may appear with microvascular and macro vascular complications which wouldn’t be seen in type 1.

Answer 557

Insulin levels are ALWAYS detectable Because of this people with type 2 diabetes do not lose weight as they do not suffer from muscle catabolism

Answer 558

In type 1: glucose and ketones In type 2: glucose

Answer 559

In type 1: muscle/fat breakdown In type 2: no muscle/fat breakdown

Answer 560

Sulphonylureas (incl gliclazide and glibenclamide) Thiazolidinediones

Answer 561

Stimulate insulin release by binding to beta cell receptors But this is at the expense of significant weight gain and does not prevent the gradual failure of insulin secretion Can also cause prolonged hypoglycaemia especially when renal function is impaired

Answer 562

Bind to receptors in adipose tissue and activate genes concerned with glucose uptake and utilisation This improves insulin sensitivity but they increase weight and risk of heart failure

Answer 563

A protein secreted from L cells in the intestine It slows gastric emptying, stimulates insulin secretion and suppresses glucagon secretion and improves beta cell funtion (Hence improves insulin sensitivity and enhances douches disposal)

Answer 564

It is rapidly degraded by DPP-IV circulating enzyme But can be prescribed with analogues that extend the duration of action of GLP-1

Answer 565

They are medication for type 2 diabetes that reduce weight and lower glucose Eg. Exanatide, liraglutide, lixisenatide

Answer 566

SGLT2 is a transport protein that acts to reabsorb glucose in the kidney proximal tubules Inhibitors of this increase glucose excretion and lower blood glucose Eg. Empagliflozin canagliflozin

Answer 567

It is rare because low insulin levels are sufficient to suppress catabolism and prevent ketogenesis

Answer 568

The insulin that is longer active and keeps blood glucose steady for hours/in fasted state

Answer 569

Insulin that is released in the spike of glucose after feeding Short-active

Answer 570

Level 3 is less severe but still serious- patient has impaired cognitive function and sufficient enough to require external help to recover Level 2 is serious biochemical- plasma glucose of <3mmol/l Level 1 is alert value where plasma glucose is <3.9mmol/l with no symptoms

Answer 571

Trembling Palpitations Sweating Anxiety Hunger

Answer 572

Basal and bolus insulin are separated and given at appropriate times Blouses given pre meal based on the carb content of the food given Basal given either twice daily or adjusted to maintain fasting blood glucose

Answer 573

Cognitive dysfunction Blackouts Seizures Comas Psychological effects

Answer 574

Increased risk of myocardial ischaemia and cardiac arrhythmias

Answer 575

Falls, accidents, driving accidents, fractures and dislocations

Answer 576

Inflammation, blood coagulation abnormalities, haemodynamic changes, endothelial dysfunction

Answer 577

Difficulty concentrating Confusion Weakness Drowsiness, dizziness Vision changes Difficulty speaking

Answer 578

Having diabetes for a long time (at the beginning of type 1 there remains some insulin and glucagon levels but these diminish years of having diabetes go on) Tight glycemic control with repeated episodes of non-severe hypoglycaemia Increasing age (as body responses are slower) Increased physical activity Sleeping Use of drugs and alcohol (alcohol is toxic to liver so it cannot break down glycogen to restore glucose)

Answer 579

It has no arterial blood supply Receives blood through portal venous circulation from the hypothalamus

Answer 580

Benign pituitary adenoma Craniopharyngioma Trauma Apoplexy/Sheehans Sarcoid/TB

Answer 581

Pressure on local structures (eg. Optic nerves -> Bitemporal hemianopia) Pressure on normal pituitary (hypo-pituitary) Functioning tumour? (Ie does it produce hormones- prolactinoma, acromegaly, Cushing’s disease)

Answer 582

Pale, no body hair, central obesity

Answer 583

Possible in men but more common in women Present with galactorrhoea and amenorrhoae and infertility Causes loss of libido and maybe visual field defect Dopamine agonists often shrink the tumours

Answer 584

Stages of puberty In boys it measures pubic hair, testicular length and testicular volume (also colour of scrotum and growth of penis) In girls it measure pubic hair, papilla and areola

Answer 585

Breast development = first visible sign of puberty

Answer 586

Prepubertal- tubular shape, endometrium single layer of cuboidal cells Adult- pear shape, endometrium increased thickness

Answer 587

Maturation process of adrenal gland where specialised subset of cells arise to form the (androgen producing) zona reticularis

Answer 588

= true early puberty Most are females Most is idiopathic early puberty But in boys it is more risky and may be due to brain tumours

Answer 589

GnRH super-agonist that is so powerful it ultimately stops pulsatility of GnRH secretion and therefore cutting off the axis

Answer 590

No breast development by 13 yrs More than 5 years between breast development and menarche Lack of pubic hair by 14 yrs Absent menarche by 15-16yrs

Answer 591

Lack of testicular enlargement by 14yrs Lack of pubic hair by 15yrs More than 5 years to complete genital enlargement

Answer 592

Complete red blood count U&E, renal, LFT and coeliac LH, FSH, Testosterone/ Oestradiol- though these levels will be low during early puberty and quiescent phase Thyroid function, prolactin DHEA-S, ACTH, Cortisol Karyotyping (esp in all girls with short stature - could be turner’s)

Answer 593

Bone age= skeletal maturity does not mean chronological age Delayed bone age can be seen in GH deficiency Advanced bone age can be seen in precocious puberty

Answer 594

Chronic renal or gastrointestinal disease CF Anorexia/ extreme exercise Stress Drugs Sickle cell/iron overload Cushing’s

Answer 595

Primary= the target organ eg gonads Secondary= eg pituitary Tertiary= eg hypothalamus

Answer 596

Hypogonadotrophic hypogonadism caused by X-linked autosomal recessive or dominant mutation

Answer 597

1 in 2000 girls 45XO genetics Causes hypergonadotrophic hypogonadism Causes cardiovascular malformations, short stature, broad chest and small mandible (jaw)

Answer 598

47XXY Affects males- 1 in 1000 Causes primary hypogonadism (and therefore hypergonadotrophism) Causes tall stature, breast cancer risk, slightly reduced IQ

Answer 599

Decreased phosphate reabsorption Increased Ca2+ reabsorption Increased bone remodelling

Answer 600

Small decrease in Ca2+ -> large increase in PTH Small increase in Ca2+ -> large increase in PTH

Answer 601

Parasthesia (tingling and numbness) Muscle spasm Seizures Basal ganglia calcification Cataracts ECG abnormalities (LONG QT)

Answer 602

Syndromes (incl Di George, HDR etc) Radiation Surgery Genetics Autoimmune

Answer 603

Resistance to parathyroid hormone

Answer 604

Thirst, polyuria Nausea, constipation Confusion -> coma Renal stones SHORT QT on ECG

Answer 605

In 90% of cases: Malignancy Primary hyperparathyroidism Otherwise: Sarcoidosis, thiazides, adrenal insufficiency etc

Answer 606

BONES, STONES, GROANS and MOANS Osteoporosis Kidney stone Confusion (psychic groans) Abdominal moans = constipation and acute pancreatitis

Answer 607

80% due to a single benign adenoma 15-20% due to four gland hyperplasia Less than 0.5% due to malignancy

Answer 608

The hypothalamus releases TRH (thyrotropin releasing hormone) Causes the pituitary to release TSH Causes the thyroid to release T4 and T3 T4 and T3 inhibit the release of TRH from the hypothalamus

Answer 609

Hypothalamus release GnRH (gonadatropin releasing hormone) The pituitary releases LH and FSH The gonads release testosterone/oestrogen Testosterone/oestrogen inhibit the release of both GnRH and LH&FSH

Answer 610

The hypothalamus releases CRH (corticotropin releasing hormone) The pituitary releases ACTH Adrenals release cortisol Cortisol inhibits the release of CRH and ACTH

Answer 611

The hypothalamus releases GHRH (growth hormone releasing hormone) The pituitary releases GH The liver releases IGF-1 IGF-1 inhibits the release of GRHR Hypothalamus also releases Somatostatin which acts in an opposite way to GRHR!

Answer 612

The hypothalamus releases dopamine The pituitary releases LESS prolactin Prolactin encourages release of dopamine

Answer 613

Prepubertal is red in colour, thin strophic columnar epithelium with a neutral pH Adult is duller red with thicker epithelium, superficial layers in epithelium and acidic pH. Labia increase in size and thickness, the hymen thickens and the clitoris enlarges

Answer 614

Has it never started or did it start then stop? Family history Prenatal history Prior illnesses/meds Nutrition/exercise Injury (testicular)

Answer 615

When the lack of sex hormones produced is DUE to the lack of gonadotrophins

Answer 616

When gonads aren’t responding and aren’t producing sex hormones HENCE the Gonadotrophins are released in excess to try to get sex hormones to release = primary gonadal failure

Answer 617

Oestrogen by tablet or transdermal Start with low dose and gradually increase Once a full dose is achieved, add progesterone

Answer 618

Testosterone enanthate = IM injection Several incremental steps for 2-4 years until full adult replacement dose is achieved

Answer 619

In vit D deficiency: PTH is up Calcium is down Phosphate is down PTH levels are appropriate

Answer 620

In hypoparathyroidism: PTH is down Calcium is down Phosphate is up PTH levels are inappropriate

Answer 621

In pseudohypoparathyroidism: PTH is up Calcium is down Phosphate is up PTH levels are appropriate

Answer 622

In hypercalcaemia of malignancy: PTH is down Calcium is up Phosphate is ? PTH levels are appropriate

Answer 623

In primary hyperparathyroidism: PTH is up Calcium is up Phosphate is down PTH levels are inappropriate

Answer 624

Thirst (osmotic activation of hypothalamus) Polyuria Weight loss and fatigue (loss of muscle and lipid due to unrestrained gluconeogenesis) Hunger (lack of useable energy source) Pruritis vulvae (itchy vulva) and Balanitis (red sore head of penis) Blurred vision (altered acuity due to uptake of glucose)

Answer 625

Risk if mother has it: 2% Risk if father has it: 8% (and symptoms are worse) Risk if both parents have it: 30% Risk if sibling has it: 10% (15% if twin, 40% if identical twin)

Answer 626

Anti- GAD Pancreatic islet cells Ab Islet antigen-2 Ab ZnT8 Also associated with other autoimmune diseases incl hypothyroidism, addisons and coeliac

Answer 627

Reduced insulin leads to fat breakdown to form glycerol + FREE FATTY ACIDS (FFA) FFA are transported to the liver to provide energy for gluconeogenesis FFA are oxidised to form ketone bodies

Answer 628

Hyperglycaemia Raised plasma ketones Metabolic acidosis

Answer 629

Symptoms develop over days, incl: polyuria, nausea, vomiting, weight loss, weakness, abdominal pain, drowsiness/confusion Signs also are hyperventilation, dehydration, hypotension, tachycardia and comas

Answer 630

Hyperglycaemia = <50mmol/l glucose Acidosis = <15 mol/l HCO3- Urinary ketone dipstick of 2+ ketones/ blood ketones of 3 ketones

Answer 631

Insulin Rehydration Replacement of electrolytes Start immediately!

Answer 632

Diabetic nephropathy (kidney disease) Retinopathy

Answer 633

Acute deprivation of glucose within the brain -> cerebral dysfunction Release of glucagon and adrenaline Sweating, tremor, palpitations, loss of concentration and hunger

Answer 634

Dose Adjusting For Normal Eating

Answer 635

Maturity-onset diabetes of the young

Answer 636

Commonest monogenic diabetes Diagnosed younger than 25 Autosomal dominant Single gene defect altering beta cell function

Answer 637

Transcription factor MODY (where hepatic nuclear factor HNF alters insulin secretion and reduces beta cell proliferation) MODY 3 = HNF1A mutation MODY 1 = HNF4A mutation (neonatal hypoglycaemia) MODY 2 = GCK mutation (GCK is the glucose sensor or beta cells- causes mild diabetes)

Answer 638

Parent with diabetes Absence of islet antibodies Evidence of non-insulin dependence No ketosis and measurable to C-peptide Sensitive to sulphonylurea (especially MODY 3)

Answer 639

Insulin is released as Pro-peptide (insulin + c-peptide) Very measurable in blood Significant levels= they’re making their own insulin

Answer 640

Maternally inherited diabetes and deafness Caused by mutation to mitochondrial DNA & loss of beta cell mass

Answer 641

Selective loss of adipose tissue Associated with insulin resistance, hyperandrogenism and PCOS

Answer 642

Acute pancreatitis -> short lasting hyperglycaemia due to glucagon secretion Chronic pancreatitis alters secretion and causes blocked ducts, must be treated with insulin

Answer 643

It is autosomal recessive causing a traid of cirrhosis, diabetes and bronzed hyperpigmentation Excess iron is deposited in the liver, pancreas, pituitary, heart and parathyroids Most people with it need insulin

Answer 644

The viscous secretions caused by CF lead to duct obstruction and pancreatic fibrosis

Answer 645

Enlargement of the thyroid causing swelling in the neck Can be benign or malignant

Answer 646

Overproduction Leakage Ingestion of excess hormone

Answer 647

Weight loss Tachycardia Anxiety High temperature/sweating Diarrhoea

Answer 648

Graves’ disease (up to 80% of all cases) -> diffused goitre Toxic multinodular goitre Toxic adenoma

Answer 649

Diffuse goitre Thyroid eye disease Acropachy (looks exactly the same as clubbed fingers) Pretibial myxoedema (swelling and red rash of lower leg)

Answer 650

Solitary nodule

Answer 651

Increased free T4 and T3 Suppressed TSH

Answer 652

Increased T4 and T3 (DUE TO) Inappropriately high TSH

Answer 653

Anti thyroid drugs (sometimes partial, sometimes complete and then replace hormones with thyroid meds) Radioiodine (iodine targets thyroid cells so using radioactive targets these cells) Surgery

Answer 654

Thionamides Carbimazole Propylthiouracil (good for women who are pregnant/ wanting to get pregnant)

Answer 655

Agranulocytosis (-> neutropenia = very low white blood cell count)

Answer 656

Fatigue Weight gain Too cold Constipation Slow cerebral ion

Answer 657

Hashimoto’s thyroiditis (autoimmune) Radioiodine therapy Thyroidectomy Hormone resistance Pituitary an hypothalamic disease

Answer 658

High TSH Low free T4 and T3

Answer 659

Inappropriately low TSH considering how low T4 and T3 are

Answer 660

Synthesis levothyroxine (synthetic T4) of a weight based dose (1.6microg per kilo) Also synthetic T3 but on NHS they use T4

Answer 661

Autoimmune where body attacks/makes antibodies for the tyroid Causes HYPERthyroidism

Answer 662

Thyroglobulin Thyroid peroxidase (TPO)

Answer 663

Once called ‘long acting thyroid stimulators’ Now called thyroid stimulating antibodies They are TSH-receptor antibodies

Answer 664

Genetic and environmental Being female Immunoregulatory genes eg HLA-DR3 Stress, iodine intake, smoking

Answer 665

Type 1 diabetes Addison’s Pernicious (harmful) anaemia Vitiligo Slope is Coeliac Hepatitis RA Grave’s

Answer 666

Swelling of the extraocular muscles (Present in most Grave’s patients)

Answer 667

Vasopressin and oxytocin are made in the paraventricular nucleus and supraoptic nucleus They are transported to the posterior pituitary in the axoplasm of the neurons

Answer 668

V1a= binding causes vasoconstriction and therefore increased BP V2= causes reabsorption of water in the renal collecting tubules V1b= binds to the anterior pituitary to cause release of ACTH

Answer 669

Extracellular has much more Na+ than intra Intracellular has much more K+ than extra Extra has a little Ca2+, intra has a little (more) Mg2+ Extracellular has much more Cl- than intra Intracellular has much more phosphate and organic anions than extra Extracellular has some HCO3-, more than intra Intracellular has some protein, more than extra

Answer 670

Makes LESS urine So more reabsorption of water by kidneys

Answer 671

Vasopressin activates V2 receptors in collecting ducts Aquaporin-2 proteins are synthesised and inserted into the apical membrane Permeability of CD is increased Water is reabsorbed and returned to the blood

Answer 672

Concentration of substances in blood/plasma per kilo (Size of particle is not important but number is!) Sodium, potassium, chloride, bicarbonate, urea and glucos are present at high enough concentrations to affect osmolality

Answer 673

The more plasma ADH, the greater the osmolality of urine (ie. The less water, so the more substances per kilo)

Answer 674

Lack of vasopressin= ADH deficiency (cranial diabetes insipidus) = uncommon but life threatening Resistance to action of ADH= ADH resistance (nephrogenic diabetes insipidus) = uncommon but life threatening Too much vasopressin (when it should not be released)= SAID (syndrome of anti-diuretic hormone secretion)= really common but can be life threatening, causes can be ectopic carcinomas

Answer 675

= ADH deficiency and resistance Polyuria Polydipsia No glycosuria Inappropriately dilute urine for plasma osmolality

Answer 676

Acquired causes include tumours, trauma, infection (incl TB, encephalitis, meningitis), inflammation (guillian barre and granuloma), vascular (incl aneurysm, infarction and sickle cell) and idiopathic Primary causes include genetics and developmental disease

Answer 677

= ADH resistance Familial nephrogenic DI is rare but can occur (X-inked or autosomal) Acquired causes incl osmotic diuresis (eg diabetes mellitus), drugs, renal impairment etc

Answer 678

Tests for release of ADH and therefore change in urine osmolality under water deprivation.

Answer 679

A normal response should show an increase in ADH causing an increase in urine osmolality over hours, with a large increase after ~13hrs. An ADH deficiency response would show no increase in urine osmolality until 16hrs. An ADH resistance response would show a very slow, steady and small increase in urine osmolality.

Answer 680

Copeptin is released at a 1:1 ratio with ADH It is measured to see levels of ADH because ADH levels are hard to measure- it has a short half life but copeptin doesn’t and it therefore is measurable

Answer 681

= ADH deficiency Any underlying conditions/causes should be treated Give desmopressin= high acuity at V2 receptors (Tablets of 100-600 mg/day Nasal spray of 10-20 mg/day Injection of 1-2 mg/day)

Answer 682

Non-functioning pituitary adenomas Endocrine active pituitary adenomas Malignant pituitary tumours (functional and non-functional carcinomas) Metastasis in the pituitary (from breast, lung, stomach and kidney) Pituitary cysts

Answer 683

Pituitary cysts (can be arising in the squamous epithelial remnants of Rathke’s pouch) These are benign but often infiltrate surrounding structures

Answer 684

Cysts on the pituitary that arise from remnants of Rathke’s pouch Mostly asymptomatic and small May present with headaches, amenorrhoea, hypopituitarism and hydrocephalus

Answer 685

Common tumours of regions after pituitary adenoma as a complication of radiotherapy Can cause visual and endocrine disturbance

Answer 686

Inflammation of the pituitary gland due to an autoimmune reaction (occurs often in women at the end of/after pregnancy- 6:1 more common in women)

Answer 687

Tumours on the pituitary that are not producing any hormones Often found incidentally Often only found when they grow to a point where they are causing other organs to misfunction = tumour mass effects

Answer 688

Tumour mass effects (eg. Visual field defects, headaches) Hormone excess Hormone deficiency

Answer 689

Cranial nerve palsy/epilepsy Headaches Visual field defects CSF rhinorrhoea (leaking through the nose)

Answer 690

Hydrocortisone (Immediate release hydrocortisone gives a big peak when first taken and goes down so patients are given tablets one after the other every 6 hours with doses getting smaller to mirror the natural levels of cortisol reducing through the day) (Modified release HC has slower release)

Answer 691

Daily tablet 1.6mg/kg/day Start low and increase to mid/upper of reference range

Answer 692

Daily IGF-1 0.2-0.4mg/day for <60yrs 0.1-0.2mg/day for >60yrs

Answer 693

Desmopressin Works immediately- patients see change within days Sub-lingual, oral or sub-cutaneous

Answer 694

Testosterone replacement with gels/orals/injections Oestrogen replacements with oral oestrogen or oestrogen and progesterone

Answer 695

Excess water ( ie not insufficient salt)

Answer 696

<135 mmol/l

Answer 697

Moderate symptoms include headache, irritability, nausea/vomiting, mental slowing, falls, confusion and disorientation Severe symptoms include comas, convulsions and respiratory arrest

Answer 698

Mild: 130-135mmol/l Moderate: 125-129mmol/l Severe: <125mmol/l

Answer 699

Hypovolaemic (low fluid volume) Euvolaemic (normal/level fluid volume) Hypervolaemic (high fluid volume)

Answer 700

Syndrome of inappropriate antidiuresis (Causes 25% of all hyponatraemia) Causes too much ADH

Answer 701

= syndrome of inappropriate antidiuresis Head injury Meningitis Encephalitis Brain tumour/abscess Haemorrhage Guillian barre

Answer 702

= syndrome of inappropriate antidiuresis Pneumonia TB Severe asthma Emphysema

Answer 703

= syndrome of inappropriate antidiuresis Diagnose and trust underlying conditions Restrict fluid If Na is low, give saline on ITU

Answer 704

Very low serum Na+ Hypokalaemia Chronic excess alcohol Malnutrition Liver disease

Answer 705

Competitive antagonist to ADH Licensed to treat SIAD

Answer 706

Damage to nerves caused by diabetes

Answer 707

Causes “glove and stocking” sensory loss Burning Parasthesia (burning/prickling in periphery) Foot ulceration Erectile dysfunction Diarrhoea/constipation/incontinence Falls

Answer 708

In children the over-growth is allowed because bony epiphyses have not yet fused This causes gigantism in children In adults the bony epiphyses have fused so growth is not allowed in the same way

Answer 709

Hypertension Headaches Sleep apnea Insulin-resistant diabetes Arthritis Dental problems due to the overgrowth of the jaw Visual field defects if due to pituitary tumour

Answer 710

Acral enlargement (hands and feet) Arthralgias ( joint pain ) Maxillofacial changes (face/jaw) Hypogonadism symptoms Excessive sweating Headaches

Answer 711

GH is pulsatile and in normal people levels return to almost 0 inbetween pulses GH in acromegaly has many more pulses but will never return to the normal low level inbetween pulses Therefore one large GH measure CANNOT diagnose acromegaly but one very small measure of GH CAN rule out acromegaly

Answer 712

Pituitary surgery Radiotherapy (incl conventional, steriotactic, LINAC, proton beam or gamma knife!) Dopamine agonists can control GH and therefore IGF-1 Somatostatin analogues PEGVISOMANT= GH competitive agonist which prevents GH clearance

Answer 713

Headache Visual field defect (Rare) CSF leak Amenorrhoea Low libido Infertility Hypogonadism (prolactin-mediated supression of gonadotrophins)

Answer 714

Trans-sphenoidal surgery

Answer 715

Medically rather than surgically Dopamine agonists (mainly cabergoline) Shrinks tumours immediately

Answer 716

Cramping in the calf/thigh muscle while walking / not at rest

Answer 717

Diminished or absent pedal (foot) pulses Coolness of the feet and toes Poor skin and nails Absence of hair on feet and legs

Answer 718

To ensure there is no neuropathy or vascular disease Must check for circulation and ulcers, skin cracking and ability to feet pain

Answer 719

Long duration diabetes Poor glycaemic control Pregnancy People on insulin treatment (due to the ischaemic region or the retina)

Answer 720

Once-yearly screening for diabetic retinopathy Takes photographs of the retinas which are graded

Answer 721

Leaking and Occlusion Leakage= basement membrane thickens and pericytes are lost so junctional contact with endothelial cells is reduced Occlusion= combo of cells being lost/thickening leads to ischaemia/ glial cells grow down the capillaries = occlusion Lead to retinal hypoxia

Answer 722

Cannot be reversed, can be managed by laser treatments where abnormal blood vessels are burned

Answer 723

Proteinuria

Answer 724

Thickening of glomerulas Increase glomerular and systematic pressure Increased injury of glomerulus Filtration of proteins/ other molecules that shouldn’t be

Answer 725

Into 5 grades based on glomerular filtration rate Grade 1 being 90-105 ml/min/1.73m^2 Grade 5 being <15 or someone on dialysis

Answer 726

BP control Glycemic control Reduce proteins to prevent proteinuria

Answer 727

Adrenal insufficiency (hypocortisolism)

Answer 728

Hypothalamus releases corticotropin releasing hormone Pituitary releases ACTH Adrenals release cortisol Cortisol inhibits release of both ACTH and CRH

Answer 729

Low at night Builds up from 3am until it peaks at 8/9am ish- whenever you wake up Falls throughout the day

Answer 730

A nucleus within the anterior hypothalamus which has a role in regulating the circadian rhythms of different hormones

Answer 731

Deficiency

Answer 732

Autoimmune TB

Answer 733

Fatigue Weight LOSS Poor recovery from illness

Answer 734

Symptoms: fatigue, weight loss, poor recovery from illness History: TB, post partum haemorrhage, cancer and treatment with steroids Family history of autoimmune Pigmentation (as ACTH acts on melanin receptors) Pallor (pale) Biochemical signs (low Na, high K, eosinophilia and borderline high TSH)

Answer 735

Low Na and High K = due to cortisol is important in excretion of water load AND aldosterone from adrenal glands Eosinophilia (high levels of eosinophils) Borderline elevated TSH (in primary adrenal insufficiency)

Answer 736

Ideally would measure CORTISOL first thing in the morning- when it should be at its highest Do a stimulation test where inject synthetic ACTH You can measure CORTISONE (a derivative of cortisol) in SALIVA- ask people to spit as soon as they wake up

Answer 737

When adrenal glands make so little cortisol and someone has an illness causing the body goes into crisis

Answer 738

Immediate hydrocortisone (100mg IV or IM) Continue 50-100mg hydrocortisone every 6 hours (Hydrocortisone is cortisol) Wean dose down to replacement dose or else you will cause cushing’s (Excess steroid) Sick day rules!?

Answer 739

Have to double your dose of steroids if you are unwell (if in doubt- double dose) If vomiting/ getting more ill have emergency injection of 100mg hydrocortisone IM!!!!! Short term excess steroid is not damaging

Answer 740

Glucocorticoid replacement with daily hydrocortisone (first thing 10mg, 5mg at lunch and dinner) Mineralocorticoid replacement if primary Androgen replacement

Answer 741

They have created a drug (chronocort = efmody) which has an outer layer that cannot allow the drug polymer to escape until it reaches the small bowel = allows slow release over night as opposed to high peaks immediately after taking the drug

Answer 742

Family history Smoking Age

Answer 743

Those that affect supply (anemia, Hypoxemia) Those that affect demand (hypertension, tachyarrythmia) Environmental (stress, exercise, cold weather)

Answer 744

Hypertension Hyperlipidemia Diabetes

Answer 745

Smoking Diet Physical inactivity

Answer 746

Air pollution

Answer 747

Age Sex Ethnicity

Answer 748

Two layers: Visceral single cell (connected to epicardium) Fibrous parietal with attachments that fix the heart in the thorax

Answer 749

Commonly viral (enteroviruses, herpesvirus etc) Bacterial causes incl mycobacterium TB Non-infectious causes incl autoimmune (RA, sjorgren), neoplastic (secondary to lung/breast), metabolic or from trauma

Answer 750

Chest pain which is severe, sharp with rapid onset and relieved by sitting forward Other symptoms that would indicate viral/bacterial infection in some cases

Answer 751

Widespread ST saddle shaped J point elevation PR depression (in leads I, II, III, aVL, aVF and V2-6)

Answer 752

The pressure on the heart when there is a build up of fluid in the pericardial space (Small amounts of fluid removed or added make a large difference)

Answer 753

Because when effusion is chronic the parietal pericardium has time to slowly stretch and build up compliance

Answer 754

Reducing exercise until symptoms resolve NSAIDs in large doses

Answer 755

A sound produced during pericarditis

Answer 756

Build up of substances incl fats and cholesterol on vessel walls

Answer 757

If atherosclerotic plaques rupture they can cause partial of complete arterial blockage -> heart attacks, stroke of gangrene (tissue death)

Answer 758

Age Smoking High serum cholesterol Obesity Diabetes Hypertension Family history

Answer 759

Complex lesion consisting of lipid, necrotic core, connective tissue and fibrous ‘cap’

Answer 760

The theory that atherosclerosis is initiated by an injury to endothelial cells which leads to endothelial dysfunction- signals are then sent to cause circulating leukocytes to accumulate and migrate into the vessel wall -> inflammation (LDLs accumulate in excess witching the arterial wall and undergo oxidation and glycation)

Answer 761

LDLs accumulate in excess witching the arterial wall and undergo oxidation and glycation

Answer 762

After initiation of inflammation, chemoattractants (for leukocytes) are released from the site of injury (causing conc grad)

Answer 763

IL-1 IL-6 IL-8 (TGF B (transforming growth factor beta), Interferons and MCP-1 (monocyte chemoattractant protein -1 which induces IL release) are also present)

Answer 764

The earliest lesion of atherosclerosis Consist of lipids macrophages and T lymphocytes within the intima

Answer 765

The second lesion of atherosclerosis Consists of layers of foam cells (macrophages -> foam cells when they insult LDLs), smooth muscle cells and T lymphocytes Also platelets adhered to vessel wall

Answer 766

3rd stage of atherosclerotic lesion Blood flow is impeded These are prone to rupture Plaques are converted by the fibrous cap (made of collagen and elastin) Lesion contains SMCs, lipid core and necrotic debris, FOAM cells and T lymphocytes

Answer 767

Plaques rupture when the cap becomes weak This may be due to shit in balance of inflammatory conditions

Answer 768

Plaque erosion is in plaques with no/a small lipid core and with more fibrous tissue. Plaque rupture is of plaques rich in inflammatory cells.

Answer 769

Erosions: anti-thrombotic Ruptures= stents

Answer 770

In erosions there is less microvascular damage and better myocardial perfusion In ruptures there is no re-flow after intervention and higher risk of major cardiac event

Answer 771

In erosions there is less microvascular damage and better myocardial perfusion In ruptures there is no re-flow after intervention and higher risk of major cardiac event

Answer 772

Erosions are more common in younger women, smokers and in the summer. Often occur near a bifurcation Plaques occur more with hypertension, diabetes, kidney disease and during the winter

Answer 773

Percutaneous coronary intervention = family of non-invasive procedures that open coronary arteries

Answer 774

It is an irreversible inhibitor of the platelet cycle-oxygenate so helps to reduce risk of cardiac events due to atherosclerosis

Answer 775

Reduce cholesterol synthesis (by inhibiting HMG CoA reductase)

Answer 776

Improve clearance of cholesterol from the blood by inhibiting PCSK9 protein in the liver

Answer 777

Endothelium Macrophages Smooth muscle cells Platelets

Answer 778

Spectrum of acute cardiac conditions from unstable angina to varying degrees of evolving myocardial infarction

Answer 779

ST elevation

Answer 780

ST depression / T wave inversion

Answer 781

No changes!

Answer 782

Cardiac chest pain at rest and new onset

Answer 783

Q wave = ST elevation as usually associated with larger infarcts

Answer 784

ST elevation means MI diagnosis usually Non-ST elevation means there is a retrospective diagnosis of MI maybe due to troponin results or other investigation

Answer 785

The point after the QRS complex where you can see if there is ST elevation/depression or not

Answer 786

PCI if ST elevation 300mg aspirin immediately Pain management

Answer 787

Troponin is a marker for cardiac muscle injury (but no specific to acute coronary syndrome)

Answer 788

A combination of 4 congenital heart defects: Ventricular septal defect Pulmonary stenosis Hypertrophy of right ventricle Overriding aorta

Answer 789

Right ventricle hypertrophy and septal defect means unoxygenated blood from right ventricle passes into the left ventricle

Answer 790

Ventricular septal defect Atrial septal defect Atrio-ventricular septal defects Patent ductus arteriosus Coarctaction of aorta

Answer 791

Abnormal connection between RV and LV (‘hole’ in septum) Blood flows from high pressure LV into low pressure RV

Answer 792

Small skinny baby Breathless Tachycardia Increased resp rate Large heart Murmur

Answer 793

A complication of non-treated ventricular septal defect Causes high pressure pulmonary blood flow and hence damage to pulmonary vasculature as well as high RV pressure and BLUE patient

Answer 794

Abnormal connections between atria (pressure in LA is slightly higher than RA so blood shunts into RA)

Answer 795

Pulmonary flow murmur Delayed closure of pulmonary valve Big pulmonary arteries Big heart

Answer 796

Basically a hole in the very centre of heart Often with Down syndrome Involves A septum and V septum and mitral and tricuspid valves

Answer 797

Types describe the way in which blood is shunted due to the position/shape of any septum: Interatrial Interatrial and interventricular Interventricular

Answer 798

The presence of the ductus arteriosus (meant to disappear in birth)= more common in prem babies DA is a shunt in neonates between aorta and pulmonary vein

Answer 799

Narrowing of the aorta at the site of insertion of the ductus arteriosus

Answer 800

Complete or almost obstruction of aortic flow Needs urgent repair (Murmur)

Answer 801

Surgical or percutaneous (through skin) Either with end to end repair or with a subclavian flap

Answer 802

A normal AV valve has 3 cusps, in bicuspid there are 2, they degenerate and becomes regurgitate earlier than normal valves

Answer 803

Narrowing of pulmonary valves and of the right ventricle

Answer 804

Right ventricular failure Poor pulmonary blood flow RV hypertrophy Valve regurgitation

Answer 805

With balloon valvuloplasty/ open valvotomy/ shunt

Answer 806

Age Smoking Family history

Answer 807

Those that affect supply of oxygen to the heart (anemia, hypoxemia) Those that affect demand of oxygen (hypertension, tachyarrhythmia) Environmental factors (exercise, stress, cold weather)

Answer 808

Crescendo angina (gets worse and worse) Unstable angina= pain at rest- bad Microvascular angina= angina when the normal coronary arteries aren’t to blame

Answer 809

ASTHMA! Cannot be given to people with asthma

Answer 810

Beta blockers (slow HR) Nitrates (incl GTN spray) Statins Calcium channel blockers ACE inhibitors Aspirin

Answer 811

When new vessels are surgically placed to bypass ones that are not working properly- can either be with veins from leg or with internal mammary artery

Answer 812

The heart comprises of a single chamber until the 5th week of gestation where it becomes divided by intra-atria and intra-ventricular septa The inta-v septum grows upwards from the apex to produce the 4 chambers

Answer 813

VSD, ASD, PDA

Answer 814

Tetralogy of fallot, tricuspid atresia

Answer 815

Stiffening of the heart either primary or secondary to aortic stenosis and coarctation.

Answer 816

Normal anatomy of the heart but with rightward orientation- often associated with other organ isomerism

Answer 817

Reperfusion of tissue following ischaemia once allowed by clot-busters or angioplasty.

Answer 818

Reperfusion of completely infarcted tissue can produce significant haemorrhage and more injury

Answer 819

A dilation of part of the myocardial wall (usually associated with fibrosis and atrophy of myocytes).\dilation of thin walled sac allows blood stasis and thrombosis

Answer 820

Pericarditis

Answer 821

Cardiac enlargement due to hypertension and no other cause

Answer 822

Initially increased myocyte size, squaring of the nuclei and a slight increase of the interstitial fibrous tissue

Answer 823

Right ventricular hypertrophy/dilation due to pulmonary hypertension (disproportionate to the left). Progressive features incl right sided heart failure and oedema

Answer 824

Infective process involving cardiac valves causing valve distortion and disruption with cardiac function

Answer 825

Blocks platelet release of thromboxane A2 (a chemical which promotes the positive feedback loop for coagulation)

Answer 826

Anti-platelets

Answer 827

Anti-platelets (used in higher risk settings)

Answer 828

Heparin or low-molecular weight heparin

Answer 829

Pain relief if necessary Aspirin and p2Y12 inhibitors for anti-platelets Anticoagulants Anti-angina therapy (incl beta blockers etc) Secondary prevention

Answer 830

PCI (stent)

Answer 831

Similar with unstable angina- most commonly PCI in a less time-critical way Sometimes coronary bypass graft

Answer 832

Infective process involving cardiac valves causing valve distortion and disruption with cardiac function

Answer 833

Inflammation of the myocardium usually associated with muscle cell necrosis and degeneration. Most commonly viral.

Answer 834

Unexplained primary cardiac hypertrophy- genetic affecting 1/500 people

Answer 835

Hearts are stiffer and less elastic so are harder to fill in diastole. This is due to disorganisation of myocytes.

Answer 836

Thin cardiac walls caused by cytoskeletal gene mutations. Causes heart failure.

Answer 837

Programmed replacement of cardiac myocytes with fibrous/fatty cells caused by desmosome gene mutations

Answer 838

A group of diseases where heart has more dilation- has classic low voltage ECG.

Answer 839

Long QT Short QT Brugada CPVT

Answer 840

A lot of drugs prolong QT and therefore can kill people already suffering with long QT!

Answer 841

The cause of 75% of cardiac tumours Normally in the atria

Answer 842

Paediatric cardiac tumour

Answer 843

Pericardial effusion Haemopericardium (direct bleeding from vessels through ventricle wall following MI) Cardiac tamponade Pericarditis

Answer 844

Conversion of plasminogen into plasmin which acts on fibrin to produce fibrin degradation products

Answer 845

A vascular dilation in the cerebral circulation (in the circle of willis)

Answer 846

A tear in the aorta (mostly above the aortic ring)

Answer 847

Enlarged torturous vein predominantly in the superficial leg veins Causes progressive incompetence of valves with back pressure

Answer 848

Haemangioma Glomus tumour Haemangioendothelioma Angiosarcoma Kaposi’s sarcoma

Answer 849

It is linked to HIV and AIDS- human herpes virus 8 = purple/brown nodule often on the skin

Answer 850

Inherited abnormality of cholesterol metabolism or sometimes problems with LDL receptors. Leads to serious premature coronary/vascular disease

Answer 851

ACE inhibitors ARBs (angiotensin II receptor blockers) Calcium channel blockers Beta-adrenoreceptor blockers Diuretics

Answer 852

Narrowing of the aortic valves

Answer 853

Syncope on exertion Angina Dyspnoea (shortness of breath) on exertion

Answer 854

An ejection murmur Crescendo- decrescendo

Answer 855

AS is graded based on AVA (valve area)

Answer 856

Rate control Anticoagulants Regular ECHOs IE prophylaxis

Answer 857

Backflow of blood from LV to LA during systole

Answer 858

LA enlargement LV hypertrophy

Answer 859

A pansystolic murmur at the apex

Answer 860

Exertion dyspnoea Compensatory phase of 10-15 which causes mechanisms incl LA enlargement and LV hypertrophy

Answer 861

Leakage of blood into the LV during diastole

Answer 862

Bicuspid aortic valves Rheumatic causes Infective endocarditis

Answer 863

Diastolic decrescendo murmur at the left sternal border/ systolic ejection murmur

Answer 864

Exertion dyspnoea moving to orthopnea (dyspnoea when lying down) moving do nocturnal dyspnoea

Answer 865

Enlargement of the aortic root, enlarged cardiac silhouette

Answer 866

Obstruction of the LV inflow that prevents proper LV filling during diastole

Answer 867

99% caused by rheumatic carditis Sometimes caused by infective endocarditis

Answer 868

Diastolic low pitched murmur like a rumble which is most prominent at the apex

Answer 869

Mitral facies= pink/purple patches on the cheeks

Answer 870

LA enlargement and maybe afib

Answer 871

Anything to slow heart rate/ reduce fluid overload- beta blockers, diuretics etc IE prophylaxis

Answer 872

Inability of the heart to deliver blood at a rate which meets the requirements of the metabolising tissues despite normal or increased cardiac filling pressures

Answer 873

Valve disease Systolic dysfunction Arrhythmia Diastolic dysfunction

Answer 874

Class I= no limitation/asymptomatic Class II= slight limitation Class III= marked limitation/ symptomatically moderate Class IV= inability to carry out any physical activity without discomfort/ symptomatically severe

Answer 875

ACE inhibitors ARBs Beta blockers Diuretics Calcium channel blockers

Answer 876

Ramipril Perindopril Enalapril

Answer 877

Candesartan Valsartan Losartan

Answer 878

Propranolol Bisoprolol Metaprolol

Answer 879

Dihydropyridines (peripheral arterial vasodilators) eg amlodopine Phenylalkylamines (negatively chonotropic and ionotropic) eg verapamil Benzothiazepines (heart/peripheral vascular effects) eg diltiazem

Answer 880

Thiazides- act on distal tubules (eg bendroflumethiazide) Loop duiretics (eg furosemide) Potassium-sparing duiretics (eg spironolactone) Aldosterone agonists

Answer 881

Hypotension Acute renal failure (due to low pressure in efferent arterioles) Hyperkalaemia Fetal abnormalities

Answer 882

Hypotension Hyperkalaemia Renal dysfunction

Answer 883

Due to peripheral vasodilation= headaches, oedema, flushing Due to negative chonotropic effects= bradycardia, AV block Due to negative ionotropic effects= worsening of cardiac failure

Answer 884

Fatigue Headaches Breadycardia Hypotension (from bradycardia) Cold peripheries Erectile dysfunction (DON’T USE WITH ASTHMA!!!)

Answer 885

Hypovolaemia Hypotension Hypo- kalaemia, natramia, magnesaemia, calcaemia Raised uric acid Erectile dysfunction Impaired glucose tolerance

Answer 886

Class I= sodium channel blockers (Ia: disopyramdide, Ib: lidocaine, Ic: propafenone) Class II: beta adrenoreceptor agonists (non selective= propranalol, B1 selective= bisoprolol) Class III= prolon action potential (amiodarone) Class IV= calcium channel blockers (verapamil)

Answer 887

Haemoglobin of lower than 130 in men and 120 in women

Answer 888

Haemolytic Aplastic Microcytic Macrocytic Normocytic

Answer 889

Increased breakdown of RBCs

Answer 890

Decreased RBCs, WCs and platelets

Answer 891

Reduced mean RBC volume

Answer 892

Increased mean RBC volume (seen in haemolytic anaemia because new fresher RBCs are bigger than old ones- that are being killed off)

Answer 893

Anaemia with normal RBC mean volume (may be a mix of macro and micro?)

Answer 894

Occurs in iron defficiency and/or thalassaemia Low ferratin, low iron, raised transferrin and low transferrin saturation May be caused by infection, inflammation, neoplasia or sickle cell

Answer 895

Folate and/or B12 deficiency Seen in haemolytic anaemia May be caused by pernicious anaemia (lack of intrinsic factor so B12 can’t be absorbed)

Answer 896

Tachycardia, skin pallor, conjunctiva pallor, intermittent claudication, jaundice, koilonychia (spoon shaped nails seen in iron deficiency)

Answer 897

Neutrophilia: infection/inflammation/CML Neutropenia: antibiotics/chemotherapy/marrow failure/liver disease

Answer 898

Thrombocytosis: infection/inflammation/tissue injury/splenectomy/thrombocythemia Thrombocytopenia: production failure (from marrow failure or leptospirosis) or increased removal

Answer 899

Lymphpcytosis: EBV/CMV/hepatitis/malignancy or stress Lymphocytopenia: steroids/HIV/post viral/marrow failure/chemotherapy

Answer 900

Sickle cell Thrombotic thrombocytopenic purpura (TTP) Immune thrombocytopenic purpura (ITP) Disseminated intravascular coagulation (DIC) Haemophilia Von willebrand’s

Answer 901

Bone and joint pain Infection Dyspnoea Cough Hypoxia (Stroke)

Answer 902

Solubility test Haemoglobin electrophoresis

Answer 903

Fatigue Fever Jaundice (Raised WBCs, low platelets, low Hb)

Answer 904

Haemophilia A= factor 8 deficiency Haemophilia B= factor 9 deficiency Presents with soft tissue bleeding into muscles, joints of haemotoma formation

Answer 905

Defect in quality or quantity of Von willibrand’s factor (which protects breakdown of factor 8) = primarily a disorder of primary haemostasis

Answer 906

Acute lymphoblastic Chronic lymphoblastic Acute myeloid Chronic myeloid

Answer 907

Children years 0-4

Answer 908

Anaemia Thrombocytopenia Neutropenia

Answer 909

Anaemia Thrombocytopenia

Answer 910

Anaemia Thrombocytopenia Leukocytosis

Answer 911

Anaemia Thrombocytopenia Leukocytosis

Answer 912

Acute myeloid

Answer 913

Chronic lymphoblastic

Answer 914

Reed sternberg cells which are present in hodgkin’s!!!

Answer 915

1. Disease in one area only 2. Disease in two or more areas on the same side of the diaphragm 3. Disease in two or more areas on both sides of the diaphragm 4. Spread beyond the lymph nodes

Answer 916

Cancer of differentiated B-lymphocytes (plasma cells) Accumulation of malignant plasma cells in the bone marrow -> progressive bone marrow failure

Answer 917

CRAB Calcium is high Renal impairment Anaemia Bone lesions

Answer 918

High concentration of erythrocytes in the blood (CONCENTRATION)

Answer 919

Relative= normal no of erythrocytes but reduced plasma Absolute= increased no of erythrocytes - primary = polycythaemia Vera (abnormality of bone marrow) - secondary = overstimulation of bone marrow by external factor

Answer 920

Myeloproliferative neoplasm (Abnormality in the bone marrow leading to overproduction of erythrocytes)

Answer 921

Headaches, dizziness, fatigue, blurred vision, red skin, hypertension, hepatosplenomegaly, itching

Answer 922

The following all raised: Haemoglobin, haematocrit, white cell count, platelet count Decreased serum erythropoietin

Answer 923

Polycythaemia Vera

Answer 924

Protein synthesis Glucose & fat metabolism Defence (kupffer cells) Detoxification and excretion

Answer 925

Blood enters via the portal vein and hepatic artery Flows into a system of sinusoids Exits via hepatic/central vein

Answer 926

Malaise Nausea Anorexia Jaundice (Confusion, bleeding, liver pain, hypoglycaemia)

Answer 927

Ascites Oedema Haematemesis Malaise Easy bruising Hepatomegaly

Answer 928

Serum bilirubin Albumin Prothrombin time

Answer 929

Jaundice of unconjugated bilirubin= pre-hepatic Jaundice of conjugated bilirubin= hepatic or post hepatic

Answer 930

Normal urine Normal stool Normal liver tests

Answer 931

Dark urine Pale stool (Itching) Abnormal liver tests

Answer 932

Intra hepatic: hepatolithiasis Extrahepatic: choledocholithaisis Gallbladder stones: cholecystolithiasis

Answer 933

70% cholesterol 30% pigment +/- calcium

Answer 934

Biliary pain No cholesystitis Obstructive jaundice Cholangitis Pancreatitis

Answer 935

Biliary pain Cholecystitis (Obstructive jaundice) No cholangitis No pancreatitis

Answer 936

Laparoscopic cholecystectomy Bile acid dissolution therapy

Answer 937

ECRP (endoscopic retrograde cholangiopancreatography) with sphincterectomy and removal/crushing/placement (Surgery for large stones)

Answer 938

Spider naevus (small dilated blood vessels on surface of skin) Ascites

Answer 939

Ascites= fluid retention in abdomen Caused by portal hypertension from increased hepatic resistance Managed by fluid and salt reduction, diuretics, large-volume paracentesis (fluid removal)

Answer 940

Alcohol Non-alcoholic steatohepatitis Viral hepatitis (B and C) Immune (incl auto) Metabolic (incl haemochromatosis and Wilson’s) Vascular

Answer 941

Cirrhosis Fibrosis Portal vein thrombosis

Answer 942

ACE inhibitors Aminoglycosides

Answer 943

Malnutrition Coagulopathy (bc coag factors are synthesised in liver?) Infections Hypo- (natraemia, kalaemia, glycaemia)

Answer 944

Antinuclear Anti-smooth muscle Liver-kidney microsome

Answer 945

Chronic disease where bile ducts are slowly destroyed (unknown pathogenesis)

Answer 946

Asymptomatically Itching Fatigue (-> autonomic neuropathy) Dry eyes Joint pain Variceal bleeding Liver pain

Answer 947

Inflammation casing scarring within the bile ducts leading to areas of narrowing and sometimes gallstones

Intro To Clinical Sciences Flashcards

(997 cards)